Central Obesity Diminishes Circulating Betatrophin Level in Middle-aged Male Subjects

Abstract

Central adiposity presents an important risk factor for advancing insulin insensitivity and type 2 diabetes mellitus. Betatrophin, a liver or adipocyte-derived hormone, was assumed to improve islet insulin secretion and compensate insulin resistance but its level during obesity is still conflicted. This study aimed to explore serum betatrophin level in centrally-obese middle-aged men with diabetic potentials compared with age-matched non-obese ones. Sixty-eight male subjects of 40-60 years of age, residing in North Okkalapa Township, Yangon, Myanmar, were recruited and classified into centrally-obese group (n=34) and non-obese group (n=34). Fasting blood samples were obtained to quantify plasma glucose by glucose oxidase method, and serum insulin and betatrophin levels by ELISA. Plasma glucose levels were comparable between the two groups, while insulin concentration of obese group was significantly greater than that of non-obese group. Therefore, HOMA-IR was markedly increased in obese subjects when compared to non-obese ones (4.87±0.28 vs 1.90±0.14, p<0.001) and so did HOMA-β (310.88±26.58 vs 149.00±11.83, p<0.001). Interestingly, betatrophin hormone level was significantly reduced in obese group than non-obese group (1.72±0.21 vs 2.72±0.26 ng/ml, p<0.01). Moreover, betatrophin had a strong negative correlation with glucose and insulin levels (p<0.05) as well as with the indicator of central adiposity, waist circumference (p<0.05), among the subjects. However, significant correlation between betatrophin and HOMA-IR and HOMA-β was not observed in both groups (p=0.14 and 0.20 respectively). Taken together, betatrophin hormone has been found to decrease in adult central obesity, which is noticeably associated with insulin resistance and compensatory beta-cell hyperfunction. Betatrophin, previously regarded as beta-cell mitogen, has been denied in this study, owing to lack of correlation with HOMA indexes of diabetes.