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Diabetes 51:599-605, 2002
© 2002 by the American Diabetes Association, Inc.

Mechanism of Amino Acid-Induced Skeletal Muscle Insulin Resistance in Humans

Michael Krebs1, Martin Krssak1, Elisabeth Bernroider1, Christian Anderwald1, Attila Brehm1, Martin Meyerspeer1,2, Peter Nowotny1, Erich Roth3, Werner Waldhäusl1, and Michael Roden1

1 Division of Endocrinology and Metabolism, Department of Internal Medicine III, University of Vienna Medical School, Vienna, Austria
2 NMR-Group, Institute of Medical Physics, University of Vienna Medical School, Vienna, Austria
3 Department of Surgery, University of Vienna Medical School, Vienna, Austria

Plasma concentrations of amino acids are frequently elevated in insulin-resistant states, and a protein-enriched diet can impair glucose metabolism. This study examined effects of short-term plasma amino acid (AA) elevation on whole-body glucose disposal and cellular insulin action in skeletal muscle. Seven healthy men were studied for 5.5 h during euglycemic (5.5 mmol/l), hyperinsulinemic (430 pmol/l), fasting glucagon (65 ng/l), and growth hormone (0.4 µg/l) somatostatin clamp tests in the presence of low (~1.6 mmol/l) and increased (~4.6 mmol/l) plasma AA concentrations. Glucose turnover was measured with D-[6,6-2H2]glucose. Intramuscular concentrations of glycogen and glucose-6-phosphate (G6P) were monitored using 13C and 31P nuclear magnetic resonance spectroscopy, respectively. A ~2.1-fold elevation of plasma AAs reduced whole-body glucose disposal by 25% (P < 0.01). Rates of muscle glycogen synthesis decreased by 64% (180–315 min, 24 ± 3; control, 67 ± 10 µmol · l-1 · min-1; P < 0.01), which was accompanied by a reduction in G6P starting at 130 min ({Delta}G6P260–300 min, 18 ± 19; control, 103 ± 33 µmol/l; P < 0.05). In conclusion, plasma amino acid elevation induces skeletal muscle insulin resistance in humans by inhibition of glucose transport/phosphorylation, resulting in marked reduction of glycogen synthesis.


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