Endocrine Abstracts

Objective: Insulin insufficiency which is the result of deficiency of β-cells is the common feature for all types of diabetes. Therefore protection of functional β-cell mass is the keystone of diabetes treatment. Betatrophin, a newly determined hormone, has been identified as a potent stimulator that increases the production and expansion of β-cells in mice. However, very little is known about the physiological role of betatrophin in human.Chronic treatment of rodents with GLP-1 agonists can result in an increase in β-cell mass due to increases in β-cell proliferation, neogenesis and decreases in β-cell apoptosis.The aim of this study is to show the effect of GLP-1 agonist treatment on betatrophin levels and comparison with insülin treatment in type 2 diabetic (T2DM) patients. This is the first human study in the literature with relation between betatrophin and GLP-1 treatment.

Methods: This prospective study included 27 patients with uncontrolled T2DM which were treated with metformin and sulfonylurea. 17 patients were enrolled in GLP-1 group and 10 patients were insulin group. Fasting betatrophin levels were evaluated before and at the 6.th month of treatment.

Results: Demographical features and BMI of two groups were similar. Betatrophin levels decreased in both groups after 6 months of treatment. But no statistical difference is observed between compared groups (P=0.473). The reduction in betatrophin levels were only significant in insülin treated group (P=0.017). There were no significant relation between betatrophin and c-peptid levels (P=0.903). Also betatrophin levels were not correlated with age, sex, duration of diabetes, variables of glucose and lipid profiles.

Conclusion: Betatrophin levels were decreased significantly in insulin group but not in GLP-1 group. Incretin based treatments are known to increase β-cell mass and betarophin is a potent stimulator of β-cells. As betatrophin levels were still high in subjects on GLP-1 treatment it can be postulated that betatrophin would be a pathway on β-cell increment during GLP-1 treatment in long-term. However, in order to obtain more significant results further studies with higher number of patients and long-term follow-up is needed.