Journal of Clinical and Diagnostic Research, ISSN - 0973 - 709X

Users Online : 214606

References
Article in PDF How to Cite Citation Manager Readers' Comments (0) Audio Visual Article Statistics Link to PUBMED Print this Article Send to a Friend
Advertisers Access Statistics Resources

Dr Mohan Z Mani

"Thank you very much for having published my article in record time.I would like to compliment you and your entire staff for your promptness, courtesy, and willingness to be customer friendly, which is quite unusual.I was given your reference by a colleague in pathology,and was able to directly phone your editorial office for clarifications.I would particularly like to thank the publication managers and the Assistant Editor who were following up my article. I would also like to thank you for adjusting the money I paid initially into payment for my modified article,and refunding the balance.
I wish all success to your journal and look forward to sending you any suitable similar article in future"



Dr Mohan Z Mani,
Professor & Head,
Department of Dermatolgy,
Believers Church Medical College,
Thiruvalla, Kerala
On Sep 2018




Prof. Somashekhar Nimbalkar

"Over the last few years, we have published our research regularly in Journal of Clinical and Diagnostic Research. Having published in more than 20 high impact journals over the last five years including several high impact ones and reviewing articles for even more journals across my fields of interest, we value our published work in JCDR for their high standards in publishing scientific articles. The ease of submission, the rapid reviews in under a month, the high quality of their reviewers and keen attention to the final process of proofs and publication, ensure that there are no mistakes in the final article. We have been asked clarifications on several occasions and have been happy to provide them and it exemplifies the commitment to quality of the team at JCDR."



Prof. Somashekhar Nimbalkar
Head, Department of Pediatrics, Pramukhswami Medical College, Karamsad
Chairman, Research Group, Charutar Arogya Mandal, Karamsad
National Joint Coordinator - Advanced IAP NNF NRP Program
Ex-Member, Governing Body, National Neonatology Forum, New Delhi
Ex-President - National Neonatology Forum Gujarat State Chapter
Department of Pediatrics, Pramukhswami Medical College, Karamsad, Anand, Gujarat.
On Sep 2018




Dr. Kalyani R

"Journal of Clinical and Diagnostic Research is at present a well-known Indian originated scientific journal which started with a humble beginning. I have been associated with this journal since many years. I appreciate the Editor, Dr. Hemant Jain, for his constant effort in bringing up this journal to the present status right from the scratch. The journal is multidisciplinary. It encourages in publishing the scientific articles from postgraduates and also the beginners who start their career. At the same time the journal also caters for the high quality articles from specialty and super-specialty researchers. Hence it provides a platform for the scientist and researchers to publish. The other aspect of it is, the readers get the information regarding the most recent developments in science which can be used for teaching, research, treating patients and to some extent take preventive measures against certain diseases. The journal is contributing immensely to the society at national and international level."



Dr Kalyani R
Professor and Head
Department of Pathology
Sri Devaraj Urs Medical College
Sri Devaraj Urs Academy of Higher Education and Research , Kolar, Karnataka
On Sep 2018




Dr. Saumya Navit

"As a peer-reviewed journal, the Journal of Clinical and Diagnostic Research provides an opportunity to researchers, scientists and budding professionals to explore the developments in the field of medicine and dentistry and their varied specialities, thus extending our view on biological diversities of living species in relation to medicine.
‘Knowledge is treasure of a wise man.’ The free access of this journal provides an immense scope of learning for the both the old and the young in field of medicine and dentistry as well. The multidisciplinary nature of the journal makes it a better platform to absorb all that is being researched and developed. The publication process is systematic and professional. Online submission, publication and peer reviewing makes it a user-friendly journal.
As an experienced dentist and an academician, I proudly recommend this journal to the dental fraternity as a good quality open access platform for rapid communication of their cutting-edge research progress and discovery.
I wish JCDR a great success and I hope that journal will soar higher with the passing time."



Dr Saumya Navit
Professor and Head
Department of Pediatric Dentistry
Saraswati Dental College
Lucknow
On Sep 2018




Dr. Arunava Biswas

"My sincere attachment with JCDR as an author as well as reviewer is a learning experience . Their systematic approach in publication of article in various categories is really praiseworthy.
Their prompt and timely response to review's query and the manner in which they have set the reviewing process helps in extracting the best possible scientific writings for publication.
It's a honour and pride to be a part of the JCDR team. My very best wishes to JCDR and hope it will sparkle up above the sky as a high indexed journal in near future."



Dr. Arunava Biswas
MD, DM (Clinical Pharmacology)
Assistant Professor
Department of Pharmacology
Calcutta National Medical College & Hospital , Kolkata




Dr. C.S. Ramesh Babu
" Journal of Clinical and Diagnostic Research (JCDR) is a multi-specialty medical and dental journal publishing high quality research articles in almost all branches of medicine. The quality of printing of figures and tables is excellent and comparable to any International journal. An added advantage is nominal publication charges and monthly issue of the journal and more chances of an article being accepted for publication. Moreover being a multi-specialty journal an article concerning a particular specialty has a wider reach of readers of other related specialties also. As an author and reviewer for several years I find this Journal most suitable and highly recommend this Journal."
Best regards,
C.S. Ramesh Babu,
Associate Professor of Anatomy,
Muzaffarnagar Medical College,
Muzaffarnagar.
On Aug 2018




Dr. Arundhathi. S
"Journal of Clinical and Diagnostic Research (JCDR) is a reputed peer reviewed journal and is constantly involved in publishing high quality research articles related to medicine. Its been a great pleasure to be associated with this esteemed journal as a reviewer and as an author for a couple of years. The editorial board consists of many dedicated and reputed experts as its members and they are doing an appreciable work in guiding budding researchers. JCDR is doing a commendable job in scientific research by promoting excellent quality research & review articles and case reports & series. The reviewers provide appropriate suggestions that improve the quality of articles. I strongly recommend my fraternity to encourage JCDR by contributing their valuable research work in this widely accepted, user friendly journal. I hope my collaboration with JCDR will continue for a long time".



Dr. Arundhathi. S
MBBS, MD (Pathology),
Sanjay Gandhi institute of trauma and orthopedics,
Bengaluru.
On Aug 2018




Dr. Mamta Gupta,
"It gives me great pleasure to be associated with JCDR, since last 2-3 years. Since then I have authored, co-authored and reviewed about 25 articles in JCDR. I thank JCDR for giving me an opportunity to improve my own skills as an author and a reviewer.
It 's a multispecialty journal, publishing high quality articles. It gives a platform to the authors to publish their research work which can be available for everyone across the globe to read. The best thing about JCDR is that the full articles of all medical specialties are available as pdf/html for reading free of cost or without institutional subscription, which is not there for other journals. For those who have problem in writing manuscript or do statistical work, JCDR comes for their rescue.
The journal has a monthly publication and the articles are published quite fast. In time compared to other journals. The on-line first publication is also a great advantage and facility to review one's own articles before going to print. The response to any query and permission if required, is quite fast; this is quite commendable. I have a very good experience about seeking quick permission for quoting a photograph (Fig.) from a JCDR article for my chapter authored in an E book. I never thought it would be so easy. No hassles.
Reviewing articles is no less a pain staking process and requires in depth perception, knowledge about the topic for review. It requires time and concentration, yet I enjoy doing it. The JCDR website especially for the reviewers is quite user friendly. My suggestions for improving the journal is, more strict review process, so that only high quality articles are published. I find a a good number of articles in Obst. Gynae, hence, a new journal for this specialty titled JCDR-OG can be started. May be a bimonthly or quarterly publication to begin with. Only selected articles should find a place in it.
An yearly reward for the best article authored can also incentivize the authors. Though the process of finding the best article will be not be very easy. I do not know how reviewing process can be improved. If an article is being reviewed by two reviewers, then opinion of one can be communicated to the other or the final opinion of the editor can be communicated to the reviewer if requested for. This will help one’s reviewing skills.
My best wishes to Dr. Hemant Jain and all the editorial staff of JCDR for their untiring efforts to bring out this journal. I strongly recommend medical fraternity to publish their valuable research work in this esteemed journal, JCDR".



Dr. Mamta Gupta
Consultant
(Ex HOD Obs &Gynae, Hindu Rao Hospital and associated NDMC Medical College, Delhi)
Aug 2018




Dr. Rajendra Kumar Ghritlaharey

"I wish to thank Dr. Hemant Jain, Editor-in-Chief Journal of Clinical and Diagnostic Research (JCDR), for asking me to write up few words.
Writing is the representation of language in a textual medium i e; into the words and sentences on paper. Quality medical manuscript writing in particular, demands not only a high-quality research, but also requires accurate and concise communication of findings and conclusions, with adherence to particular journal guidelines. In medical field whether working in teaching, private, or in corporate institution, everyone wants to excel in his / her own field and get recognised by making manuscripts publication.


Authors are the souls of any journal, and deserve much respect. To publish a journal manuscripts are needed from authors. Authors have a great responsibility for producing facts of their work in terms of number and results truthfully and an individual honesty is expected from authors in this regards. Both ways its true "No authors-No manuscripts-No journals" and "No journals–No manuscripts–No authors". Reviewing a manuscript is also a very responsible and important task of any peer-reviewed journal and to be taken seriously. It needs knowledge on the subject, sincerity, honesty and determination. Although the process of reviewing a manuscript is a time consuming task butit is expected to give one's best remarks within the time frame of the journal.
Salient features of the JCDR: It is a biomedical, multidisciplinary (including all medical and dental specialities), e-journal, with wide scope and extensive author support. At the same time, a free text of manuscript is available in HTML and PDF format. There is fast growing authorship and readership with JCDR as this can be judged by the number of articles published in it i e; in Feb 2007 of its first issue, it contained 5 articles only, and now in its recent volume published in April 2011, it contained 67 manuscripts. This e-journal is fulfilling the commitments and objectives sincerely, (as stated by Editor-in-chief in his preface to first edition) i e; to encourage physicians through the internet, especially from the developing countries who witness a spectrum of disease and acquire a wealth of knowledge to publish their experiences to benefit the medical community in patients care. I also feel that many of us have work of substance, newer ideas, adequate clinical materials but poor in medical writing and hesitation to submit the work and need help. JCDR provides authors help in this regards.
Timely publication of journal: Publication of manuscripts and bringing out the issue in time is one of the positive aspects of JCDR and is possible with strong support team in terms of peer reviewers, proof reading, language check, computer operators, etc. This is one of the great reasons for authors to submit their work with JCDR. Another best part of JCDR is "Online first Publications" facilities available for the authors. This facility not only provides the prompt publications of the manuscripts but at the same time also early availability of the manuscripts for the readers.
Indexation and online availability: Indexation transforms the journal in some sense from its local ownership to the worldwide professional community and to the public.JCDR is indexed with Embase & EMbiology, Google Scholar, Index Copernicus, Chemical Abstracts Service, Journal seek Database, Indian Science Abstracts, to name few of them. Manuscriptspublished in JCDR are available on major search engines ie; google, yahoo, msn.
In the era of fast growing newer technologies, and in computer and internet friendly environment the manuscripts preparation, submission, review, revision, etc and all can be done and checked with a click from all corer of the world, at any time. Of course there is always a scope for improvement in every field and none is perfect. To progress, one needs to identify the areas of one's weakness and to strengthen them.
It is well said that "happy beginning is half done" and it fits perfectly with JCDR. It has grown considerably and I feel it has already grown up from its infancy to adolescence, achieving the status of standard online e-journal form Indian continent since its inception in Feb 2007. This had been made possible due to the efforts and the hard work put in it. The way the JCDR is improving with every new volume, with good quality original manuscripts, makes it a quality journal for readers. I must thank and congratulate Dr Hemant Jain, Editor-in-Chief JCDR and his team for their sincere efforts, dedication, and determination for making JCDR a fast growing journal.
Every one of us: authors, reviewers, editors, and publisher are responsible for enhancing the stature of the journal. I wish for a great success for JCDR."



Thanking you
With sincere regards
Dr. Rajendra Kumar Ghritlaharey, M.S., M. Ch., FAIS
Associate Professor,
Department of Paediatric Surgery, Gandhi Medical College & Associated
Kamla Nehru & Hamidia Hospitals Bhopal, Madhya Pradesh 462 001 (India)
E-mail: drrajendrak1@rediffmail.com
On May 11,2011




Dr. Shankar P.R.

"On looking back through my Gmail archives after being requested by the journal to write a short editorial about my experiences of publishing with the Journal of Clinical and Diagnostic Research (JCDR), I came across an e-mail from Dr. Hemant Jain, Editor, in March 2007, which introduced the new electronic journal. The main features of the journal which were outlined in the e-mail were extensive author support, cash rewards, the peer review process, and other salient features of the journal.
Over a span of over four years, we (I and my colleagues) have published around 25 articles in the journal. In this editorial, I plan to briefly discuss my experiences of publishing with JCDR and the strengths of the journal and to finally address the areas for improvement.
My experiences of publishing with JCDR: Overall, my experiences of publishing withJCDR have been positive. The best point about the journal is that it responds to queries from the author. This may seem to be simple and not too much to ask for, but unfortunately, many journals in the subcontinent and from many developing countries do not respond or they respond with a long delay to the queries from the authors 1. The reasons could be many, including lack of optimal secretarial and other support. Another problem with many journals is the slowness of the review process. Editorial processing and peer review can take anywhere between a year to two years with some journals. Also, some journals do not keep the contributors informed about the progress of the review process. Due to the long review process, the articles can lose their relevance and topicality. A major benefit with JCDR is the timeliness and promptness of its response. In Dr Jain's e-mail which was sent to me in 2007, before the introduction of the Pre-publishing system, he had stated that he had received my submission and that he would get back to me within seven days and he did!
Most of the manuscripts are published within 3 to 4 months of their submission if they are found to be suitable after the review process. JCDR is published bimonthly and the accepted articles were usually published in the next issue. Recently, due to the increased volume of the submissions, the review process has become slower and it ?? Section can take from 4 to 6 months for the articles to be reviewed. The journal has an extensive author support system and it has recently introduced a paid expedited review process. The journal also mentions the average time for processing the manuscript under different submission systems - regular submission and expedited review.
Strengths of the journal: The journal has an online first facility in which the accepted manuscripts may be published on the website before being included in a regular issue of the journal. This cuts down the time between their acceptance and the publication. The journal is indexed in many databases, though not in PubMed. The editorial board should now take steps to index the journal in PubMed. The journal has a system of notifying readers through e-mail when a new issue is released. Also, the articles are available in both the HTML and the PDF formats. I especially like the new and colorful page format of the journal. Also, the access statistics of the articles are available. The prepublication and the manuscript tracking system are also helpful for the authors.
Areas for improvement: In certain cases, I felt that the peer review process of the manuscripts was not up to international standards and that it should be strengthened. Also, the number of manuscripts in an issue is high and it may be difficult for readers to go through all of them. The journal can consider tightening of the peer review process and increasing the quality standards for the acceptance of the manuscripts. I faced occasional problems with the online manuscript submission (Pre-publishing) system, which have to be addressed.
Overall, the publishing process with JCDR has been smooth, quick and relatively hassle free and I can recommend other authors to consider the journal as an outlet for their work."



Dr. P. Ravi Shankar
KIST Medical College, P.O. Box 14142, Kathmandu, Nepal.
E-mail: ravi.dr.shankar@gmail.com
On April 2011
Anuradha

Dear team JCDR, I would like to thank you for the very professional and polite service provided by everyone at JCDR. While i have been in the field of writing and editing for sometime, this has been my first attempt in publishing a scientific paper.Thank you for hand-holding me through the process.


Dr. Anuradha
E-mail: anuradha2nittur@gmail.com
On Jan 2020

Important Notice

Reviews
Year : 2009 | Month : December | Volume : 3 | Issue : 6 | Page : 1953 - 1967 Full Version

Health benefits of Conjugated linoleic acid: A Review


Published: December 1, 2009 | DOI: https://doi.org/10.7860/JCDR/2009/.614
KUMAR R *, BHATIA A **, ARORA D ***

*(Lecturer) Department of Microbiology, Adesh Medical College and Hospital.Bhatinda, Punjab, India-151001**(Prof.)Department of Biotechnology,Punjabi University, Patiala Punjab-147002. (India).***(Asst. Prof.) Department of Microbiology Adesh Medical College and Hospital. Bhatinda, Punjab -151001 (India).

Correspondence Address :
Dr. Rajiv Kumar (Lecturer)Department of Microbiology,Adesh Medical College and Hospital.Bhatinda, Punjab, India-151001.Tel: +91-9915022267,Fax: +91-0164 2742902 E-mail: r.chawla@mail.com

Introduction
Conjugated linoleic acid
Conjugated linoleic acid (CLA) is a generic name for a mixture of isomers of linoleic acid with conjugated double bonds. The double bonds can be in several possible positions either as cis or trans isomers. Double bonds of CLA are mainly found at positions 9 and 11, or 10 and 12 (Ha et al., 1987), while isomers having double bonds at other positions also have been reported (Christie et al., 1997). Several scientists, based on studies primarily in animal models, have suggested that CLA has potential health or nutritional effects, including anti carcinogenic activity (Ha et al., 1990), anti atherogenic activity (Lee et al., 1994; Pariza et al.,1996), the ability to reduce the catabolic effects of immune stimulation (Cook et al., 1993), and the ability to reduce body fat (Pariza et al., 1996) Of the individual isomers of CLA, cis-9, trans-11-octadecadienoic acid has been implicated as the most biologically active because it is the predominant isomer incorporated into the phospholipids of cell membranes (Ip et al., 1994). The cis-9, trans-11 CLA isomer also is the predominant isomer found in the diet. On the other hand probiotics (lactic acid bacillus) have been reported with many health benefits. The Health impact with the consumption of microflora consisting of probioics is reported in humans (Isolauri, 2001; Kumar et al., 2002; Liu et al., 2007; Maassen and Claassen 2008) and in animals (Gill et al., 2000; Wollowski et al., 2001; Peng et al., 2007; Yadav et al., 2007). Different bacteria have different actions in different disease states, taking into account that some disease states are better treated with combination of bacteria.

Various Health Effects Of Probiotics Are :
Reduction in Serum Cholesterol, Improvement in lactose Intolerance and Calcium malabsorption, Anti-mutagenic properties, Effectiveness against Diarrhoea, Helicobacter pylori infection, Inflammatory Bowel Disease (IBD), Genitourinary Tract infection (GTI), Calcium Oxalate Stone disease (COSD), Allergies/Eczema, Inflammation/Arthritis, HIV/Compromised Immunity.

Source of CLA
Food products from ruminants, particularly dairy products, are the major dietary source of CLA for humans. They are intermediates in the bio-hydrogenation of linoleic acid, and it is generally accepted that CLA in ruminants originate from the incomplete bio-hydrogenation of the unsaturated fatty acid linoleic acid by rumen bacteria (Kelly et al., 1998). However, it has been demonstrated that cows also can synthesize CLA from trans-11-octadecenoic acid, another intermediate in the rumen bio- hydrogenation process (Kim and Liu, 2000).

Information is lacking on CLA levels required by humans, but it is estimated from animal studies that a daily intake of 3 g/d may be effective for cancer prevention (Ip et al., 1994). Dietary sources of CLA include milk fat, natural and processed cheeses, meat products, and plant oil (Ha et al., 1989; Shanta et al., 1992). Animal sources are richer in CLA than plant sources, and in general, foods from ruminants contain more CLA than foods from non ruminants. Considerable research has been conducted on the CLA content and isomer distribution in cow’s milk. The wide variation of CLA content in dairy products also may be due to processing parameters such as different heat treatment procedures during pasteurization. The CLA content in yogurt or cheese can be increased by action of the starter cultures (Lin et al., 1999).

Jiang et al. (1998) reported the formation of CLA from linoleic acid by Propionibacterium freudenreichii. Their study also included seven cultures of lactobacilli, none of which were found to form CLA. Lin et al. (1999), Lin (2000), and Ogawa et al. (2001) reported the production of CLA from free linoleic acid by Lactobacillus acidophilus. Each study included one strain, and in all cases the entire culture (i.e., growth medium plus cells) was assayed for CLA. Kishino et al. (2002) found that washed cells of Lactobacillus plantarum formed high levels of CLA from free linoleic acid upon extended incubation. They indicated most of the CLA for this culture was associated with the bacterial cells.

Conjugated Linoleic Acid Also Have Many Health Benefits. Which are described as follows:
Human Tissue.
Anti-Carcinogenic.
Anti-Atherogenic.
Anti-Diabetic.
Bone formation.
Immuno modulatory properties.
Gene Expression.
Anti Oxidant activity.

CLA in Human Tissue:
Cawood et al. (1983) studied low concentrations of CLA are found in human blood and tissues. The author suggested that CLA may be produced in vivo from free radical-mediated oxidation of linoleic acid.

Harrison et al.(1985) investigated the free radical species and subsequent diene conjugation produces an linoleic acid (LA) lipid radical with conjugated diene structure. In the presence of protein, the LA radical may react with protein instead of molecular oxygen, giving rise to a CLA molecule and a protein radical. CLA in human tissues may be derived from dietary sources, such as fried ground beef and dairy products. Blood CLA levels have been increased in human subjects by feeding CLA-rich diets.

Huang et al. (1994) studied on nine men, plasma CLA increased 19% to 27% feeding four weeks of cheddar cheese, but no appreciable changes in linoleic and arachidonic acids, cholesterol or phospholipids levels were observed. This finding may be of importance in changing the levels of CLA in biological fluids by altering specific dietary foods and fatty acids as sources of CLA and, thereby, protecting against cancer.

Effect Of CLA On Cancer:
The anticancer potential of CLA has received a great deal of research attention in both in vitro and animal models. Pariza and Hargraves et al. (1985) first reported that topical applications of a partially purified extract from grilled ground beef (enriched with mutagenesis modulator) five minutes prior to DMBA (7,12 dimethylbenz anthracene) treatment reduced the number of papillomas per mouse as well as the number of mice with papillomas. The anti carcinogenic factor was then isolated and identified as a mixture of dienoic derivatives of linoleic acid.

Ha et al. (1987) investigated that CLA had inhibited the development of mouse epidermal tumours.

Ha et al. (1989) found that Dietary sources of CLA included milk fat, natural and processed cheeses, meat products, and plant oil. Animal sources are richer in CLA than plant sources, and in general, foods from ruminants contain more CLA than foods from non ruminants.

Ha et al. (1990) reported Inhibition of benz(a) pyrene-induced mouse fore stomach neoplasia by conjugated dienoic derivatives of linoleic acid.

Schonberg et al (1995) Observed inhibition of proliferation of estrogen receptor-positive MCF-7 cells by CLA. The author found that Bovine milk fat enriched with CLA was more effective in inhibiting human MCF-7 breast cancer cells.

Durgam et al. (1997) investigated that CLA in the form of free fatty acids exerts an anti proliferate effect, Milk fat enriched with CLA appears to have even greater in vitro activity. Bovine milk fat enriched with CLA was more effective in inhibiting human MCF-7 breast cancer cells than were isolated CLA isomers. Incubation of cells with bovine milk fat enriched with CLA decreased viable cell numbers by up to 90% . Incubation with a mixture of CLA isomers or with the c-9, t-11 CLA isomer resulted in a 60% decrease. Incubation with the t-10, c-12 CLA isomer caused only a 15% decrease in cell numbers under similar conditions. In contrast to the results obtained with the various forms of CLA, incubation with linoleic acid resulted in a 25% increase in cell proliferation. In vitro evidence suggests a higher percentage of estrogen receptor-positive MCF-7 cells treated with CLA remained in the G0/G1 phase as compared to controls and those treated with linoleic acid. The effect of CLA on these cells was only temporary and was reversed when CLA was withdrawn from the media.

Ip et al. (1999) found greater in vitro antiproliferative ability of c-9, t-11 isomer and owed it due to its accumulation to a greater degree in rat mammary tissue thus author suggested that c-9, t-11 isomer might be the most important for anticancer effects.

Thomas Yeung et al. (2000) investigated in vitro anticancer activity for CLA. And inhibition the proliferation of human hepatoma cell lines by it.

Igarashi et al. (2001) observed inhibitory effects of CLA on lung adenocarcinoma cell lines and human glioblastoma cell line.

Shultz et al. (1992) observed Inhibitory effect of conjugated dienoic derivatives of linoleic acid and beta-carotene on the in vitro growth of human cancer cells.
Ip et al. (1995) Studied the effect of timing and duration of dietary conjugated linoleic acid (CLA) on mammary cancer prevention. female rats were fed a diet containing one-percent CLA between early post weaning and a period analogous to puberty (from 21 to 42 days of age) tumour formation as a result of methyl nitrosourea (MNU) administration at 56 days of age was substantially reduced.

Liew et al. (1995) Studied the anticancer effects of CLA in colon cancer in rats which were exposed to the carcinogen 2-amino-3-methylimidazol[4,5-f] quinolone to induce colon carcinogenesis. Controls (normal diet) and CLA (0.5% ) treated rats were exposed to the carcinogen during weeks 3 and 4 of the study period. After week 16 the rats were killed in order to quantify aberrant crypt foci (ACF). While CLA administration had no impact on the size of ACF the number of ACF was significantly reduced in the CLA treated group when compared with the controls.

Ip et al. (1996) studied the efficacy of conjugated linoleic acid in mammary cancer The author stated that prevention is independent of the level or type of fat in the diet. In vivo evidence has also indicated that adding CLA to the diet of female rats exposed to carcinogens results in lower levels of mammary tissue malondialdehyde (an end product of lipid peroxidation), suggesting the potential for some degree of antioxidant activity.
Banni et al. (1997) investigated that CLA exert a profound effect on protection against induced dimethylbenz[a]anthracene (DMBA) mammary tumour in mice and rats.

Ip et al. (1997a and 1997b) reported significant cancer protection was found only in the rats receiving CLA for the entire 20 weeks. As soon as CLA feeding was discontinued, protection against carcinogen-induced cancer formation was lost. The authors stated that Conjugated linoleic acid and linoleic acid as distinctive modulators of mammary carcinogenesis.

Belury et al. (1997) reported modulation of hepatic lipid composition in mice by Conjugated linoleic acid.

Wong et al. (1997) investigated the effects of dietary conjugated linoleic acid on lymphocyte function and growth of mammary tumours in mice.

Visonneau et al. (1997) found that Conjugated linoleic acid suppresses the growth of human breast adenocarcinoma cells in SCID mice. Feeding CLA to SCID mice resulted in protection against cancer formation and metastasis via mechanisms independent of the host immune system. The author stated that it was unlikely that CLA ability to protect rats and mice against cancer is directly related to immune system activation.

Cesano et al.(1998) investigated the anticancer activity and antimetastatic activity in animal models of prostate cancer by dietary CLA In vitro. The authors suggested CLA’s anticancer activity might be partially a result of CLA-inducing lipid peroxidation. However lipid peroxidation as the role mechanism of action in vitro.

Banni et al. (1999) investigated the decrease in linoleic acid metabolites as a potential mechanism in cancer risk reduction by conjugated linoleic acid. Evidence of the study suggested that degree of CLA’s activity might be a result of modifying eicosanoid production. Feeding CLA to mice resulted in a decrease in arachidonic acid production.

Kavanaugh et al.(1999) observed Effect of dietary conjugated linoleic acid on phorbol ester-induced PGE2 production and hyperplasia in mouse epidermis. Dietary CLA also reduced PGE2 synthesis approximately twofold in mice treated topically with the tumour promoter 12-O-tetradecanoylphorbol-13-acetate.

Ip et al. (2000) reported the induction of apoptosis by conjugated linoleic acid in cultured mammary tumour cells and pre malignant lesions of the rat mammary gland. In vivo evidence suggests an ability of CLA to induce apoptosis, suggested that some of CLA ability to decrease tumour mass might be a result of inducing programmed cell death.

Hubbard et al. (2000) studied reduction of murine mammary tumour metastasis by conjugated linoleic acid.

Anee et al. (2006) reported reduction in human cancer Cell growth by Beef Conjugated linoleic acid (CLA) isomers.

Effect of CLA On Atherosclerosis
Briggs et al. (1993) studied that CLA isomers could modulate atherogenesis is regulating the production of lipoproteins in the liver. Sterol element binding proteins (SREBP) are a group of membrane-bound transcription factors that bind to their specific DNA binding sites (SRE-1) to activate the expression of target genes that encode enzymes necessary for lipid synthesis, including the LDL receptor (LDLR) gene in sterol-depleted cells.

Lee et al. (1994) observed that Lipid levels among the CLA-supplemented rabbits consisted of lower triglycerides and low density lipoprotein (LDL) cholesterol levels. Further examination of the aortas of CLA-fed rabbits showed less atherosclerosis.

Nicolosi et al.(1997) investigated reduction in early atherosclerosis in the CLA-supplemented animals.

Brashears et al.(1998) founded the bile salt de conjugation of CLA and cholesterol removal from media by Lactobacillus casei.

Stangl et al. (1999) found that HDL cholesterol ratio was significantly increased by feeding CLA to the animals.

Munday et al. (1999) substituted CLA (0.5% of the diet) in diet for linoleic acid for C57BL/6 mice. This strain of mice is genetically susceptible to the development of fatty streaks in the intima of the aortic sinus when placed on a diet similar to the control diet used in the study. In these mice, CLA addition to the diet resulted in a lipid profile considered less atherogenic (lower triglycerides, and a higher serum HDL total cholesterol ratio)

Kritchevsky et al. (2000) found one percent CLA to the diet for 90 days resulted in an average regression of established atherosclerosis of 30%. CLA supplementation in conjunction with an atherosclerotic diet fed to rabbits showed similar beneficial effect in retarding atherosclerosis in his second study.

Blankson et al. (2000) did a clinical studied in human subjects with BMIs between 25-35 kg/m2, The author noticed statistically significant reductions in LDL. HDL and total cholesterol in all groups receiving CLA. However these changes were not large enough to be clinically significant. An increase in lipoprotein(a)was found in the groups receiving 3.4 grams or more of CLA per day.

Kritchevsky et al. (2004) investigated that Conjugated linoleic acid isomer effects in regression of lesions in atherosclerosis.

Nicholson et al.(2004) reported that CD36 oxidized LDL and PPAR gamma Pathological interactions in macrophages and atherosclerosis. LDL oxidation also results in changes in apolipoprotein B -epitope. The oxidized apo lipoprotein portion of LDL is subsequently recognized and internalized by SR-A where as the oxidized lipid moiety of LDL is bound to CD36 on macrophages.

Antonius et al. (2004) observed the effect of conjugated linoleic acid reduces body composition and plasma lipids in humans.

Desroches et al. (2004) investigated the Metabolic syndrome and effect of Conjugated linoleic acid on obesity and lipoprotein disorders.

Effect Of CLA On Insulin
Houseknecht et al. (1998) and Banni et al.(1999) reported that CLA isomers are potent modulators of Peroxisome proliferators-activated receptors (PPARs). PPARs bind to target gene and resultant change in gene expression accounts for effects on Glucose metabolism, lipid metabolism, atherosclerosis and carcinogenic activity.

Houseknecht et al. (1998) investigated the effect of CLA on insulin levels, glucose tolerance, and glucose homeostasis was investigated in male Zucker diabetic rats (an animal model of type 2 diabetes). An improvement in glucose disposal and a more rapid return to baseline glucose levels subsequent to a glucose infusion was also observed in the CLA-fed rats.

West et al. (2000) observed in AKR/J mice (a strain susceptible to dietary obesity), adding CLA as one percent of dietary calories resulted in a nearly two-fold increase in plasma insulin levels. In these mice there was also a trend toward higher blood glucose levels.

Belury et al. (2003) studied that conjugated linoleic acid (CLA) isomer, t-10, c-12-CLA is inversely associated with changes in body weight and serum leptin in subjects with type 2 diabetes mellitus.

Moloney et al. (2004) observed conjugated linoleic acid (CLA) supplementation in some animals may have therapeutic potential with respect to insulin sensitivity and lipid metabolism, which is important cardiovascular disease (CVD) risk factors associated with type 2 diabetes mellitus.

CLA and Bone Formation
Jameela Banu et al. (2006) observed the Effects of conjugated linoleic acid and exercise on bone mass in young male Balb/C mice.

Hur et al. (2007) investigated that Dietary CLA inhibits endosteal bone resorption, increases endocortical bone formation, and modulates the action and expression of cyclo oxygenase (COX) enzyme, thereby decreasing prostaglandin-dependent bone resorption. CLA also enhances calcium absorption and may improve bone formation in animals, although results are not consistent. Since CLA can also affect inflammatory cytokines, it is hypothesized that CLA may be a good tool for prevention or reduction of rheumatoid arthritis symptoms. The possible mechanisms by which CLA prevents rheumatoid arthritis as well as other inflammatory diseases.
Ilana Platt et al.(2007) investigated Isomer-Specific Effects of Conjugated Linoleic Acid on Mineralized Bone Nodule Formation from Human Osteoblast-Like Cells. The cis-9,trans-11 isomer increased the number and size of mineralized bone nodules from 25 to 100 µM, but the 10trans,12cis isomer did not. The increase in mineralized bone nodule formation by cis-9, trans-11 CLA was accompanied by a variable increase in ALP activity. These results show that the cis-9, trans-11 isomer of CLA increases the formation of mineralized bone nodules using bone cells of human origin, and provide evidence for isomer-specific effects of CLA on bone health.

CLA Modulation Of Immune Response
The immune system of body is central defence against cancer, it is possible that the anticancer activity of CLA may be mediated through enhanced immune function. The physiological role of CLA in normal and immune-stimulated animals has been studied. Most of the studies show the relation of body growth and immune stimulation by conjugated linoleic acid.

Klasing et al. (1987) investigated the ability of CLA to influence growth in baby chicks following immune stimulation with bacterial lipo-polysaccharide (LPS, otherwise known as endotoxin). Typically chicks lose body weight for 24 hours after being injected with LPS, a loss as a result of cytokines released by immune cells. These cytokines (primarily interleukin-1 and tumour necrosis factor, TNF) induce skeletal muscle catabolism.
Cook (1991) conducted studies that how nutritional methods could prevent growth suppression that is usually observed with immune stimulation in animals, e.g. vaccination.

Cook et al. (1993) documented antioxidant properties of CLA and hypothesized that this LA isomer may have an impact on the immune response in aging mammalian species. Chicks fed CLA and injected with the endotoxin lipo-polysaccharide (LPS) continued to grow, whereas those not fed CLA either failed to grow or lost weight following LPS injection. In addition, dietary CLA enhanced the phytohemagglutinin response and alleviated the catabolic effect of immune stimulation in rats.

Hotamisligil and Spiegelman et al. (1993) concluded that the cytokine produced biochemical changes in a wide variety of cells attributable to its capacity for using multiple signaling pathways through its cell surface receptors. Hence TNF- , like CLA, is multifunctional. Mice were fed control diet or diet supplemented with 0.5% CLA for 32 days, then injected with TNF- as indicated. The CLA-fed mice experienced less weight loss indicating that they were partially protected against the cachexia that was induced by the cytokine. These results provide evidence indicating that CLA may modulate a cellular response to TNF- , possibly through the regulation of eicosanoid and CLA.

Miller et al. (1994) observed the ability of conjugated linoleic acid to prevent endotoxin-induced growth suppression. Conjugated linoleic acid prevented anorexia from endotoxin injection. Splenocyte blastogenesis was increased by conjugated linoleic acid. Based on the observation that CLA feeding decreased tissue arachidonic acid content, the authors concluded that CLA may be preventing the catabolism of tissue by removing eicosanoid precursors.

Suganuma et al. (1996) Studied the process of cancer prevention mediated through inhibition of tumour necrosis factor- expression. TNF- appears to be a key mediator in many chronic pathologies including cachexia, atherosclerosis, carcinogenesis .

Wong et al. (1997 ) studied the effects of conjugated linoleic acid on lymphocyte function and growth of a transplantable murine mammary tumor. In one experiment Female Balb/c mice eight-week-old were fed 0.1%, 0.3% or 0.9% CLA for three or six weeks. Lymphocyte proliferation, interleukin-2 production and lymphocyte cytotoxicity were assessed using splenic lymphocytes. Plasma CLA concentrations increased in a dose-dependent manner with CLA feeding. Lymphocyte proliferation in mice and phytohemagglutinin and production of IL-2 also was stimulated by CLA. Therefore, dietary CLA modulated certain aspects of the immune defense but had no obvious effect on the growth of an established, aggressive mammary tumor.
Moya et al.(1999) investigated that CLA is potent naturally occurring ligand and activator of PPARs. The author observed that PPARs involved in regulating expression of various gene involved in proliferation of lymphocytes monocytes and macrophages, apoptosis and inflammation.

Hayek et al. (1999) found that young and old C57BL / 6NCrlBR mice fed 1% CLA had greater splenocytes proliferation in response to concanavalin A and phytohemagglutinin-A (PHA) than mice fed the control diet. CLA-supplemented young mice had significantly higher splenocyte interleukin-2 production than those fed the control diet. These findings suggest that CLA is effective in preventing the catabolic effect of immune stimulation, and possesses a potent immuno stimulatory effect in mammalian species. The potential of preventing the catabolic losses without affecting the generation of adaptive immunity could provide benefit to growth and development.
Bassaganya et al. (2002) reported that CLA interacts with peroxisome proliferator-activated receptors (PPARs). Which are the fatty acid receptor that regulates the expression of genes involved in immune functions and energy homeostasis.

Iwakiri et al. (2002) investigated the Suppression of cyclooxygenase-2 and inducible nitric oxide synthase expression by conjugated linoleic acid (CLA) in murine macrophages.

Alber et al. (2003) studied that CLA supplementation beneficial for immunocompromised individuals which are slow or low responders to vaccination.

Torres et al. (2003) observed that Conjugated linoleic acid exhibits stimulatory and inhibitory effects on prostanoid production in human endothelial cells and platelet.

Yang et al. (2003) reported that Dietary conjugated linoleic acid decreased cachexia, Macrophages and production of cytokines. CLA was shown to inhibit lipopolysccharide (LPS)-stimulated tumour necrosis factor-α (TNF-α). The authors observed decrease in interleukin-4 (IL-4) in CLA fed mice when splenocytes were stimulated with concanavalin-A (con-A) for 44 hours.
Yamasaki et al. (2003) reported the Immunoglobulin and Cytokine production from spleen lymphocytes is modulated in C57BL/6J mice by dietary cis-9, trans-11 and trans-10, cis-12 conjugated linoleic acid. The author observed that spleen lymphocytes isolated from the mice fed with trans-10, cis-12- CLA produced more immunoglobulin (Ig)A and (Ig)M but (Ig)G. (Ig)A production was greater in t-10, c-12- CLA treated group than controls. Conversely, C-9, t-11-CLA did not affect the production of any Ig subclasses. Lymphocytes isolated from C-9, t-11-CLA fed mice produced more tumour necrosis factor- α than control group. The proportion of B-cells in the spleen lymphocytes was significantly lower in C-9, t-11-CLA group than and higher in t-10, c-12- CLA group than in controls. Moreover the percentage of CD4+ T cells lower in the t-10, c-12-CLA and percentage of CD8+ T was higher in C-9, t-11-CLA. The ratio of CD4+ T/ CD8+ T was lower in control groups.

Marianne et al. (2004) demonstrated that conjugated linoleic acid modulates immune function. The author observed both the innate and adaptive immune response are affected by dietary CLA supplementation. CLA decrease tumour necrosis factor-α (TNF- α) and interleukin 6 (IL-6) and isomers of CLA cis-9, trans-11 and trans-10, cis-12 exerts distinct effects on T-cells population and immunoglobulin subclasses in rats models.

Li et al. (2006) studied that conjugated linoleic acid suppresses NF-kB activation and lipo polysaccharide (LPS)-induced IL-12 by a conjugated linoleic acid. The author observed that cis-9, trans-11 suppresses IL-12 production by LPS- stimulated dendritic cells by ERK mediated IL-10 induction. The IL-10 mediated effects are inhibition of NF-kB activation indicated that cis-9, trans-11 can enhance transcription and production of anti-inflammatory cytokine IL-10.

Mullen et al. (2007) investigated that Conjugated linoleic acid supplementation reduces peripheral blood mononuclear cell interleukin-2 production in healthy middle-aged males.

CLA mediated Gene Expression:
Yu et al. (2004) demonstrated that a CLA isomer mixture (50:50, 400 μmol/L final concentration) up-regulated LDL receptor (LDLR) mRNA and protein expression at three- to five-fold in HepG2 cells. The results of the study suggest the up regulation of the LDLR gene by CLA through a mechanism that is independent of SREBP-1 and acyl CoA cholesterol acyl- transferase (ACAT).
Ringseis et al. (2006) reported that the trans-10, cis-12 CLA isomer, not the cis-9, trans-11 CLA isomer, induced LDLR gene expression via SREBP-2 in human hepatoma cells (HepG2). They concluded that the enhanced uptake of VLDL and LDL cholesterols by hepatic LDLR may account for the decreased plasma cholesterol levels in response to CLA isomer.

Alibin et al. (2008) observed the Suppression of cardiac myocyte hypertrophy by conjugated linoleic acid and role of peroxisome proliferator-activated receptors (PPARs).

CLA and Antioxidant Activity
CLA has been investigated for antioxidant activity by several researches since it was considered as a possible explanation for some of its health effects such as carcinogenesis and atherosclerosis. However it is clear that the conjugated double bonds made contribution to the radical scavenging capacity of CLA. The difference in the reaction kinetics between CLA-radicals and linoleic acid- radical perhaps provide a reasonable explanation for CLA have anticarciongenic. While increase linoleic acid was observed to promote tumour formation (MacDonald, 2000).

Ha et al. (1987) reported that CLA was more effective in preventing linoleic acid oxidation than α- tocopherols.

Wu et al. (1994) and Beharka et al. (1997) investigated that antioxidant nutrients (e;g Vitamin E, p-carotene and glutathione) can enhance the immune response in rodents and humans.

Yurawecz et al. (1995) found that CLA could be converted to furan fatty acid by air oxidation in methanol and should be consider as a source of furan fatty acids in biological systems. Formation of furan fatty acids may contribute to the antioxidant properties of CLA.

Cantwell et al. (1999) reported the effect of conjugated linoleic acid on the antioxidant enzymes defence system in rat hepatocytes.

O’ Shea et al. (1999) investigated the antioxidant enzyme defence responses of human MCF-7 and SW480 cancer cells to conjugated linoleic acid.

Leung et al. (2000) reported that trans-10, cis-12 conjugated linoleic acid has strong oxy radical scavenging capacity. Their study also showed that t-10, c-12 CLA have high antioxidant activity than c-9, t-11 CLA.

Liangli Yu. (2001) investigated free radical scavenging properties against the stable 2,2- diphenyl-1- picry hydrazyl radical (DPPH). Kinetics of CLA- DPPH reactions was different to that linoleic acid (LA). The author observed CLA had reacted and quenched DPPH radicals while LA had showed no radical quenching activity indicating that CLA can provide immediate protection against free radicals.

Liangli Yu et al. (2002) reported the conjugated linoleic acid cis-9, trans-11 and cis-12, trans-10 isomers differ in free radical scavenging properties. The author concluded that individual CLA isomers differ in their biological actions and indicate that interaction between isomers contribute to their beneficial health effects.

Bioconversion Of CLA
CLA can be formed from linoleic acid by the ruminal bacteria (Butyrivibrio fibrisolvens) and other prebiotics Lactobacillus. Free linoleic acid can be converted to CLA in rats but esterified linoleic acid cannot do so. However germ-free rats were not capable of converting linoleic acid to CLA, suggesting that the intestinal micro-flora of non-ruminants also has a limited ability to isomerise linoleic acid to CLA.

Kepler et al. (1966) studied the intermediates and products of the bio hydrogenation of linoleic acid by Butyrivibrio fibrisolvens. A rumen bacterium, Butyrivibrio fibrisolvens was able to convert linoleic acid to oleic acid via conjugated linoleic acid.

Chin et al. (1994) reported that Conjugated linoleic acid (9,11- and 10,12-octadecadienoic acid) is produced in conventional but not germ-free rats fed linoleic acid.

Buck et al. (1994) studied comparisons of freshly isolated strains of Lactobacillus acidophilus of human intestinal origin. Two strains of L. acidophilus (L1 and O16) and two of L. casei (E5 and E10) isolated from human intestinal sources were used to produced conjugated linoleic acid
Boyaval et al. (1995) observed CLA production in that .Less was produced in the presence of 0.05% than in 0.02% linoleic acid by propionic acid bacteria.

Lin et al. (1999,2000) reported that Conjugated linoleic acid concentration is affected by lactic cultures and added linoleic. Their study revealed that a culture of L.acidophilus produced cis-9, trans-11 in sterilized skim milk supplemented with free linoleic acid after 24 h of incubation at 37°C.

Ogawa et al. (2001) investigated Conjugated linoleic acid accumulation via 10-hydroxy-12-octadecaenoic acid during micro aerobic transformation of linoleic acid by Lactobacillus acidophilus.

Kishino et al. (2002) reported Conjugated linoleic acid production from linoleic acid by lactic acid bacteria. The authors found that washed cells of Lactobacillus plantarum formed high levels of CLA from free linoleic acid upon extended incubation. They indicated most of the CLA of culture was associated with the bacterial cells.

Alonso et al. (2003) investigated the production of free conjugated linoleic acid by Lactobacillus acidophilus and Lactobacillus casei of Human intestinal Origin. Their study has shown that two cultures each of Lactobacillus acidophilus (016, L1) and Lactobacillus casei (E5, E10) were able to convert free linoleic acid to CLA. Of the possible isomers of CLA, cis-9 and trans-11, cis-12 and trans-10 formed. cis-9 trans-11 comprised more than 90% of the total CLA.

John Wallace et al. (2007) reported that the isomers of conjugated linoleic acids are synthesized via different mechanisms in ruminal digesta and bacteria. Digesta samples from the ovine rumen and pure ruminal bacteria were incubated with linoleic acid (LA) in deuterium oxide-containing buffer to investigate the mechanisms of the formation of conjugated linoleic acids (CLA)




References

Alibin, C.P., Kopilas, M.A. and Anderson, H.D. (2008) Suppression of cardiac myocyte hypertrophy by conjugated linoleic acid: role of peroxisome proliferator-activated receptors alpha and gamma. Journal of Biological Chemistry. 283 : 10707-10715.

2.
Albers. R., Brink, E.J., Hendrick, H.F.J. and Mohede, I.C.M. (2003) Effect of Cis-9, trans-11 and trans-10, cis12 Conjugated linoleic acidisomers on immune functions in healthy men. Eur. J. Clin. Nutr. 57: 595-603
3.
Alonso, L., Custea, E. P. and Gilliland, S.E. (2003) Production of free conjugated linoleic acid by
4.
Lactobacillus acidophilus and Lactobacillus casei of Human intestinal Origin. Journal of Diary Science. 86 (6): 1941-1946.
5.
Anee, D., La, T., and Eric, D.(2006) Beef Conjugated linoleic acid (CLA)isomers reduces human cancer Cell growth even associated with other beef fatty acids. British Journal of Nutrition. 95 : 346-352.
6.
Antonius, H.M. (2004) Effect of conjugated linoleic acid on bodycomposition and plasma lipids in humans. American Journal of Clinical Nutrition. 79 (3) : 352-361.
7.
Banni, S., Angioni, E. and Casu,V.(1999) Decrease in linoleic acid metabolites as a potential mechanism in cancer risk reduction by conjugated linoleic acid. Carcinogenesis. 20: 1019-1024.
8.
Banni, S., Angioni, E. and Carta,G.(1999) Influence of dietary conjugated linoleic acid on lipid metabolism in relation to its carcinogenic activity. Champagien. IL: 307-318.
9.
Bassaganya, R.J., Hontecillas. R. and Beitz, D. (2002) Colonic anti- inflammatory mechanism of conjugated linoleic acid. Clin. Nutr. 21: 451-459.
10.
Beharka, A.A., Wu, D., Han,S.N.,and Meydani, S.N., (1997) Macrophage prostaglandin production contributes to the age-associated decrease in T cell function which is reversed by the dietary antioxidant vitamin E. Mech. Ageing Dev. 94 :157-165.
11.
Belury, M.A., Mahon, A. and Banni, S., (2003) The conjugated linoleic acid (CLA) isomer, t-10, c-12-CLA, is inversely associated with changes in body weight and serum leptin in subjects with type 2diabetes mellitus. J. Nutr. 133(1) :257S-260S.
12.
Belury, M.A. and Kempa-Steczko, A. (1997) Conjugated linoleic acid modulates hepatic lipid composition in mice. Lipids. 32:199-204.
13.
Blankson, H., Stakkestad, J.A. and Fagertun, H. (2000) Conjugated linoleic acid reduces body fat mass in overweight and obese humans. J. Nutr. 130 : 2943-2948.
14.
Boyaval, P., Corre, C., Dupuis, C., and Roussel, E. (1995) Effects of free fatty acids on propionic acid bacteria. Lait. 75: 17–29.
15.
Brashears, M. M., Gilliland, S. E., and Buck, L.M. (1998) Bile salt deconjugation and cholesterol removal from media by Lactobacillus casei. J. Dairy Sci. 81: 2103–2110.
16.
Briggs, M.R., Yokoyama, C., Wang, X., Brown, M.S. and Goldstein, J.L. (1993) Nuclear protein that binds sterol regulatory element of low density lipoprotein receptor promoter: 1Identification of the proteinand delineation of its target nucleotide sequence. Journal of Biological Chemistry. 268 : 14490-14496.
17.
Buck, L. M. and S. E. Gilliland. (1994) Comparisons of freshly isolated strains of Lactobacillus acidophilus of human intestinal origin for ability to assimilate cholesterol during growth. J. Dairy Sci. 77: 2925–2933.
18.
Cawood, P., Wickens, D.G., Iverson, S.A., Braganza, J.M. and Dormandy, T.L.,(1983) The nature of diene conjugation in human serum, bile and duodenal juice. FEBS Lett 162: 239–243.
19.
Cesano, A., Visonneau, S. and Scimeca, J.A., (1998) Opposite effects of linoleic acid and conjugated linoleic acid on human prostatic cancer in SCID mice. Anticancer. Res.18:1429-1434.
20.
Chin, S.F., Storkson, J.M., Liu, W., Albright, K.J. and Pariza, M.W. (1994) Conjugated linoleic acid (9,11- and 10,12-octadecadienoic acid) is produced in conventional but not germ-free rats fed linoleic acid. J. Nutr. 124: 694–701.
21.
Christie, W.W., Dobson, G., and Gunstone, F. D. (1997). Isomers in commercial samples of conjugated linoleic acid. Lipids. 32: 1231–1232.
22.
Cook, M.E. (1991) Nutrition and the immune response of domestic fowl. Crit. Rev. Poultry. Biol. 3 :167–189.
23.
Cook, M.E., Miller, C.C., Park, Y. and Pariza, M.W. (1993) Immune modulation by altered nutrient metabolism: nutritional control of immune-induced growth depression. Poultry. Sci. 72 :1301–1305.
24.
De Man, J.C., Rogosa, M. and Sharpe, M.E. (1960) A medium for the cultivation of Lactobacilli. J. Appl. Baceriol., 23 : 130-35.
25.
Desroches Sophie. and Lamarche Benoit. (2004) Metabolic syndrome and effect of conjugated linoleic acid on obesity and lipoprotein disorders. American Journal of Clinical Nutrition. 79 (6) : 1149S- 1152S.
26.
Durgam, V.R. and Fernandes, G. (1997) The growth inhibitory effect of conjugated linoleic acid on MCF-7 cells is related to estrogens response system. Cancer. Lett. 116 :121-130.
27.
Gill, H.S., Rutherfurd, K.J., Prasad, J. and Gopal, P.K. (2000) Enhancement of natural and acquired immunity by Lactobacillus acidophilus (HN017) and Bifidobacterium lactis (HN019). Br. J. Nutr., 83(2) : 164-67.
28.
Ha, Y. L., Grimm, N.K., and Pariza, M.W. (1989) Newly recognized Anti carcinogenic fatty acids: identification and quantification in natural and processed cheeses. J. Agric. Food Chem. 37:75–81.
29.
Ha, Y.L., Grimm, N.K. and Pariza, M.W. (1987) Anticarcinogens from fried ground beef: heat-altered derivatives of linoleic acid. Carcinogenesis 8: 1881–1887.
30.
Ha, Y.L., Storkson, J. and Pariza, M.W. (1990) Inhibition of benz(a)pyrene-induced mouse forestomach neoplasia by conjugated dienoic derivatives of linoleic acid. Cancer. Res. 50: 1097–1101.
31.
Harrison, K., Cawood, P., Iverson, A. and Dormandy, T.L. (1985) Diene conjugation patterns in normal serum. Life Chem Rep 3 : 41–44.
32.
Hayek, M.G., Han, S.N., Wu, D., Watkins, B.A., Meydani, M., Dorsey,J.L., Smith,D.E. and Meydani, S.N. (1999) Dietary conjugated linoleic acid influences theimmune response of young and old C57BL/ 6NCrlBR mice. J. Nutr. 129 : 32–38.
33.
Hotamisligil, G.S. and Spiegelman, B.M. (1994) TNF : A key component of obesity-diabetes link. Diabetes 43 : 1271–1278.
34.
Houseknecht, K.L., Vanden Heuvel, J.P. and Moya-Camarena, S.Y.(1998) Dietary conjugated linoleic acid normalizes impaired glucose tolerance in the Zucker diabetic fatty fa/fa rat. Biochem. Biophys. Res. Commun. 244 : 678- 682.
35.
Huang, Y.C., Luedecke, L.O. and Schultz, T.D.,(1994) Effect of cheddar cheese consumption on plasma conjugated linoleic acid concentrations in men. Nutr. Res. 14: 373–386.
36.
Hubbard, N.E., Lim, D., Summers, L. and Erickson, K.L. (2000) Reduction of murine mammary tumor metastasis by conjugated linoleic acid. Cancer. Lett. 150 : 93-100.
37.
Hur., S. J. and Park Yeonhwa. (2007) Effect of conjugated linoleic acid on bone formation and rheumatoid arthritis. Eur J Pharmacol. 30: 568-570.
38.
Igarashi, M. and Miyazawa, T. (2001) The growth inhibitory effect of conjugated linoleic acid on a human hepatoma cell line, HepG2, is induced by a change in fatty acid metabolism, but not the facilitation of lipid peroxidation in the cells. Biochim. Biophys. Acta.1530 :162- 171.
39.
Ilana Platt., Leticia, G., Rao Ahmed. and El-Sohemy. (2007). Isomer-Specific Effects of Conjugated Linoleic Acid on Mineralized Bone Nodule Formation from Human Osteoblast-Like cells. Experimental Biology and Medicine 232 : 246-252.
40.
Ip, C., Jiang, C., Thompson, H.J. and Scimeca, J.A.(1997) Retention of conjugated linoleic acid in the mammary gland is associated with tumour inhibition during the post-initiation phase of carcinogenesis. Carcinogenesis.18: 755- 759.
41.
Ip. C., Banni, S. and Angioni, E.(1999) Conjugated linoleic acid-enriched butter fat alters mammary gland morphogenesis and reduces cancer risk in rats. J. Nutr.129 : 2135-2142.
42.
Ip, C., Scimeca, J.A. and Thompson, H.(1995) Effect of timing and duration of dietary conjugated linoleic acid on mammary cancer prevention. Nutr. Cancer.24:241-247.
43.
Ip, C. and Scimeca, J.A. (1997) Conjugated linoleic acid and linoleic acid are distinctive modulators of mammary carcinogenesis. Nutr. Cancer. 27 : 131-135.
44.
Ip, C., Briggs, S.P. and Haegele, A.D. (1996) The efficacy of conjugated linoleic acid in mammary cancer prevention is independent of the level or type of fat in the diet. Carcinogenesis.17: 1045-1050.
45.
Ip, C., Ip, M.M., Loftus, T., Shoemaker, S. and Shea-Eaton, W. (2000) Induction of apoptosis by conjugated linoleic acid in cultured mammary tumour cells and premalignant lesions of the rat mammary gland. Cancer Epidemiol Biomarkers Prev. 9 : 689-696.
46.
Isolauri, E., Sutas, Y., Kankaanpaa, P., Arvilommi, H. and Salminen, S. (2001) Probiotics: effects on immunity. Am J Clin Nutr., 73 : 444S-450S.
47.
Iwakiri, Y., Sampson, D.A. and Allen, K.G.(2002) Suppression of cyclooxygenase-2 and inducible nitric oxide synthase (INO’S) expression by conjugated linoleic acid in murine macrophages. Prostaglandins, Leukotrienes, and Essential Fatty Acid. 67:435- 443.
48.
Jameela Banu., Arunabh Bhattacharya., Mizanur Rahman and Marianne O'Shea. (2006) Effects of conjugated linoleic acid and exercise on bone mass in young male Balb/C mice. Lipids Health Dis; 5 : 7-10
49.
John Wallace, R., Nest McKain., Kevin J., Shingfield. and Estelle Devillard. (2007) Isomers of conjugated linoleic acids are synthesized via different mechanisms in ruminal digesta and bacteria. Journal of Lipid Research, Vol. 48: 2247-2254.
50.
Kavanaugh, C.J., Liu, K.L. and Belury, M.A. (1999) Effect of dietary conjugated linoleic acid on phorbol ester-induced PGE2 production and hyperplasiain mouse epidermis. Nutr. Cancer. 33 :132-138.
51.
Kelly, M. L., Berry, J. R., Dwyer, D.A., Griinari, J. M., Chouinard, P. Y., Van Amburgh, M.E., and Bauman, D.E. (1998) Dietary fatty acid sources affect conjugated linoleic acid concentrations in milk from lactating dairy cows. J. Nutr. 128 : 881–885.
52.
Klein, A., Friedrich, U., Vogelsang, H. and Jahreis, G.(2008) Lactobacillus acidophilus 74-2 modulate unspecfic cellular immune response in healthy adults. Eur. J. Clin. Nutr., 62(5) : 583-593.
53.
Kepler, C.R, Hirons, K.P., McNeill, J.J. andTove. S.B.(1966) Intermediates and products of the biohydrogenation of linoleic acid Butyrivibrio fibrisolvens. J. Biol. Chem. 6: 1350–1354.
54.
Kishino, S., Ogawa, J., Omura, Y., Matsumura, K., and Shimizu, S., (2002) Conjugated linoleic acid production from linoleic acid by lactic acid bacteria. J. Am. Oil Chem. Soc. 79: 159–163.
55.
Klasing, K.C., Laurin, D.E., Peng. R.K. and Fry, D.M.(1987) Immunologically mediated growthdepression in chicks: influence of feed intake, corticosterone, and interleukin-1. J. Nutr. 117 : 1629–1637.
56.
Kolb, H. and Kolb-Bachofen, V. (1998) Nitric oxide in autoimmune disease: cytotoxic or regulatory mediator. Immunol. Today, 19 : 556-561.
57.
Kritchevsky, D., Tepper, S.A. and Wright, S. (2000) Influence of conjugated linoleic acid (CLA) on establishment and progression of atherosclerosis in rabbits. J. Am. Coll. Nutr.19 : 472S- 477S.
58.
Kumar, R., Mukherjee, M., Bhandari, M., Kumar, A., Sidhu, H. and Mittal, R.D. (2002) Role ofOxalobacter formigenesin calcium oxalate stone disease: a study from North India. Eur. Urol., 41:318-322.
59.
Lee, K.N., Kritchevsky, D. and Pariza, M.W. (1994) Conjugated linoleic acid and atherosclerosis in rabbits. Atherosclerosis.108 :19-25.
60.
Li, G., Dong, B., Butz, D.E., Park, Y., Pariza, M.W. and Cook, M.E. (2006) NF-kappa B independent inhibition od lipopolysaccharide-induced cycloxygenase by a conjugated linoleic acid cognate, conjugated nonadecadienoic acid. Biochemica et Biophysica Acta.1761: 969-972.
61.
Liangli (Lucy), Yu., Dwayne Adams., and Michael Gabel. (2001) Free Radical scavenging Properties of conjugated linoleic acid J. Agri. Food. Chem., 49 : 3452-3456.
62.
Liangli (Lucy), Yu., Dwayne Adams., and Michael Gabel. (2002) Conjugated linoleic acid isomer differ in their Free radical cavenging Properties. J. Agri. Food. Chem. 50: 4135-4140.
63.
Liew, C., Schut, H.A. and Chin, S.F.(1995) Protection of conjugated linoleic acids against 2-amino-3- methyl imidazol[4,5-f] quinolone-induced colon carcinogenesis in the F344 rat: a study of inhibitory mechanisms. Carcinogenesis.16: 3037-3043.
64.
Lin, T. Y. (2000) Conjugated linoleic acid concentration as affected by lactic cultures and additives. Food Chem. 69 : 27–31.
65.
Lin, T. Y., Lin, C. W., and Lee, C. H. (1999) Conjugated linoleic acid concentration as affected by lactic cultures and added linoleic. Food Chem. 67: 1–5.
66.
Liu, Z., Jiang, Z., Zhou, K., and Zhang, B. (2007) Screening of Bifidobacteria with acquired tolerance to human gastrointestinal tract. Anaerobe., 13 (5-6) : 215-19.
67.
Maassen, C.B.M. and Claassen, E. (2008) Strain – dependent effect of probiotics Lactobacilli on EAE autoimmunity. Vaccine. 26: 2056-2057
68.
Macdonald, H.B. (2000) Conjugated linoleic acid and disease prevention. J. Am. Coll. Nutr. 19 : 111-118.
69.
Marianne, O’ Shea. and Josep, Bassaganya. (2004). Immunomodulatory Properties of conjugated linoleic acid. J. Am. Coll. Nutr. 79 :119-206.
70.
Medici, M., Vinderolla, C.G., Weill, R. and Perdigon, G. (2005) Effect of fermented milk containing probiotic bacteria in the prevention of an enteroinvasive E.coli infection in mice. J. Dairy. Res., 72 : 243-249.
71.
Miller, C.C., Park, Y., Pariza, M.W. and Cook, M.E., (1994) Feeding conjugated linoleic acid to animals partially overcomes catabolic responses due to endotoxin injection. Biochem. & Biophy. Res. Commun. 198 : 1107–1112.
72.
Miller, R.A. (1994) Aging and immune function: Cellular and biochemical analyses. Exp. Gerontol. 29 : 21-35.
73.
Moloney, F., Yeow, T.P., Mullen, A., Nolan, J.J. and Roche, H.M. (2004) ipoprotein metabolism in patients with type 2 diabetes mellitus. Am. J. Clin. Nutr. 80 (4) : 887-95.
74.
Moya, S.Y., Vanden, J.P., Leesnitzer, L.A. and Belury, M.A.(1999) Conjugated linoleic acid is potent naturally occurring ligand and activator of PPAR alpha. J. Lipid. Res. 40: 1426-1433.
75.
Mullen, A., Moloney, F., Nugent, A.P., Doyle, L., Cashman, K.D. and Roche, H. M. (2007) Conjugated linoleic acid supplementation reduces peripheral blood mononuclear cell interleukin-2 (IL-2) production in healthy middle-aged males. Journal of Nutritional Biochemistry. 8: 658-666.
76.
Munday, J.S., Thompson, K.G. and James, K.A.(1999) Dietary conjugated linoleic acids promote fatty streak formation in the C57BL/6 mouse atherosclerosis model. Br. J. Nutr. 81 : 251- 255.
77.
Nakamura, Y.K. and Omaye, S.T. (2008) Conjugated linoleic acid isomers increases PPAR gamma and NF-kappa B DNA binding activities in human umbilical vein endothelial cells: involvement of expression of Cu/Zn superoxide dismutase, catalse and lipid peroxidation. PhD thesis (in progress). University of Nevada.
78.
Namba, Y., Hidaka, Y., Taki, K. and Morimoto, T. (1981) Effect of oral administration of lysozyme or digested bacterial cell walls on immuostimulation in guinea pigs. Infect. Immun., 31 : 580-583.
79.
Nicholson, A.C. and Hajjar, D.P. (2004) CD36, oxidized LDL and PPAR gamma: pathological interactions in macrophages and atherosclerosis. Vascular Pharmacology. 41 :139-146.
80.
Nicolosi, R.J., Rogers, E.J. and Kritchevsky, D.(1997) Dietary conjugated linoleic acid reduces plasma lipoproteins and early aortic atherosclerosis in hypercholesterolemic hamsters. Artery. 22 : 266-277.
81.
Ogawa, J., Matsumura, K., Kishino, S., Omura, Y., and Shimizu, S. (2001) Conjugated linoleic acid accumulation via 10-hydroxy-12-octadecaenoic acid during micro aerobic transformation of linoleic acidby Lactobacillus acidophilus. Appl. Environ. Microbiol. 67: 1246–1252.
82.
O’ Shea, M., Stanton, C. and Devery, R., (1999) Antioxidant enzyme defense responses of human MCF-7 and SW480 cancer cells to conjugated linoleic acid. Anticancer. Res. 19 : 1953-1960.
83.
Pariza, M. W., Park, Y., Cook, M., Albright, K., and Liu, M. (1996) Conjugated linoleic acid reduces body fat. FASEB J. 10 : 27-32.
84.
Pariza, M.W. and Hargraves, W.A. (1985) A beef-derived mutagenesis modulator inhibits initiation of mouse epidermal tumors by 7,12 dimethylbenz[a]anthracene. Carcinogenesis. 8 : 1881–1887.
85.
Peng, S., Lin, J.Y. and Lin, M. Y. (2007) Antiallergic effect of milk fermented with lactic acid bacteria in a murine animal model. J. Agric. Food Chem., 55 (13): 5092-96.
86.
Robert, J. B., Roy, M., Robins, B. and Mimi, L.K. (2006) Probiotic use in clinical practice: what are the risks. Am. J. Clin. Nutr.83:1256– 1264.
87.
Ringseis, R., Konig, B., Leuner, B., Schubert, S., Nass, N., Stangl, G. and Eder, K. (2006) LDLreceptor gene transcription is selectively induced by t-10,c-12-CLA but not by c-9,t-11-CLA in the human hepetoma cell line HepG2. Biochemica et Biophysica Acta.1761 :1235-1243.
88.
Schonberg, S. and Krokan, H.E. (1995)The inhibitory effect of conjugated dienoic derivatives (CLA) of linoleic acid on the growth of human tumour cell lines is in part due to increased lipid peroxidation. Anticancer. Res.15 :1241- 1246.
89.
Shanta, N. C., Decker, E.A., and Ustunol, Z. (1992) Conjugated linoleic acid concentration in processed cheese. J. Am. Oil Chem. Soc. 69: 425–428.
90.
Shultz, T.D., Chew, B.P., Seaman, W.R. and Luedecke, L.O. (1992) Inhibitory effect of conjugated dienoic derivatives of linoleic acid and beta-carotene on the in vitro growth of human cancer cells. Cancer Lett (Netherlands) 63 (2) :125-133.
91.
Stangl, G.I., Muller, H. and Kirchgessner, M. (1999)Conjugated linoleic acid effects on circulating
92.
hormones, metabolites and lipoproteins, and its proportion in fasting serum and erythrocyte membranes of swine. Eur. J. Nutr.38 : 271- 277.
93.
Stanton, C., Lawless, F., Kjellmer, G., Harrington, D., Devery, R., Connolly, J.F., Murphy, J. (1997)
94.
Dietary influences on Bovine milk cis-9, trans-11-conjugated linoleic acid content. J. Food. Sci. 62: 1083–1086.
95.
Sugano, M., Tsujita, A. and Yamasaki, M. (1998) Conjugated linoleic acid modulates tissue levels of chemical mediators and immunoglobulins in rats. Lipids.33 : 521-527.
96.
Suganuma, M., Okabe, S., Sueoka, E., Iida, N., Komori, A., Kim, S.J. andFugiki, H., (1996) A new process of cancer prevention mediated through inhibition of tumour necrosis factor expression. Cancer Res. 56 : 3711–3715.
97.
Thomas Yeung, C.H., Yang, L. and Huang, Y. (2000) Dietary conjugated linoleic acid mixture affects the activity of intestinal acyl coenzyme A: cholesterol acyl-transferase in hamsters. Br. J. Nutr. 84 : 935-941.
98.
Thompson, H., Zhu, Z. and Banni, S. (1997) Morphological and biochemical status of the mammary gland as influenced by conjugated linoleic acid: implication for a reduction in mammary cancer risk.Cancer. Res57 : 5067-5072.
99.
Torres-Duarte, A.P. and Vanderhoek, J.Y. (2003) Conjugated linoleic acid exhibits stimulatory and inhibitory effects on prostanoid production in human endothelial cells and platelet. Biochemica et Biophysica Acta. 1640 : 69-76.
100.
Visonneau, S., Cesano, A. and Tepper, S.A.(1997) Conjugated linoleic acid suppresses the growth of human breast adenocarcinoma cells in SCID mice. Anticancer. Res.17: 969-973. [101] West, D.B., Blohm, F.Y., Truett, A.A. and DeLany, J.P. (2001) Conjugated linoleic acid persistently increases total energy expenditure in AKR/J mice without increasing uncoupling protein gene expression. J. Nutr.130 : 2471-2477. [102] Wollowski, I., Ji, S.T., Bakalinsky, A.T., Neudecker, C., and Pool-Zobel (2001) Bacteria used for the production of yoghurt inactivate Carcinogens and prevent DNA-damage in the colon cells. J. of Nutr., 129 : 77-82. [103] Wong, M.W., Chew, B.P., Wong, T.S., Hosick, H.L., Boylston, T.D. and Shultz, T.D.(1997) Effects of dietary conjugated linoleic acid on lymphocyte function and growth of mammary tumours in mice. Anticancer. Res. 17(2A) : 987–993. [104] Wong, M.W., Chew, B.P. and Wong, T.S.(1997) Effects of dietary conjugated linoleic acid on lymphocyte function and growth of mammary tumors in mice. Anticancer. Res.17: 987-993. [105] Wu, D., Meydani, S.N., Sastre, J., Hayek, M., and Meydani, M.(1994)In vitro glutathione supplementation enhances interleukin-2 production and mitogenic response of peripheral blood mononuclear cells from young and old subjects. J. Nutr. 124: 655-663. [106] Yadav, H., Jain, S. and Sinha, P.R. (2007) Anti diabetic effect of probiotic dahi containing L. acidophilus and L. casei in high fructose fed rats. Nutr., 23 : 62-68. [107] Yang, M., Cook, M.E., and Pariza, M.W. (2003) Dietary conjugated linoleic acid decreased cachexia, Macrophage and production of cytokines. Experimental Biology and Medicine. 228: 51-58. [108] Yamasaki, M. and Chujo, H. (2003) Immunoglobulin and Cytokine production from spleen lymphocytes is modulated in C57BL/6J mice by dietary cis-9, trans-11 and trans-10, cis-12 conjugated linoleic acid. J. Nutr. 133: 784-788. [109] Yu-Poth, S., Yin, D., Zhao, G.,Kris-Etherton, P.M. and Etherton, T.D. (2004) Conjugated linoleic acid up regulates LDL receptor gene expression in HepG2 cells. Journal of Nutrition.134: 68-71.

JCDR is now Monthly and more widely Indexed .
  • Emerging Sources Citation Index (Web of Science, thomsonreuters)
  • Index Copernicus ICV 2017: 134.54
  • Academic Search Complete Database
  • Directory of Open Access Journals (DOAJ)
  • Embase
  • EBSCOhost
  • Google Scholar
  • HINARI Access to Research in Health Programme
  • Indian Science Abstracts (ISA)
  • Journal seek Database
  • Google
  • Popline (reproductive health literature)
  • www.omnimedicalsearch.com