The influence of physical training on glucose tolerance, insulin sensitivity, and lipid and lipoprotein concentrations in middle-aged hypertriglyceridaemic, carbohydrate intolerant men

The effects of 9 weeks of moderate intensity exercise training while on a weight-maintaining diet were studied in 19 untrained middle-aged, hypertriglyceridaemic, carbohydrate intolerant men. Initial mean maximum oxygen consumption was low (29.7±1.0 ml-min −1 · kg −1 ; mean±SEM) and improved (34.2±1.4ml·min −1 ·kg −1 , p <0.01) with exercise training. Fasting glucose, insulin, lipid and lipoprotein concentrations did not change. While the abnormal glucose response to oral glucose did not change with training, insulin concentrations were significantly ( p <0.05) lower at 90 and 120 min during the final oral glucose tolerance test. Insulin mediated glucose uptake did not change, indicating that the degree of exercise training failed to improve in vivo insulin sensitivity. Significant associations were found between the following parameters measured: fasting concentrations of triglycerides and insulin, very low density lipoprotein-triglycerides and glucose, and measures of in vivo insulin resistance and fasting insulin levels, suggesting that insulin resistance in these glucose intolerant subjects may play a role in their hypertriglyceridaemia. These data indicate that moderate increases in physical training alone are not sufficient to improve the carbohydrate, insulin and lipid metabolism of hypertriglyceridaemic, glucose intolerant men.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/46020/1/125_2004_Article_BF00292538.pd

Impaired glucose tolerance in mice with a targeted impairment of insulin action in muscle and adipose tissue

Type 2 diabetes is a complex metabolic disorder characterized by peripheral insulin resistance and impaired beta cell function. Insulin resistance is inherited as a non-mendelian trait. In genetically predisposed individuals, resistance of skeletal muscle and adipose tissue to insulin action precedes the onset of clinical diabetes, and is thought to contribute to hyperglycaemia by leading to impaired beta cell function and increased hepatic glucose production. It is not clear whether beta cell and liver defects are also genetically determined. To test the hypothesis that insulin resistance in muscle and fat is sufficient to cause type 2 diabetes in the absence of intrinsic beta cell and liver abnormality, we generated transgenic mice that were insulin-resistant in skeletal muscle and adipose tissue. These mice developed all the prodromal features of type 2 diabetes but, despite the compounded effect of peripheral insulin resistance and a mild impairment of beta cell function, failed to become diabetic. These findings indicate the need for a critical re-examination of the primary site(s) of insulin resistance in diabetes