The Effect of Insulin on the Metabolism of Parenteral Maltose in Man Maltose in Man*

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Abstract
Intravenously administered maltose has been suggested as a useful carbohydrate source of greater caloric density per mol than glucose, and its utilization may be significantly influenced by insulin. To study the effect of insulin on the metabolism of parenteral maltose, a 10% maltose solution containing 25 μCi [U-14C/]maltose/liter was infused iv (2.5 or 5.0 mg/ kg.min) in healthy males (21–26 yr) for a 12-h period either with or without insulin. Blood glucose, maltose, insulin, and FFA as well urine maltose, glucose, and 14C and breath 14CO2 were measured hourly. At the 2.5 mg/kg-min rate, 18.8% and 25.3% of the administered dose were recovered as 14CO2 in the expired mg/kg-min rate, 18.8% and 25.3% of the administered dose were recovered as 14CO2 in the expired breath over a 12-h period without and with insulin, respectively. At the 5.0 mgmg/kg-min rate, 10.7% and 11.8% of the infused maltose were expired as 14CO2 without and with insulin, respectively. Serum maltose increased to 100 and 225 mgmg/100 ml by 6 h at the slow and fast rates of infusion, respectively, remaining constant thereafter. Serum glucose and insulin were unaltered during maltose infusion alone. Insulin significantly depressed serum glucose while elevating serum insulin. Plasma FFA decreased in response to maltose at both rates of infusion with and without insulin. At the slow infusion rate, insulin reduced the total sugar excreted in the urine from 34.8% to 9.2% (P < 0.01) of the administered dose. At the fast infusion rate, 53.3% and 48.8% (P =NS) of the administered sugar were excreted in the urine during infusion without and with insulin, respectively. Calculation of the specific activity of the urinary [l4C]glucose as well as the maximal amount of maltose transported per U by the renal tubules suggested that the metabolism of continuously infused infused maltose was dependent upon renal hydrolysis of maltose to glucose, with subsequent reabsorption as glucose.(J Clin Endocrinol50: 764,1980)

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