Importance of hypoglycemia-induced glucose production during isolated glucagon deficiency.

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Abstract
Studies were undertaken to assess the ability of the body to compensate for glucagon lack. Somatostatin and basal replacement amounts of insulin were infused into overnight fasted dogs for 4.5 h to create a period of prolonged glucagon deficiency. Glucose production (GP) was measured using a primed constant infusion of [3H]glucose and gluconeogenesis (GNG) was assessed by measuring the conversion of circulating alanine and lactate into glucose. Glucagon lack of 4 h duration was associated with a 28 .+-. 4% sustained fall in overall GP, a 136 .+-. 49% increase in GNG and a 39 .+-. 5 mg/dl decrease in the plasma glucose level. When the hypoglycemia attendant on glucagon lack was prevented by the infusion of glucose, endogenous GP decreased by 67 .+-. 7% and GNG remained mildly suppressed (20%). In postabsorptive dogs basal glucagon is responsible for over 2/3 of GP, its primary role being a stimulation of glycogenolysis. Basal glucagon is essential for the maintenance of normal GP and euglycemia when insulin is present. The hypoglycemia attendant on selective glucagon deficiency plays an important role in maintaining GP and limiting glucose utilization under this circumstance. The stimulation of GP induced by hypoglycemia involves a glycogenolytic and gluconeogenic response.