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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
Original article / research
Full Version
Serum Lipid Peroxidation And Leptin Levels In Male And Female Type 2 Diabetic Patients In Gorgan (South East Of Caspian Sea), Iran
Correspondence Address :
Abdoljalal Marjani,Gorgan Faculty of Medicine,Department of Biochemistry and Biophysics,Biochemistry and Metabolic Disorder Research Center, Golestan University of Medical Sciences,Gorgan, Golestan province,.Iran.Tel & Fax: +98(171)4421651 & 4440225 E.mail:abdoljalal@yahoo.com
Background: The aim of the present study was to determinate the possible relationship between serum leptin and lipid peroxidation in male and female type 2 diabetic patients in Gorgan, Iran.
Methods: The subjects consisted of fifty type 2 diabetic patients and fifty age and sex-matched control subjects. The concentration of leptin, malondialdehyde, lipid parameters and insulin were measured in all subjects. The results were evaluated by using Independent sample ‘t’ test and Spearman’s correlation coefficient test.
Results: Leptin was correlated with BMI (male: r=0.339 and female: r=0.426, p<0.05) and malondialdehyde levels (male: r=0.124 and female: r=0.271, p<0.05) in the type-2 diabetic patients. In the control subjects, only a correlation between leptin and BMI was found (male: r=0.165, female: r= 0.037, p<0.05).
Conclusions: In the correlation analysis using leptin as the dependent variable, BMI was found to be the predictor of leptin in males and females. Increased lipid peroxidation and hyperleptinaemia may play a role in the beginning and development of type 2 diabetes mellitus in this area.
Leptin, Lipid peroxidation, Type 2 diabetes mellitus, Gorgan
Introduction
Diabetes is a major public health problem that is approaching epidemic proportions globally. This metabolic disease is one of the most common endocrine disorders affecting almost 6% of the world’s population (1). The prevalence of type 2 Diabetes mellitus (DM) ranges from 1.2% to 14.6% in Asia, 4.6% to 40% in the Middle East and 1.3% to 14.5 % in Iran (2),(3). Diabetes mellitus is considered to be one of a rank of free radical diseases. It causes complications, with increased free radical formation (4). The process of lipid peroxidation is one of the oxidative conversions of polyunsaturated fatty acids to products known as malondialdehyde (MDA). MDA is a highly toxic molecule and its secondary products such as thiobarbutiric acid reactive substance (TBARS), are commonly used to evaluate lipid peroxidation (5). A major development in energy balance regulation came with the discovery in 1994, of leptin, the protein product of the ob gene (6).The functions attributed to leptin are extensive, including the regulation of food intake and energy balance through central hypothalamic pathways, its role as a major signal to the reproductive system in theinhibition of insulin secretion by pancreatic-cells and in the stimulation of glucose transport (7). Previous studies of leptin in type 2 diabetes have shown no difference in basal levels, apart from expected differences due to BMI (8),[9) or a reduced leptin level, which may be explained by differences in fat distribution (10). Importantly however, the relationship between leptin and variables involved in glucose homeostasis and diabetes might show ethnic differences. A recent population study of Peruvian Indians compared with a Caucasian population showed that the Indians had higher insulin and lower leptin levels than the Caucasians (11). Similarly, Chilean Indians also had higher insulin and lower leptin levels than the Caucasians (12). Furthermore, Mexican American subjects showed higher levels of leptin as compared to age and sex-matched non-Hispanic whites (13). These results observed in different ethnic groups reinforce that studies have to be undertaken in different populations. Thus, the aim of the present study was to investigate the possible relationship between serum leptin and the lipid peroxidation of male and female patients diagnosed with type 2 diabetes mellitus in Gorgan,Iran.
This study was performed in the Biochemistry and Metabolic Disorder Research Center of Gorgan, Iran, in 2008. We had a study group including 50 patients of type-2 diabetes mellitus who referred to the Department of Diabetes Center in 5th Azar Hospital in Golestan University of Medical Sciences and 50 age and sex matched healthy control subjects. At the point of entry into the study, all diabetic patients underwent clinical and biochemical investigations. The data were collected by trained interviewers. The exclusion criterion was the coexistence of any other serious illness. Type-2 diabetes mellitus was defined as nonketosis diabetes by medical history and it is currently treated with oral agents. None of the patients had micro vascular complications (diabetic nephropathy or retinopathy). Administration of insulin for glycaemic control was considered to be an exclusion criterion. In the controls, diabetes was excluded by the fasting blood glucose test. Ten ml of fasting blood was collected from each subject by veinpuncture. The samples were centrifuged for 10 minutes at 3000rpm. The serum was used for the analyses of malondialdehyde (14), fasting blood sugar (15), lipid profile (total cholesterol (16) including the analysis of triglycerides (17), HDL-cholesterol (18) VLDL-cholesterol and LDL cholesterol (19) in those who had type-2 diabetes mellitus and in controls. Lipids levels were measured by biochemical kits and Lipid peroxidation (the level of lipid peroxidation expressed as malondialdehyde [MDA]) was determined using previously described methods and spectrophotometry techniques (Model JENWAY 6105 UV / VIS ) in the Biochemistry and Metabolic Disorder Research Center (Faculty of Medicine). The results were reported as mean± SD. The statistical analysis was done with SPSS version -11.5 software. The results were evaluated by using Independent sample ‘t’ test and Spearman’s correlation coefficient test. P values < 0.05 were considered to be statistically significant.
The Measurement Of Serum Leptin
Serum leptin levels were measured using a human leptin ELISA test kit (Biovendor, Research and Diagnostic Products, Czech).
The Measurement Of Serum Insulin
Serum insulin levels were measured using a human insulin ELISA test kit (DiaPlus, Immunoenzymometric assay, USA).
The Measurement Of Serum Malondialdehyde
2.5 ml of trichloroacetic acid was added to 0.5 ml serum and the tube was left to stand for 10 min at room temperature. After centrifugation at 3500 rev. / min for 10 min, the supernatant was decanted and the precipitate was washed once with sulfuric acid. Then, 2.5 ml of sulfuric acid and 3 ml of thiobarbituric acid (TBA) in sodium sulfate were added to this precipitate and the coupling of lipid peroxide with TBA was carried out by heating this mixture in a boiling water bath for 30 min. After cooling in cold water, the resulting chromogen was extracted with 4 ml of n-butyl alcohol by vigorous shaking. Separation of the organic phase was facilitated by centrifugation at 3000 rev./min for 10 min and its absorbance was determined at awavelength of 530 nm.
The clinical characteristics of the type-2 diabetic patients and control subjects are described in (Table/Fig 1). The mean duration of diabetes mellitus in type-2 diabetes mellitus patients was 1.5 years (range 1-3 years). The mean age of male and female patients in the type-2 diabetic and control subjects were 50.38±10.78 (18 males) and 50.46±9.53 (32 females), and 48.40± 10.49 years (20 females) and 48.46± 10.65 years (30 females), respectively. A number of obvious differences were found between the two subjects. The female type 2 diabetes mellitus patients had higher levels of fasting blood sugar, total cholesterol, LDL-cholesterol, HDL-cholesterol, VLDL-cholesterol, triglycerides, malondialdehyde, leptin and insulin as compared to the male subjects. Notably, the BMI (32.88±5.82 kg/m²), malondialdehyde (2.57±1.38 nmol/ml) and leptin levels (34.99±10.19 ng/ml) were significantly higher in female type-2 diabetes mellitus patients than in diabetic male subjects (25.05±1.85 kg/m², 2.10±0.67 nmol/ml and 11.04±7.76 ng/ml,) (P< 0.05) (Table/Fig 1). The data shown in Table 1 reveals that the BMI (30.60±5.50 kg/m²) and leptin levels (26.34±12.02 ng/ml) was significantly higher in female control subjects than in male subjects (25.97±4.36 kg/m² and 11.26±5.46 ng/ml,) (P< 0.05). There was no significant difference in other parameters in female type-2 diabetes mellitus patients and male subjects. The data of (Table/Fig 1)shows that the levels of fasting blood sugar, total cholesterol, LDL-cholesterol, VLDL-cholesterol, triglycerides, malondialdehyde and insulin were significantly higher in male and female (leptin was also higher) type-2 diabetes mellitus patients than in male and female controls (P< 0.05). But this is not the same for HDL-cholesterol, age and BMI in female type-2 diabetes mellitus patients(Table/Fig 1). There were no significant differences in age, BMI, HDL-cholesterol and leptin in male type-2 diabetes mellitus patients and in male control subjects. Leptin correlated positively and significantly with the BMI of diabetic and control males (r=0.339and r=0.165, p<0.05) and females (r=0.426 and r=0.037, p<0.05). Leptin also correlated positively and significantly with malondialdehyde (MDA) in the male and female type-2 diabetes mellitus patients (r= 0.124, r= 0.271, p<0.05) (Table/Fig 2).
In the present study, we have observed that the levels of malondialdehyde (MDA), a lipid peroxidation product and a marker of oxidative stress, is increased significantly in male as well as in female diabetic patients [Table/Fig 1]. This apparently shows that diabetic patients are exposed to an increased oxidative stress via lipid peroxidation. Some other researchers have also reported elevated lipid peroxidation products in the blood samples of type 2 diabetic patients (20),(21). Several studies have shown that lipid peroxidation is increased in diabetes, particularly in type 2 diabetes mellitus (22),(23),(24). Jain (25) demonstrated that hyperglycaemia stimulates the lipid peroxidation of RBC and Kannan and Jain (26) later showed that it increases oxidative stress in cells in vitro. Contrary to our observations and to that of others, there are several studies which did not find increased oxidative stress in type 2 diabetes mellitus patients (27).
In an animal study, Midaoui and Champlain (28) sufferred the rat from type 2 diabetes mellitus and examined oxidative stress in the model of rat. Notably, they observed that hyperglycaemia alone does not induce oxidative stress unless it was accompanied by insulin resistance; thereby, implying that the involvement of reactive oxygen species is selectively related to insulin resistance (29).
Our results reveal a significant increase in the concentration of MDA in type 2 diabetic patients as compared to the control subjects (Table/Fig 1). This is in agreement with the other published reports (22),(23),(24),(25),(26). Our results show that BMI, MDA and leptin are statistically increased in female diabetic patients as compared to male subjects (Table/Fig 1).
Many investigators have demonstrated that leptin has a major relationship with BMI (30),(31),(32),(33),(34),(35). In our study, also, leptin showed a correlation with BMI, both inmales and females with diabetes and in control subjects. Leptin showed a correlation with MDA in both males and females with diabetes. A clear tendency towards being obese and overweight was apparent in female and male diabetic patients (BMI, 30.07±6.08 and 25.05±1.85 kg/m2) and in control subjects (BMI, 30.60±5.50 and 25.97±4.36 kg/m2). Some of the type 2 diabetes mellitus patients suffered from Hyperlipidaemia. Therefore, our results apparently showed that being obese and overweight gave rise to increased oxidative stress in type 2 diabetes mellitus patients. Being obesity and overweight did not change the oxidative stress in the control subjects. Our study focussed on the association between serum leptin concentration and lipid peroxidation in type 2 diabetics. Recent studies have showed that leptin significantly increases intracellular reactive oxygen species in microvascular endothelial cells, particularly in diabetics (36). According to our study,increased leptin levels observed in male and female diabetics may be related to increased lipid peroxidation (Table/Fig 2).Literature findings on the role of leptin in diabetes is conflicting. Investigators have reported either increased (37), decreased (38),(37),(38),(39) or unchanged (40),(41) leptin levels in diabetics. As Wauters et al. (42) have pointed out, adiposity and gender are the main determinants of leptin levels in normal controls and diabetic patients. Therefore, part of the controversy among previous reports could be related to the difference in the adiposity or the gender of the patients. Many investigators have described leptin alterations only in obese or overweight patients (38), (37),[40). Few workers have studied only men (37) or women (39). The mechanism by which leptin stimulates oxidative stress conditions is unclear, but it may be related to the fact that leptin stimulates mitochondrial fatty acid oxidation and the increased generation of reactive radicals (43). Sebnem et al. (44) have observed a significant decrease in the leptin levels in the plasma of streptozotocin- induced diabetic rats. Streptozotocin-induced hypoleptinaemia may be related to a reduced adipose tissue mass and to the reduced assimilation and storage of energy substrates in the fat tissue in insulin deficiency and/or to the direct toxic effect of streptozotocin on the adipose tissue (45). Panarotto et al. (46) has described lower leptin concentrations in females with diabetes as compared to those in the control subjects. Our data only appear to be in contrast with this finding; our patients actually had higher leptin levels and higher fasting serum glucose concentrations than those studied by Panarotto's group. Moreover, in correlation analysis, BMI is considered to be a significant predictor of hyperleptinaemia (Table/Fig 2). In the correlation analysis using leptin as the dependent variable, BMI and MDA were found to be significant predictors of leptin. In the present study, it was found that there was a correlation between serum leptin and BMI in males and females in normal and diabetic subjects. Gender specific correlation showed an association between leptin and MDA in diabetic patients. Serum leptin showed a significant relationship to MDA in male and female diabetic patients (r = 0.124 and r= 0.271, p < 0.05). This trend reflects the increased MDA in males and females. Therefore, serum MDA levels are confounded by leptin or vice versa, such that in diabetes. Nakanishi et al. (47) have investigated the association between leptin and oxidative stress and have explained this association exclusively through obesity. Many investigators demonstrated that leptin had a major correlation with BMI [48,(49),(50),(51),(52). There is still a controversy that leptin concentrations are affected by type 2 diabetes. Surveys of Mexican-American (53) and German (54) subjects showed that leptin did not differ between normal subjects and subjects with type 2 diabetes, with matched BMI in males and females. In another report, it was found that baseline plasma leptin levels in subjects with newly diagnosed or long-standing type 2 diabetes were not significantly different from nondiabetic controls matched for BMI (54). Other reports comparing plasma leptin levels between controls and weight-matched subjects with type 2 diabetes have led to discrepant conclusions, showing no effect (55),(56) or a decrease in leptin (57),(58). Our present study shows a similar relationship between leptin and oxidative stress in obese and overweight type 2 diabetes mellitus hyperleptinaemic patients. Finally, our study on individuals who were referred to the Department of Diabetes Center in 5th Azar Hospital in the Golestan University of Medical Sciences on the South East of the Caspian Sea indicated that Type 2 diabetes was associated with higher leptin and MDA levels and BMI. In the correlation analysis, we found a significant relation between leptin levels and BMI in males and females. Increased lipid peroxidation and hyperleptinaemia may play a role in the beginning and in the development of type 2 diabetes mellitus.
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