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Metabolism

High Oxidative Capacity Due to Chronic Exercise Training Attenuates Lipid-Induced Insulin Resistance

  1. Esther Phielix1,
  2. Ruth Meex2,
  3. D. Margriet Ouwens3,
  4. Lauren Sparks1,
  5. Joris Hoeks1,
  6. Gert Schaart2,
  7. Esther Moonen-Kornips1,2,
  8. Matthijs K.C. Hesselink2 and
  9. Patrick Schrauwen1⇓
  1. 1Department of Human Biology, NUTRIM School for Nutrition, Toxicology, and Metabolism, Maastricht University Medical Center, Maastricht, the Netherlands
  2. 2Department of Human Movement Sciences, NUTRIM School for Nutrition, Toxicology, and Metabolism, Maastricht University Medical Center, Maastricht, the Netherlands
  3. 3Institute of Clinical Biochemistry and Pathobiochemistry, German Diabetes Center, Dusseldorf, Germany
  1. Corresponding author: Patrick Schrauwen, p.schrauwen{at}maastrichtuniversity.nl.
Diabetes 2012 Oct; 61(10): 2472-2478. https://doi.org/10.2337/db11-1832
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Abstract

Fat accumulation in skeletal muscle combined with low mitochondrial oxidative capacity is associated with insulin resistance (IR). Endurance-trained athletes, characterized by a high oxidative capacity, have elevated intramyocellular lipids, yet are highly insulin sensitive. We tested the hypothesis that a high oxidative capacity could attenuate lipid-induced IR. Nine endurance-trained (age = 23.4 ± 0.9 years; BMI = 21.2 ± 0.6 kg/m2) and 10 untrained subjects (age = 21.9 ± 0.9 years; BMI = 22.8 ± 0.6 kg/m2) were included and underwent a clamp with either infusion of glycerol or intralipid. Muscle biopsies were taken to perform high-resolution respirometry and protein phosphorylation/expression. Trained subjects had ∼32% higher mitochondrial capacity and ∼22% higher insulin sensitivity (P < 0.05 for both). Lipid infusion reduced insulin-stimulated glucose uptake by 63% in untrained subjects (P < 0.05), whereas this effect was blunted in trained subjects (29%, P < 0.05). In untrained subjects, lipid infusion reduced oxidative and nonoxidative glucose disposal (NOGD), whereas trained subjects were completely protected against lipid-induced reduction in NOGD, supported by dephosphorylation of glycogen synthase. We conclude that chronic exercise training attenuates lipid-induced IR and specifically attenuates the lipid-induced reduction in NOGD. Signaling data support the notion that high glucose uptake in trained subjects is maintained by shuttling glucose toward storage as glycogen.

Footnotes

  • Clinical trial reg. no. NTR2002, http://www.trialregister.nl.

  • This article contains Supplementary Data online at http://diabetes.diabetesjournals.org/lookup/suppl/doi:10.2337/db11-1832/-/DC1.

  • See accompanying commentary, p. 2397.

  • Received December 26, 2011.
  • Accepted April 22, 2012.
  • © 2012 by the American Diabetes Association.

Readers may use this article as long as the work is properly cited, the use is educational and not for profit, and the work is not altered. See http://creativecommons.org/licenses/by-nc-nd/3.0/ for details.

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High Oxidative Capacity Due to Chronic Exercise Training Attenuates Lipid-Induced Insulin Resistance
Esther Phielix, Ruth Meex, D. Margriet Ouwens, Lauren Sparks, Joris Hoeks, Gert Schaart, Esther Moonen-Kornips, Matthijs K.C. Hesselink, Patrick Schrauwen
Diabetes Oct 2012, 61 (10) 2472-2478; DOI: 10.2337/db11-1832

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High Oxidative Capacity Due to Chronic Exercise Training Attenuates Lipid-Induced Insulin Resistance
Esther Phielix, Ruth Meex, D. Margriet Ouwens, Lauren Sparks, Joris Hoeks, Gert Schaart, Esther Moonen-Kornips, Matthijs K.C. Hesselink, Patrick Schrauwen
Diabetes Oct 2012, 61 (10) 2472-2478; DOI: 10.2337/db11-1832
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