Is Type 2 Diabetes a Different Disease in Obese and Nenobese Patients?
OBJECTIVE The main purpose of this work was to study the possible differences in insulin secretion in a large group of type 2 diabetic patients in relation to diabetes duration, obesity, and the presence of secondary failure after treatment with oral hypoglycemic agents.
RESEARCH DESIGN AND METHODS There were 147 nonobese and 215 obese type 2 diabetic subjects, aged 35–80 years, investigated in a cross-sectional descriptive study. Subjects were grouped according to whether glycemic control was good (mean blood glucose <8.5 mmol/l) or poor. β-Cell function was assessed by measuring meal-stimulated insulin and C-peptide concentrations, as the mean of the three postprandial increments above the premeal value.
RESULTS Basal C-peptide concentrations were significantly higher in obese than nonobese patients of both groups. The mean of meal-stimulated C-peptide concentrations was also significantly higher in obese than nonobese patients with good glycemic control, but not in the secondary failure groups. In nonobese and obese patients considered separately, a significant negative correlation between the mean of daily blood glucose and meal-stimulated C-peptide was observed (r = −0.705 and r = −0.679, respectively, P < 0.001) and the residual β-cell function was significantly correlated with the known duration of diabetes and metabolic control, but not with BMI, in both groups.
CONCLUSIONS On average, obese diabetic subjects showed higher meal-stimulated Cpeptide than nonobese subjects only in well-controlled groups. In both obese and nonobese patients, an inverse association between meal-stimulated insulin secretion and duration of diabetes was observed. In obese patients, as in nonobese patients, the lower β-cell function seems likely to be the major pathogenetic factor in the appearance of secondary failure, while being overweight plays only a minor role, thus showing that type 2 diabetes is the same disease in obese and nonobese patients.
- Received June 13, 1997.
- Revision received June 29, 1998.
- Accepted June 29, 1998.
- Copyright © 1998 by the American Diabetes Association