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  • Title: Enhanced hepatic gluconeogenic capacity for selected precursors after endurance training.
    Author: Sumida KD, Donovan CM.
    Journal: J Appl Physiol (1985); 1995 Dec; 79(6):1883-8. PubMed ID: 8847248.
    Abstract:
    The effects of endurance training (running 90 min/day, 30 m/min, approximately 10% grade) on hepatic gluconeogenesis were studied in 24-h-fasted rats by using the isolated liver perfusion technique. After isolation, livers were perfused (single pass) for 30 min with Krebs-Henseleit bicarbonate buffer and fresh bovine red blood cells (hematocrit 20-24%) with no added substrate. Alanine (10 mM), dihydroxyacetone (20 mM), or glutamine (10 mM) was then added to the reservoir, and perfusions continued for 60 min. No significant differences were observed in perfusate pH, hematocrit, bile production, or serum alanine aminotransferase effluxing from livers from trained or control animals for any perfusion. Livers from trained animals that were perfused with 10 mM alanine demonstrated significantly higher rates of glucose production compared with livers from control animals (0.51 +/- 0.04 vs. 0.40 +/- 0.02 micromol.min-1.g liver-1, respectively). Elevations of a similar magnitude were observed for rates of [14C]alanine incorporation into [14C]glucose in livers from trained vs. control animals (8,797 +/- 728 vs. 6,962 +/- 649 dpm.min-1.g liver-1, respectively). Significant increases were also observed in hepatic alanine uptake (30%), oxygen consumption (23%), urea release (22%), and 14CO2 production (29%) of livers of endurance-trained animals. In contrast, no significant differences between groups were observed for hepatic glucose output after perfusions with either dihydroxyacetone (1.75 +/- 0.06 micromol.min-1.g liver-1) or glutamine (0.62 +/- 0.04 micromol.min-1.g liver-1). Further, during perfusions with dihydroxyacetone and glutamine, training had no significant impact on precursor uptake, oxygen consumption, or urea output. The current findings indicate a training-induced adaptation for hepatic gluconeogenesis located below the level of the triose phosphates.
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