The physiological mechanisms of hypoglycaemic glucose counterregulation have been clarified in recent years. Glucagon plays a primary role in promoting glucose recovery from hypoglycaemia and epinephrine largely compensates for deficient glucagon secretion. Recovery from hypoglycaemia fails to occur only in the absence of both glucagon and adrenaline. To the extent that they have deficient glucagon secretory responses to plasma glucose decrements, patients with IDDM are dependent upon adrenaline mediated β-adrenergic mechanisms to promote recovery from hypoglycaemia. Thus, they are at increased risk for prolonged hypoglycaemia if they are treated with β-adrenergic antagonists such as propranolol. The precise mechanisms of nonhypoglycaemia glucose counterregulation - those that blunt physiologic decrements in plasma glucose, prevent hypoglycaemia and restore euglycaemia - have not been fully defined. However, these can be expected to be clarified in the near future and should lead to a better understanding of human hypoglycaemic states.
|Number of pages||7|
|State||Published - Jan 1 1982|