Abstract
Betatrophin is a newly identified circulating adipokine playing a role in the regulation of glucose homeostasis and lipid metabolism. But its role in metabolic syndrome (MetS) remains unknown. Therefore, we aimed to compare the circulating betatrophin concentrations between patients with MetS and healthy controls. We recruited 47 patients with MetS and 47 age and sex matched healthy controls. Anthropometric and biochemical measurements were performed, and serum betatrophin levels were detected by ELISA. Full-length betatrophin levels in patients with MetS were significantly higher than those in controls (694.84 365.51 pg/ml versus 356.64 287.92 pg/ml; P <0.001). While no significant difference of total betatrophin levels was found between the two groups (1.20 0.79 ng/ml versus 1.31 1.08 ng/ml; P = 0.524). Full-length betatrophin level was positively correlated with fasting plasma glucose (FPG) (r = 0.357, P = 0.014) and 2-hour plasma glucose (2hPG) (r = 0.38, P <0.01). Binary logistic regression models indicated that subjects in the tertile of the highest full-length betatrophin level experienced higher odds of having MetS (OR, 8.6; 95% CI 2.8-26.8; P <0.001). Our study showed that full-length betatrophin concentrations were increased in drug-naïve MetS patients.
Highlights
Metabolic syndrome (MetS) is a cluster of multiple metabolic disorders including abdominal obesity, hypertension, glucose intolerance and dyslipidemia [1]
Betatrophin, known as lipasin, angiopoietinlike protein 8 (ANGPTL8) and refeeding induced fat and liver (RIFL), is a newly identified circulating adipokine predominantly synthesized in the liver and adipose tissue [3,4,5,6]
Since participants were matched for age and gender distribution, both were similar between the two groups
Summary
Metabolic syndrome (MetS) is a cluster of multiple metabolic disorders including abdominal obesity, hypertension, glucose intolerance and dyslipidemia [1]. The prevalence of MetS is increasing at alarming rates threatening people’s health by placing them at a higher risk of cardiovascular diseases, stroke and kidney diseases. Overweight/obesity and insulin resistance are definite risk factors for MetS [2], the underlying causes remain inconclusive. Betatrophin was supposed to be a regulatory mediator of glucose homeostasis and lipid metabolism in previous studies [7, 8]. Yi and colleagues showed that betatrophin promotes beta cell proliferation and expansion in insulin resistant mice [9]. Controversy remains concerning the role of betatrophin in glucose homeostasis and insulin sensitivity [12,13,14]
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