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1 Institute of Physiology, Medical School, University of Lausanne, 1005; 2 Surgical Intensive Care Unit, University Hospital, 1011 Lausanne, Switzerland; and 3 Laboratory of Fundamental and Applied Bioenergetics, University Joseph Fourier, 38041 Grenoble, France
Hyperinsulinemia increases
lactate release by various organs and tissues. Whereas it has been
shown that aerobic glycolysis is linked to
Na+-K+-ATPase activity, we hypothesized that
stimulation by insulin of skeletal muscle
Na+-K+-ATPase is responsible for increased
muscle lactate production. To test this hypothesis, we assessed muscle
lactate release in healthy volunteers from the
[13C]lactate concentration in the effluent
dialysates of microdialysis probes inserted into the tibialis anterior
muscles on both sides and infused with solutions containing 5 mmol/l
[U-13C]glucose. On one side, the microdialysis probe was
intermittently infused with the same solution additioned with
2.10
5 M ouabain. In the basal state,
[13C]lactate concentration in the dialysate was not
affected by ouabain. During a euglycemic-hyperinsulinemic clamp,
[13C]lactate concentration increased by 135% in the
dialysate without ouabain, and this stimulation was nearly entirely
reversed by ouabain (56% inhibition compared with values in the
dialysate collected from the contralateral probe). These data indicate
that insulin stimulates muscle lactate release by activating
Na+-K+-ATPase in healthy humans.
aerobic glycolysis; [13C]lactate; microdialysis; ouabain
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