Postprandial insulin deficiency is the most powerful explanatory factor of deteriorating glucose control in newly presenting type 2 diabetes. "Indices of insulin sensitivity and pancreatic beta-cell responsiveness explain fasting glucose and HbA1c (glycated hemoglobin) well but fail to explain postprandial glucose," add investigators from City University in London and the University of Wales College of Medicine, United Kingdom.
The investigators examined the ability of indices of insulin sensitivity and pancreatic beta-cell responsiveness to explain interindividual variability of glucose control measures in 65 patients with newly presenting type 2 diabetes.
Minimal model-derived insulin sensitivity, glucose effectiveness, first-phase insulin secretion and disposition index were determined using an insulin-modified iv glucose tolerance test.
Fasting/basal and postprandial pancreatic beta-cell responsiveness was measured by a standard meal tolerance test.
Stepwise linear regression was used with these indices to explain the interindividual variability of fasting and postprandial concentrations of plasma glucose, plasma insulin and HbA1c.
Results showed a negative correlation between measures of pancreatic beta-cell responsiveness and fasting plasma glucose. Pancreatic beta-cell responsive measures were positively correlated with fasting plasma insulin and insulin response to the meal tolerance test.
Minimal model-derived insulin sensitivity was found to be negatively correlated with fasting plasma insulin but was not correlated with any glucose variable.
Postprandial beta-cell responsiveness and disposition index were the "most informative in explaining interindividual variability," according to the investigators. J Clin Endocrinol Metab 2002; 87(1): 198-203