Insulin and glucagon in prevention of hypoglycemia during exercise in humans
- 1 May 1991
- journal article
- research article
- Published by American Physiological Society in American Journal of Physiology-Endocrinology and Metabolism
- Vol. 260 (5) , E695-E704
- https://doi.org/10.1152/ajpendo.1991.260.5.e695
Abstract
To assess the roles of decrements in insulin and increments in glucagon in the prevention of hypoglycemia during moderate exercise (approximately 60% peak O2 consumption for 60 min), normal young men were studied during somatostatin infusions with insulin and glucagon infused to 1) hold insulin and glucagon levels constant, 2) decrease insulin, 3) increase glucagon, and 4) decrease insulin and increase glucagon during exercise. In contrast to a comparison study (saline infusion), when insulin and glucagon were held constant, glucose production did not increase and plasma glucose decreased from 5.5 +/- 0.2 to 3.4 +/- 0.2 mmol/l (P less than 0.001) initially during exercise. Notably, plasma glucose then plateaued and was 3.3 +/- 0.2 mmol/l at the end of exercise. This decrease was at most only delayed when either insulin was decreased or glucagon was increased independently. However, when insulin was decreased and glucagon was increased simultaneously, there was an initial increase in glucose production, and the glucose level was 4.5 +/- 0.2 mmol/l at 60 min, a value not different from that in the comparison study. Thus we conclude that both decrements in insulin and increments in glucagon play important roles in the prevention of hypoglycemia during exercise and do so by signaling increments in glucose production. However, since hypoglycemia did not develop during exercise when changes in insulin and glucagon were prevented, an additional counterregulatory factor, such as epinephrine, must be involved in the prevention of hypoglycemia during exercise, at least when the primary factors, insulin and glucagon, are inoperative.Keywords
This publication has 27 references indexed in Scilit:
- Role of changes in insulin and glucagon in glucose homeostasis in exercise.Journal of Clinical Investigation, 1986
- Enhanced glycemic responsiveness to epinephrine in insulin-dependent diabetes mellitus is the result of the inability to secrete insulin. Augmented insulin secretion normally limits the glycemic, but not the lipolytic or ketogenic, response to epinephrine in humans.Journal of Clinical Investigation, 1985
- Interactions between glucagon and other counterregulatory hormones during normoglycemic and hypoglycemic exercise in dogs.Journal of Clinical Investigation, 1984
- Adrenergic blockade alters glucose kinetics during exercise in insulin-dependent diabetics.Journal of Clinical Investigation, 1984
- Mechanisms of postprandial glucose counterregulation in man. Physiologic roles of glucagon and epinephrine vis-a-vis insulin in the prevention of hypoglycemia late after glucose ingestion.Journal of Clinical Investigation, 1983
- Neuroendocrine responses to glucose ingestion in man. Specificity, temporal relationships, and quantitative aspectsJournal of Clinical Investigation, 1983
- Identification of Type I Diabetic Patients at Increased Risk for Hypoglycemia during Intensive TherapyNew England Journal of Medicine, 1983
- Exercise in diabetic man: glucose turnover and free insulin responses after glycemic normalization with intravenous insulinCanadian Journal of Physiology and Pharmacology, 1982
- Role of Glucagon, Catecholamines, and Growth Hormone in Human Glucose CounterregulationJournal of Clinical Investigation, 1979
- Physical exercise and fuel homeostasis in diabetes mellitusDiabetologia, 1978