Variation in Circulating Betatrophin/ANGPTL8 Levels in Normal and Overweight/Obese Pregnant Women BC04-BC08
Mohammad Ahmad Hamza,
Assistant Lecturer, Department of Biochemistry, University of Zakho, Zakho, Kurdistan, Iraq.
Introduction: Betatrophin as hepatokine and adipokine influences glucose homeostasis and implicates in the pathophysiological process of obesity and pregnancy. Various studies suggest that metabolic changes in normal weight/lean Pregnant women (PL) are significantly different from overweight/obese pregnant women (PO). However, the exact mechanism of how pre-gravid Body mass index (preBMI) affects betatrophin levels during normal pregnancy and the relationship of betatrophin to other clinical variables in PL and in PO have not been elucidated.
Aim: To elucidate the effect of preBMI on betatrophin level in the initial three trimesters of pregnancy, and to determine the possible correlation between betatrophin and lipid profile parameters/thyroid profile.
Materials and Methods: The cross-sectional study was carried out from December 2016 to May 2017 at Maternity Hospital, Zakho City, Kurdistan Region (Iraq). Betatrophin levels were estimated in 59 pregnant women in initial three trimester of pregnancy. Among 32 PL (pre BMI=24.9 kg/m2) and 27 PO (pre BMI>25 kg/m2), 10 and 8 were in First trimester (FT), 10 and 10 were in Second trimester (ST), 12 and 9 were in Third trimester (TT) respectively. Ten Non-pregnant normal weight/lean (NPL) (BMI=24.9 kg/m2) and 12 Non-pregnant overweight/obese (NPO) (BMI>25 kg/m2) healthy married women of reproductive age were selected as controls. Serum total betatrophin, total triiodothyronine (T3), total-thyroxin (T4), thyroid stimulating hormone (TSH), and estradiol (E2) were estimated by Enzyme linked immunosorbent assay (ELISA) and Triglyceride (TG) was estimated by the glycerophosphate oxidase colorimetric method. One-way analysis of variance (ANOVA), Welch test, Kruskal Wallis test, Games-Howell test, Independent t-test, Mann-Whitney test, and Pearson/Spearman correlation analysis were performed to assess the parameters. The p-value <0.05 was considered statistically significant.
Results: Betatrophin levels were elevated by 21.3% in the PL as compared to NPL group. The raised levels in FT gradually decreased towards the end of gestation. Conversely, in the PO, betatrophin was significantly decreased as compared to NPO group (p-value=0.03). In FT, betatrophine showed a significant decline compared to ST, TT and NPO groups (p= 0.017, 0.006 and 0.001 respectively). In PL, betatrophin was correlated with TSH in ST (r=0.721, p=0.019) and with T3 in TT (r=0.759, p=0.004). In NPL, betatrophin correlated with T3 (r=0.823, p=0.003). In PO, Betatrophin correlated with T3 (r=0.433, p=0.024), T4 (r=0.499, p=0.008), E2 (r=0.609, p=0.001), TG (r=0.570, p=0.002) and Gestational weight gained (GWG) (r=0.676, p=0.0001). TG levels were elevated in all trimesters in PO than in PL.
Conclusion: Our results highlight the potential involvement of T3 and TSH in regulating betatrophin levels during pregnancy. Therefore, T3 and TSH levels beside TG level should be taken into consideration when interpreting clinical studies of betatrophin. Depending upon the preBMI; betatrophin change in different ways in PL and PO women. Conversely to PL, betatrophin levels increased during pregnancy in PO, and correlated with TG. Therefore, maintaining an ideal weight before pregnancy is recommended to avoid pregnancy-related complications such as hypertriglyceridemia and insulin resistance.