In skeletal muscle, at the level of glucose transport, insulin resistance appears to be a major alteration responsible for decreased glucose disposal rates in non-insulin-dependent (type II) diabetes mellitus. This study focuses on in vitro studies of the glucose transport process in human and rat skeletal muscle. Muscle strips from a group of lean type II diabetic patients demonstrated a 50% decrease in insulin responsiveness for glucose transport when compared with nondiabetic subjects. These findings indicate the presence of postreceptor defects in type II diabetic muscles. Furthermore, in an isolated muscle preparation, it could be demonstrated that epitrochlearis muscles from streptozocin-induced diabetic rats were not only resistant to insulin, but also to exercise-induced increase in glucose transport. However, both regular physical exercise and insulin therapy normalized the decreased capacity for glucose transport in the diabetic rat muscles. Therefore, it appears that regular physical exercise and, in some cases insulin therapy, would be advisable for type II diabetic patients with marked muscular insulin resistance to improve peripheral glucose disposal rates.
Skip Nav Destination
Supplement 4: Diabetes & Exercise ‘90| November 01 1992
Interaction of Exercise and Insulin in Type II Diabetes Mellitus
Address Correspondence and reprint requests to Harriet Wallberg-Henriksson, MD, Department of Clinical Physiology, Karolinska Hospital, Box 60500, S-104 01, Stockholm, Sweden.
Harriet Wallberg-Henriksson; Interaction of Exercise and Insulin in Type II Diabetes Mellitus. Diabetes Care 1 November 1992; 15 (11): 1777–1782. https://doi.org/10.2337/diacare.15.11.1777
Download citation file: