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A possible mechanism for explaining this phenomenon is that an increased FFA availability enhances the hepatic NADH/NAD ratio, creating a metabolic condition horsefeed which inhibits the activity of BCKA horsefeed dehydrogenase activity (TESSARI et al., 1987; BUSE, HERLONG and WEIGAND, 1976; HARRIS and PAXTON, 1985; TISCHLER and FAGAN, 1982). Another possible mechanism by which fat infusion might contribute to nitrogen sparing is through an effect of FFA on the binding to albumin of µ-ketoisocaproate (KIC), the µ-ketoacid produced by leucine desamination. During triglyceride infusion with heparin in humans, NISSEN et al. (1982) showed that the elevation of plasma FFA levels horsefeed significantly increased the circulating free KIC concentration, by displacing KIC which is bound to albumin. An increase in the circulating free KIC pool may affect the concentration gradient between plasma and tissues favoring the uptake of free KIC by the liver, where reamination of KIC to leucine occurs.
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