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Background  Butyrate, end-product of intestinal fermentation, is known to impair oxidative phosphorylation in rat liver and could disturb glycogen synthesis depending on the ATP supplied by mitochondrial oxidative phosphorylation and cytosolic glycolysis.    Methods  In 48 hr-fasting rats, hepatic changes of glycogen and total ATP contents and unidirectional flux of mitochondrial ATP synthesis were evaluated by  ex vivo   31 P NMR immediately after perfusion and isolation of liver, from 0 to 10 hours after force-feeding with (butyrate 1.90 mg + glucose 14.0 mg.g -1  body weight) or isocaloric glucose (18.2 mg.g -1  bw); measurements reflected  in vivo  situation at each time of liver excision. The contribution of energetic metabolism to glycogen metabolism was estimated.    Results  A net linear flux of glycogen synthesis (~11.10 ± 0.60 μmol glucosyl units.h -1 .g -1  liver wet weight) occurred until the 6 th  hr post-feeding in both groups, whereas butyrate delayed it until the 8 th  hr. A linear correlation between total ATP and glycogen contents was obtained (r 2  = 0.99) only during net glycogen synthesis. Mitochondrial ATP turnover, calculated after specific inhibition of glycolysis, was stable (~0.70 ± 0.25 μmol.min -1 .g -1  liver ww) during the first two hr whatever the force-feeding, and increased transiently about two-fold at the 3 rd  hr in glucose. Butyrate delayed the transient increase (1.80 ± 0.33 μmol.min -1 .g -1  liver ww) to the 6 th  hr post-feeding. Net glycogenolysis always appeared after the 8 th  hr, whereas flux of mitochondrial ATP synthesis returned to near basal level (0.91 ± 0.19 μmol.min -1 .g -1  liver ww).    Conclusion  In liver from 48 hr-starved rats, the energy need for net glycogen synthesis from exogenous glucose corresponds to ~50% of basal mitochondrial ATP turnover. The evidence of a late and transient increase in mitochondrial ATP turnover reflects an energetic need, probably linked to a glycogen cycling. Butyrate, known to reduce oxidative phosphorylation yield and to induce a glucose-sparing effect, delayed the transient increase in mitochondrial ATP turnover and hence energy contribution to glycogen metabolism.

A metabolic link between mitochondrial ATP synthesis and liver glycogen metabolism: NMR study in rats re-fed with butyrate and/or glucose