Time sequence of changes in the responsiveness of glycogen breakdown to adrenergic agonists in perfused liver of rats with insulin-induced hypoglycemia

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Abstract

The time-course changes of the responsiveness of glycogen breakdown to a- and ß-adrenergic agonists during insulin-induced hypoglycemia (IIH) were investigated. Blood glucose levels were decreased prior to the alteration in the hepatic responsiveness to adrenergic agonists. The activation of hepatic glucose production and glycogenolysis by phenylephrine (2 µM) and isoproterenol (20 µM) was decreased in IIH. The changes in the responsiveness of glycogen catabolism were first observed for isoproterenol and later for phenylephrine. Hepatic ß-adrenergic receptors showed a higher degree of adrenergic desensitization than did a-receptors. Liver glycogen synthase activity, glycogen content and the catabolic effect of dibutyryl cyclic AMP (the ß-receptor second messenger) were not affected by IIH.

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Glucose counterregulation: prevention and correction of hypoglycemia in humans.

P Cryer (1993)

The prevention or correction of hypoglycemia in humans is the result of both dissipation of insulin and activation of glucose counterregulatory (glucose-raising) systems. Whereas insulin is the dominant glucose-lowering factor, there are redundant glucose counterregulatory factors. Furthermore, there is a hierarchy among the glucoregulatory factors. The first defense against a decrement in plasma glucose is decreased insulin secretion; this occurs with glucose decrements within the physiological range at a glycemic threshold of 4.6 +/- 0.2 mmol/l. However, biological glucose recovery from hypoglycemia can occur despite mild (approximately 2-fold) peripheral hyperinsulinemia and can occur in the absence of portal hypoinsulinemia. Thus additional (glucose counterregulatory) factors must be involved. Critical glucose counterregulatory systems are activated at glycemic thresholds of approximately 3.8 mmol/l (the level at which brain glucose uptake is first measurably reduced), well above the thresholds for symptoms of hypoglycemia (approximately 3.0 mmol/l) and those for cognitive dysfunction resulting from neuroglycopenia (approximately 2.7 mmol/l). Among the glucose counterregulatory factors, glucagon plays a primary role. Indeed, it may be that hypoglycemia does not occur if the secretion and actions of both glucagon and insulin, among the glucoregulatory hormones, are normal. Epinephrine is not normally critical, but it becomes critical to glucose counterregulation when glucagon is deficient. Because hypoglycemia develops or progresses when both glucagon and epinephrine are deficient and insulin is present, these three hormones stand high in the hierarchy of redundant glucoregulatory factors.(ABSTRACT TRUNCATED AT 250 WORDS)