Glucose-dependent insulin-releasing peptide [GIP] in patients with type 2 diabetes mellitus with and without autonomic neuropathy

ABSTRACT

This study was conducted to investigate the role of glucose-dependent insulin-releasing peptide or gastric inhibitory polypepetide [GIP] in the control of glycemic state in patients with type 2 diabetes mellitus in the presence and absence of autonomic neuropathy. Twenty patients with type 2 jiabetes mellitus and 10 healthy normal subjects were studied. The diabetic patients were divided into 2 equal groups one group with autonomic neuropathy [AN] and the other without AN according to cardiovascular autonomic function tests. Patients and controls were subjected to clinical examination and determination of HbA[1c]%, fasting blood sugar and basal insulin level. One-hour after ingestion of standard mixed meal [50 gm carbohydrate and 8% amino acid in 400 ml water] blood samples were collected for determination of glucose, insulin, and GIP plasma levels. Insulin resistance index was calculated from the homeostasis model assessment equation [HOMA]. A significantly impaired postprandial GIP and insulin levels as well as their responses to the ingestion of the mixed meal in the type 2 diabetics with AN was observed compared to those without AN. Postprandial GIP level was found to be correlated negatively with postprandial glucose level [r=-0.54] and positively with postprandial insulin level [r=-0.45], P < 0.05 for all diabetic patients. In diabetic patients with AN, significant -negative correlations were detected between duration of diabetes and postprandial GIP level [r= -0.66], absolute GIP response [r= -0.74], as well as% GIP response [r=- 0.71] [P < /= 0.05 for all.]. GIP plays an important role in the physiologic control of postprandial glucose homeostasis. GIP responses were lower in the diabetics as a group compared with healthy subjects despite similar basal levels. Moreover, In diabetic patients with autonomic neuropathy, there was a delayed and impaired GIP response to the mixed meal. Their absolute and% GIP responses were significantly lower than those of control subjects and patients without autonomic neuropathy