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Activation of Liver Branched-Chain -Keto Acid Dehydrogenase in Rats by Excesses of Dietary Amino Acids¹

Departments of Biochemistry and Nutritional Sciences, College of Agricultural and Life Sciences, University of Wisconsin-Madison, Madison, WI 53706

As part of an effort to explain the leucine-induced depressions of plasma isoleucine and valine concentrations, and the concomitant stimulation of valine oxidation in vivo, branched-chain -keto acid dehydrogenase (BCKAD) activity was measured in livers from rats that were fed for only 6 h/d large quantities of individual amino acids in a low protein diet. Preincubation of homogenates with buffer containing Mg²⁺ and Ca²⁺ allowed estimation of fully active complex. Cytosolic and mitochondrial branched-chain-amino-acid aminotransferase (BCAAT) activities were also measured in livers of rats fed an excess of leucine. The percentage of BCKAD in the active form in livers of rats fed the low protein diet containing an excess of leucine, isoleucine, valine or phenylalanine for 2 d was double that of rats fed the low protein control diet (control, leucine, isoleucine, valine and phenylalanine groups having, respectively, 45 ± 2, 85 ± 7, 85 ± 3, 95 ± 5, and 81 ± 4% of hepatic BCKAD in the active form). Consumption of a low protein diet containing an excess of leucine had no significant effect on either cytosolic or mitochondrial BCAAT activities of liver. The response of BCKAD in liver can contribute to the leucine-induced stimulation of valine oxidation in vivo but analysis of the results of this study leads to the conclusion that other mechanisms, probably in nonhepatic tissues, must also be involved.

KEY WORDS: • branched-chain amino acid antagonism • branched-chain -keto acid dehydrogenase • branched-chain-amino-acid aminotransferase • amino acid toxicity

¹ Research supported in part by the College of Agricultural and Life Sciences, University of Wisconsin-Madison, and by grants AM10748 and P30 AM 26659 from the U.S. Public Health Service, National Institutes of Health.

² Present address: Department of Medicine, Endocrinology Division, Medical University of South Carolina-Charleston, Charleston, SC 29425.

³ To whom reprint requests should be sent.

Manuscript received 18 January 1985. Revision accepted 6 August 1985.

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