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Objective:To investigate the relationship between body fat distribution and insulin resistance, islet β cell function and metabolic disorders in adult population.Methods:A total of174subjects aged20-68years were recruited. Information of anthropometric parameters, blood biochemical indexes blood pressure, serum lipid, liver function, kidney function, free fatty acid (FFA), high sensitivity C reaction protein (hs-CRP) and the results gained from oral glucose tolerance test (OGTT), insulin releasing test (IRT) were collected. Body fat distribution was measured with Dual energy X-ray absorptiometry (DEXA).Results:(1) The trunk fat mass/total fat mass (TTFM%) and android fat mass/gynoid fat mass (A/G) were positively correlated to the blood pressure, blood lipid, serum glucose, ALT, UA, InHOMA-IR and hs-CRP.(2) The group of obesity had higher DBP, serum insulin, TG, ALT, UA, InHOMA-IR and hs-CRP compared with the normal weight group(P<0.05).(3) The group of abdominal obesity had higher blood pressure, serum glucose, HbA1c, serum insulin, TG, TC, FFA and hs-CRP than the non-abdominal obesity group (P<0.05).(4) Compared with the group of normal metabolism, the group of metabolic disorders had higher TTFM%and A/G (P<0.05).(5) After multiple stepwise regression analysis, the main influencing factors of InHOMA-IR and InHOMA-β were TFFM%and G%, respectively. Logistic regression showed that A%(OR=3.0,95%CI1.86-8.17) was a risk factor for diabetes, A/G(OR=21,95%CI1.75-6.56) was a risk factor for and dyslipidemia.Conclusions:The DEXA method is used to measure the body fat distribution in this study and the conclusions are:(1) It is more likely to get insulin resistance, metabolic disorders and low-grade inflammation in adults either overall obesity or abdominal obesity.(2) The trunk and android fat deposition aggravates insulin resistance, metabolic disorders and low-grade inflammation.(3) The main influencing factors of insulin resistance and islet β cell function are trunk and gynoid fat, respectively.(4) Android fat mass is a major risk factor for glycolipid metabolism.
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