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Am J Physiol Endocrinol Metab 280: E296-E300, 2001;
0193-1849/01 $5.00
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Vol. 280, Issue 2, E296-E300, February 2001

Role of Na+-K+-ATPase in insulin-induced lactate release by skeletal muscle

Valérie Novel-Chaté1, Valentine Rey1, René Chioléro2, Philippe Schneiter1, Xavier Leverve3, Eric Jéquier1, and Luc Tappy1

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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