THE INFLUENCE OF REGIONAL ADIPOSITY ON ATHEROGENIC RISK-FACTORS IN MEN AND WOMEN WITH TYPE-2 DIABETES

To determine firstly whether body fat distribution could predict the presence of atherogenic risk factors better than overall adiposity in Type 2 diabetes, and secondly whether sex differences in these risk factors could be explained by sex differences in fat distribution, waist-to-hip girth ratio (WHR), serum lipids, lipoproteins, apolipoproteins, plasma lipolytic activity, and blood pressure were assessed in 47 patients with Type 2 diabetes, 21 women matched for age, body mass index (BMI) and blood glucose control with 26 men. The men had higher WHR (0.95 (range 0.83-1.07) vs 0.82 (0.74-0.94), p < 0.001), lower HDL-cholesterol (1.03 +/- 0.05 vs 1.38 +/- 0.06 mmol l-1, p < 0.001) and apolipoprotein A1 (1.40 +/- 0.06 vs 1.76 +/- 0.06 g l-1, p < 0.001) concentrations, and higher hepatic lipase activities (16.2 (6.4-38.0) vs 8.6 (2.3-23.1) mmol h-1 l-1, p < 0.01). In both men and women, BMI and WHR were positively related to serum triglyceride, insulin and C-peptide concentrations. In women, HDL-cholesterol was negatively related to BMI (r = -0.45, p < 0.05) but only possibly related to WHR (r = -0.33, NS). In men, by contrast, WHR was related negatively to HDL-cholesterol (r = -0.60, p < 0.005), HDL2-cholesterol (r = -0.43, p < 0.05), and apolipoprotein A1 (r = -0.70, p < 0.001) and positively to hepatic lipase activity (r = 0.65, p < 0.001), whereas the same relationships with BMI were not significant. Neither WHR nor BMI was significantly related to systolic or diastolic blood pressure in men or women. When 10 men and 10 women were matched for WHR, the sex difference in HDL-cholesterol, HDL2-cholesterol and hepatic lipase activity lost statistical significance but apolipoprotein A1 and HDL3-cholesterol remained significantly lower in men. WHR is thus a better predictor than BMI of several atherogenic risk factors in men (but not women) with Type 2 diabetes. The observed sex differences in factors relating to HDL metabolism can be only partially explained by differences in regional adiposity.