Failure of Hyperketonemia to Alter Basal and Insulin-Mediated Glucose Metabolism in Man

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Abstract
The effect of physiologic elevations of plasma hydroxy-butyrate induced by the infusion of sodium D,L-β-hydroxy-butyrate (15 μmol · kg-1 · min-1) on carbohydrate metabolism was examined with the euglycemic insulin clamp technique in nine healthy volunteers. Plasma insulin concentration was acutely raised and maintained at 126 ± 6 μU/ml and plasma glucose was held constant at the fasting level by a variable glucose infusion. Glucose uptake of 6.53 ± 0.80 mg · kg-1 · min-1 was unchanged by hyperketonemia when compared with an intraindividual control study using saline instead of β-OH-butyrate infusion (6.26 ± 0.59 mg · kg-1 · min-1). In studies, in which the degree of metabolic alkalosis accompanying butyrate infusion was mimicked by the continuous administration of bicarbonate, glucose uptake was also unaffected (6.25 ± 0.45 mg · kg-1 · min-1), Furthermore, hyperketonemia had no effect on basal glucose production or the suppression of hepatic glucose production following hyperinsulinemia. It is concluded that moderate elevations in plasma β-hydroxy-butyrate do not alter hepatic or peripheral glucose metabolism.

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