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J Korean Diabetes Assoc. 2000 Apr;24(2):216-224. Korean. Original Article.
Jun DW , Kim SH , Lee JH , Choi WH , Park YS , Kim TH .
Department of internal medicine, Han yang University, Collage of Medicine, Seoul, Korea.
Abstract

BACKGROUND: There is growing evidence for a adipoinsular axis, between adipose tissue and pancreatic beta cells via the hormones leptin and insulin, in mice models, Insulin is adipogenic and increases the production of leptin by adipose tissue, Leptin feeds back to reduce both insulin secretion and insulin gene expression. But human obesity is a complex disorder, with many factors playing a parts; the pathophysiology of leptin is not as simple as it seems to be in mice models of obesity. We therefore explored the dysregulation between leptin and insulin concentration in human model. METHOD: Using radioimmunoassay, we measured serum leptin concentrations in Type 2 diabetic patients (male 26, male 52). Using body composition, we measured total and regional adiposity. The data were analyzed using t-tast to test difference in serum leptin concentration, and other factors were evaluated by partial correlation analysis. RESULT: Serum leptin concentrations in both sex was strongly and positively correlated with total adiposity (r=0.588, p<0.001), Serum leptin concentration was correlated with serum insulin concentration (r=0.41, p=0.002) even after adjusting for adiposity in both sex (r=0.32, p=0.021). Serum leptin concentration was more highly correlated with abdominal adiposity than peripheral adiposity(r=0.693 vs r=0,628). Leptin concentration were higher in women than men, even at the same adiposity, However, no independent association was seen between leptin and hypertension as well as total cholesterol. CONCLUSION: Serum leptin concentration was correlated with serum insulin concentration even after adjusting for adiposity in both sex, In human, such a putative loss of leptin reception by beta cell could result in dysregulation of the adipoinsular axls and a corresponding failure to suppress insulin secretion, resulting in chronic hyperinsutinemia.

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