Lipid profile and its relation to fasting insulin level in non-insulin dependent diabetes mellitus (NIDDM).

Atherosclerotic cardiovascular disease is the major cause of morbidity and mortality in NIDDM patients. But the exact pathophysiology of accelerated atherosclerosis seen in NIDDM is not completely understood. Hyperinsulinemia and hyperlipidemia frequently coexist in these subjects. Present study was undertaken to demonstrate relationship of serum insulin with atherogenic lipids in 92 (male = 62, female = 30) newly diagnosed, middle-aged, nonsmoking, uncomplicated and untreated NIDDM patients with normal body mass index (BMI). Fourty (male = 20, female = 20) non-diabetic healthy subjects with a negative family history of diabetes served as control. After an overnight fasting, venous blood was collected for plasma glucose, serum insulin and lipid profile. ECG and oral glucose tolerance test (OGTT) were done in all subjects. Diabetes mellitus was diagnosed by WHO criteria. Total cholesterol, LDL-c, LDL/HDL ratio, TG (p always < 0.001) and fasting serum insulin (p = 0.033) were significantly higher and HDL-c was significantly lower (p = 0.001) in NIDDM than control subjects. Fasting serum insulin was inversely related to the degree of hyperglycemia in NIDDM subjects (r = -0.1867; p = 0.037). NIDDM with hyperinsulinemia (n = 18) had a strong negative correlation (r = -0.449, p = 0.031) with HDL-c. Neither total cholesterol nor LDL-c had any significant correlation with insulin. The results indicate that diabetic state itself is associated with atherogenic lipid disorder.

The relationship between blood pressure and serum insulin response in glucose intolerant subjects.

One hundred newly diagnosed IGT and type 2 diabetic subjects both normotensive and hypertensive and of age between 40-55 years were studied by oral glucose stimulation. Serum insulin concentrations were measured in the fasting and at 30, 60 and 120 minutes after glucose administration. Postglucose serum insulin responses were found to be significantly higher in the hypertensive subjects with FPG < 7.8 mmol/l (p < 0.05 at 30, 60 and 120 minutes) as compared with the corresponding values of the normotensive subjects with comparable fasting hyperglycemia. No significant difference in insulin responses between hypertensive and normotensive subjects was found in those with FPG > 7.8 mmol/l. A positive correlation was observed between diastolic blood pressure and 2 hour postglucose serum insulin concentration in those with FPG < 7.8 mmol/l (P < .05). The results suggested that hyperinsulinemia is a feature of hypertensive subjects with mild glucose intolerance and not of those with severe glucose intolerance. The absence of elevated insulin response in hypertensive subjects with advanced type 2 diabetes might be due to severe B cell decompensation. It appears that insulin resistance is somehow associated with essential hypertension and hyperinsulinemia is not necessary for the maintenance of raised blood pressure.