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Effects of Euglycemic Hyperinsulinemia on Neonatal Canine Hepatic and Muscle Metabolism

ABSTRACT: The effects of euglycemic hyperinsulinemia on hepatic and muscle metabolism were determined in the fasted newborn dog during the first day of life. Hyperinsulinemia was sustained with a primed constant infusion of insulin whereas euglycemia was maintained with an intravenous infusion of 10% glucose using the insulin clamp technique. Euglycemic hyperinsulinemia caused an increase of glucose utilization from 43.9 ± 3.7 to 66.5 ± 5.4 µmol/kg/min (p<0.001) and reduced endogenous glucose production to 44.4 ± 5.4% of basal values obtained before the induction of hyperinsulinemia. Hepatic tissue glycogen, triglycerides, or intermediates were not altered by hyperinsulinemia nor was the incorporation of [3H]glucose into glycogen. However, the hepatic cytoplasmic redox state was more oxidized, and the incorporation of [3H]glucose into triglycerides was higher among hyperinsulinemic pups. Pups who demonstrated incomplete suppression of endogenous glucose production had metabolite perturbation suggestive of ongoing gluconeogenesis. Despite very few changes in hepatic tissue metabolite levels, pups subjected to hyperinsulinemia demonstrated a linear uptake of 2- deoxyglucose into hepatic tissue as a function of circulating insulin levels during hyperinsulinemia. Muscle tissue demonstrated no alterations of tissue metabolites, glycogen, or triglycerides levels or precursor incorporation into these storage pools. Nonetheless, 2-deoxyglucose incorporation into neonatal muscle tissue was a significant linear function of plasma insulin concentration. Total tissue 2-deoxyglucose uptake was lower in muscle tissue than in hepatic tissue (245 ± 19 versus 514 ± 20 dpm/g/min) (p<0.001). These data suggest that hyperinsulinemia has little effect on neonatal net glycogen or triglyceride synthesis but does augment tissue glucose uptake. In newborn liver, part of the insulin-stimulated glucose uptake may be used in futile cycles such as triglyceride synthesis and lipolysis. Furthermore, hyperinsulinemia probably does not suppress hepatic gluconeogenesis as evident by persistent glucose production during the clamp period.