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Exercise Science Research Institute, Arizona State University, Tempe, Arizona 85287-0404
High-fat (HF) and high-sucrose (SU)
diets increase gluconeogenesis. The present study was
designed to determine the contributions of pyruvate dehydrogenase,
pyruvate carboxylase, phosphoenolpyruvate carboxykinase
(PEPCK), and pyruvate kinase fluxes to this accelerated gluconeogenesis
(GNEO) in the absence and presence of fatty acids. Male Sprague-Dawley
rats were fed an HF, SU, or starch (ST) diet for 1 wk, and hepatocytes
or mitochondria were isolated. In the absence of palmitate, the tracer
estimated rates of GNEO
(nmol · min
1 · mg1) were
elevated in hepatocytes isolated from SU (32.3 ± 1.8) and HF
(35.4 ± 1.8) vs. ST (22.8 ± 1.5). Pyruvate carboxylase and PEPCK flux rates
(nmol · min1 · mg1) were
increased in the SU (47.5 ± 2.2 and 34.8 ± 1.5) and HF (49.4 ± 1.8 and 38.2 ± 1.8) groups compared with the ST
group (32.8 ± 3.2 and 44.3 ± 2.0). Palmitate
(250-1,000 µM) stimulation of these fluxes was not significantly
different among groups. Bromopalmitate, an inhibitor of fat oxidation,
abolished differences in GNEO, pyruvate carboxylase, and PEPCK fluxes
in HF and SU vs. ST. In isolated mitochondria, pyruvate carboxylation
and palmitoyl carnitine oxidation were not significantly different
among groups. The results of this study suggest that the increased
gluconeogenic flux observed with HF and SU diets is associated with an
increased pyruvate flux through pyruvate carboxylase and PEPCK.
Moreover, the ability of bromopalmitate to normalize gluconeogenic
fluxes suggests that endogenous fatty acids contribute to diet-induced increases in GNEO.
liver; glucose; precursors; lipids
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