Role of insulin in regulating amino acid metabolism in normal and alloxan-diabetic cattle.
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Experimental diabetes was induced in the bovine in two experiments by intravenous injection of alloxan (110 mg/kg or 60 mg/kg) in order to determine the role of insulin on nitrogen and amino acid metabolism. In experiment 1, insulin was injected to control hyperglycemia in one group of steers immediately after alloxan treatment (110 mg/kg). In experiment 2, insulin was injected beginning 6 days following alloxan treatment (60 mg/kg) to control hyperglycemia. Plasma glucose increased to 800-1400 mg/100 ml within 5-6 days following alloxan administration (experiment 1). A large surge of insulin release occurred immediately after alloxan administration, which was followed by a decrease in insulin concentrations to subnormal levels in those animals not treated with insulin. Alloxan-treated steers became acidotic by day 2 as indicated by a drop in blood pH, bicarbonate and base excess. Acid-base status improved in steers treated with alloxan plus insulin but did not return to normal. Alloxan treatment caused a marked increase in serum urea-N and creatinine concentrations and insulin treatment of the alloxanized animal decreased both serum urea-N and creatinine concentrations. Treatment with alloxan caused a two- to threefold increase in the plasma concentrations of valine, isoleucine, leucine, lysine and 3-methylhistidine and a decrease in alanine, threonine, citrulline and arginine. Insulin treatment of the alloxanized bovine maintained normal plasma concentrations of valine, isoleucine and leucine. In a third experiment, the injection of insulin (6 U/kg) into normal cattle caused a transient decline in plasma concentrations of branched-chain amino acids (BCAA); however, if glucose was continuously infused (125 mmol/hour) in addition to insulin injection, a sustained decrease in plasma BCAA concentrations was observed. These data support the concept that insulin promotes decreased plasma concentrations of BCAA either by promoting tissue anabolism by stimulating tissue uptake and protein synthesis or decreasing proteolysis and BCAA release.