BACKGROUND: The aim of this study was to investigate insulin sensitivity and secretion in lean and obese Asian (Thai) type 2 diabetic patients. METHODS: Insulin sensitivity and insulin secretion was assessed with the hyperinsulinemic euglycemic (80 mU/m(2) per min) and hyperglycemic clamp technique in 9 lean and 10 obese patients with type 2 diabetes and 4 lean and 4 obese nondiabetic control subjects. RESULTS: Obese type 2 diabetics had a lower M-value (sensitivity to exogenous insulin) than lean type 2 diabetics (8.7 +/- 1.3 versus 16.5 +/- 1.6 mg . fat free mass kg(-1) . min(-1), P < 0.001) and obese control subjects (15.9 +/- 4.0 mg . fat free mass kg(-1) . min(-1), P < 0.05). Insulin sensitivity (M-value) was similar in lean type 2 diabetics as compared to lean nondiabetic control subjects. During the hyperglycemic clamp, the first (P < 0.001) and second phase (P < 0.02) of insulin and C-peptide response (P < 0.02) was significantly decreased in lean type 2 diabetics as compared to lean nondiabetic subjects. In obese type 2 diabetics, the first and second phase of insulin response was significantly decreased (P < 0.05) compared to obese nondiabetic subjects. CONCLUSIONS: Obese type 2 diabetics have significant defects in both insulin sensitivity and insulin secretion whereas lean type 2 diabetics demonstrate primarily a defect in insulin secretion. Lean diabetics have similar insulin sensitivity when compared to healthy age- and sex-matched nondiabetic subjects during the euglycemic clamp study, suggesting the lack of significant insulin resistance in lean type 2 diabetics.
BACKGROUND: The aim of this study was to investigate insulin sensitivity and secretion in lean and obese Asian (Thai) type 2 diabeticpatients. METHODS:Insulin sensitivity and insulin secretion was assessed with the hyperinsulinemic euglycemic (80 mU/m(2) per min) and hyperglycemic clamp technique in 9 lean and 10 obesepatients with type 2 diabetes and 4 lean and 4 obese nondiabetic control subjects. RESULTS:Obese type 2 diabetics had a lower M-value (sensitivity to exogenous insulin) than lean type 2 diabetics (8.7 +/- 1.3 versus 16.5 +/- 1.6 mg . fat free mass kg(-1) . min(-1), P < 0.001) and obese control subjects (15.9 +/- 4.0 mg . fat free mass kg(-1) . min(-1), P < 0.05). Insulin sensitivity (M-value) was similar in lean type 2 diabetics as compared to lean nondiabetic control subjects. During the hyperglycemic clamp, the first (P < 0.001) and second phase (P < 0.02) of insulin and C-peptide response (P < 0.02) was significantly decreased in lean type 2 diabetics as compared to lean nondiabetic subjects. In obese type 2 diabetics, the first and second phase of insulin response was significantly decreased (P < 0.05) compared to obese nondiabetic subjects. CONCLUSIONS:Obese type 2 diabetics have significant defects in both insulin sensitivity and insulin secretion whereas lean type 2 diabetics demonstrate primarily a defect in insulin secretion. Lean diabetics have similar insulin sensitivity when compared to healthy age- and sex-matched nondiabetic subjects during the euglycemic clamp study, suggesting the lack of significant insulin resistance in lean type 2 diabetics.