Metabolism - Clinical and Experimental
Volume 46, Issue 2 , Pages 164-167, February 1997

Splanchnic versus whole-body production of α-ketoisocaproate from leucine in the fed state

  • Gianni Biolo

      Affiliations

    • Present address for G.B.: Institute of Clinica Medica, Hospital of Cattinara, 34149 Trieste, Italy.
  • ,
  • Paolo Tessari

      Affiliations

    • Corresponding Author InformationAddress reprint requests to Paolo Tessari, MD, Department of Metabolic Disease, Policlinico, Via Giustiniani 2, 35128 Padova, Italy.

Department of Metabolic Diseases, University of Padova, Padova, Italy

Received 7 February 1996; accepted 6 September 1996.

Abstract 

The extent to which dietary branched-chain amino acids are deaminated by the splanchnic tissues (ie, the liver and gut) in the fed state and released as ketoacids into the systemic circulation is not known. To determine this, we combined the oral (L-[1-13C]-leucine, [13C]-Leu) and intravenous (l-[5,5,5-2H3]leucine, [2H3]-Leu) leucine tracer infusion with the intravenous administration of an independent isotope of the leucine ketoanalog α-ketoisocaproic acid (KIC) ([4,5-3H]KIC). The study was conducted during constant administration of a complete mixed meal. We found that 26% ± 5% of the orally administered leucine was taken up by the splanchnic organs at first pass, whereas 74% ± 5% appeared in the systemic circulation. The rate of splanchnic KIC release from deamination of dietary leucine accounted for 3% ± 0.2% of the oral leucine administration rate and 13% ± 2% of leucine splanchnic uptake (fractional splanchnic deamination). The fraction of whole-body total leucine uptake that was deaminated to KIC was 41% ± 5% (P < .05 v fractional splanchnic deamination of dietary leucine uptake). We conclude that (1) the release of KIC from leucine deamination within splanchnic tissues constitutes a minimal fraction of first-pass dietary leucine uptake, and (2) splanchnic tissues are relatively less efficient than the whole body in KIC production from leucine deamination.

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PII: S0026-0495(97)90296-1

Metabolism - Clinical and Experimental
Volume 46, Issue 2 , Pages 164-167, February 1997