High oxidative capacity due to chronic exercise training attenuates lipid-induced insulin resistance.

Research output: Contribution to journalArticleAcademicpeer-review

27 Citations (Scopus)

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/m(2)) and 10 untrained subjects (age = 21.9 +/- 0.9 years; BMI = 22.8 +/- 0.6 kg/m(2)) 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 similar to 32% higher mitochondrial capacity and similar to 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. Diabetes 61:2472-2478, 2012

Original languageEnglish
Pages (from-to)2472-2478
Number of pages7
JournalDiabetes
Volume61
Issue number10
DOIs
Publication statusPublished - Oct 2012

Keywords

  • FREE FATTY-ACIDS
  • PHOSPHATIDYLINOSITOL 3-KINASE ACTIVITY
  • TYPE-2 DIABETIC PARENTS
  • HUMAN SKELETAL-MUSCLE
  • MITOCHONDRIAL-FUNCTION
  • TRIGLYCERIDE
  • DYSFUNCTION
  • HUMANS
  • SENSITIVITY
  • OBESITY

Cite this

@article{e3b1b6fb2b5b456fb71b4ffb4ed9362c,
title = "High oxidative capacity due to chronic exercise training attenuates lipid-induced insulin resistance.",
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/m(2)) and 10 untrained subjects (age = 21.9 +/- 0.9 years; BMI = 22.8 +/- 0.6 kg/m(2)) 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 similar to 32{\%} higher mitochondrial capacity and similar to 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. Diabetes 61:2472-2478, 2012",
keywords = "FREE FATTY-ACIDS, PHOSPHATIDYLINOSITOL 3-KINASE ACTIVITY, TYPE-2 DIABETIC PARENTS, HUMAN SKELETAL-MUSCLE, MITOCHONDRIAL-FUNCTION, TRIGLYCERIDE, DYSFUNCTION, HUMANS, SENSITIVITY, OBESITY",
author = "E. Phielix and R. Meex and DM. Ouwens and L.M. Sparks and J. Hoeks and G. Schaart and C.F.P. Kornips and M.K.C. Hesselink and P. Schrauwen",
year = "2012",
month = "10",
doi = "10.2337/db11-1832",
language = "English",
volume = "61",
pages = "2472--2478",
journal = "Diabetes",
issn = "0012-1797",
publisher = "American Diabetes Association",
number = "10",

}

High oxidative capacity due to chronic exercise training attenuates lipid-induced insulin resistance. / Phielix, E.; Meex, R.; Ouwens, DM.; Sparks, L.M.; Hoeks, J.; Schaart, G.; Kornips, C.F.P.; Hesselink, M.K.C.; Schrauwen, P.

In: Diabetes, Vol. 61, No. 10, 10.2012, p. 2472-2478.

Research output: Contribution to journalArticleAcademicpeer-review

TY - JOUR

T1 - High oxidative capacity due to chronic exercise training attenuates lipid-induced insulin resistance.

AU - Phielix, E.

AU - Meex, R.

AU - Ouwens, DM.

AU - Sparks, L.M.

AU - Hoeks, J.

AU - Schaart, G.

AU - Kornips, C.F.P.

AU - Hesselink, M.K.C.

AU - Schrauwen, P.

PY - 2012/10

Y1 - 2012/10

N2 - 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/m(2)) and 10 untrained subjects (age = 21.9 +/- 0.9 years; BMI = 22.8 +/- 0.6 kg/m(2)) 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 similar to 32% higher mitochondrial capacity and similar to 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. Diabetes 61:2472-2478, 2012

AB - 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/m(2)) and 10 untrained subjects (age = 21.9 +/- 0.9 years; BMI = 22.8 +/- 0.6 kg/m(2)) 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 similar to 32% higher mitochondrial capacity and similar to 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. Diabetes 61:2472-2478, 2012

KW - FREE FATTY-ACIDS

KW - PHOSPHATIDYLINOSITOL 3-KINASE ACTIVITY

KW - TYPE-2 DIABETIC PARENTS

KW - HUMAN SKELETAL-MUSCLE

KW - MITOCHONDRIAL-FUNCTION

KW - TRIGLYCERIDE

KW - DYSFUNCTION

KW - HUMANS

KW - SENSITIVITY

KW - OBESITY

U2 - 10.2337/db11-1832

DO - 10.2337/db11-1832

M3 - Article

VL - 61

SP - 2472

EP - 2478

JO - Diabetes

JF - Diabetes

SN - 0012-1797

IS - 10

ER -