Markers of mitochondrial biogenesis and metabolism are lower in overweight and obese insulin-resistant subjects

Leonie Heilbronn, Khee Gan Seng, Nigel Turner, Lesley V. Campbell, Donald J. Chisholm

Research output: Contribution to journalArticle

114 Citations (Scopus)

Abstract

Background: Impaired mitochondrial function in skeletal muscle is implicated in the development of insulin resistance. However, potential differences in fatness and fitness may influence previous results. Methods: Subjects (n =18) were divided into insulin-sensitive (IS) and insulin-resistant (IR) groups by median glucose infusion rate during a hyperinsulinemic euglycemic clamp. Weight, VO2max (maximal aerobic capacity), and percentage body fat were measured before and after 6 continuous weeks of aerobic exercise training at 55-70% VO2max (40 min/session, 4 d/wk). Results: Age, percentage fat, and VO2max were not different between IS and IR groups at baseline. Expression of the nuclear encoded PGC1α and mitochondrial encoded gene COX1 were significantly lower in the IR group (P < 0.05). Citrate synthase activity and protein levels of subunits from complexes I and III of the respiratory chain were also lower in the IR group (P < 0.05). Insulin sensitivity and aerobic fitness were increased after exercise training in both groups (P < 0.001), and the expression of mitochondrial encoded genes CYTB and COX1 was also increased (P < 0.01). However, there was no change in PGC1α expression, mitochondrial enzyme activity, or protein levels of complexes of the respiratory chain in response to exercise in either group. Conclusion: This study confirms that IR men have reduced markers of mitochondrial metabolism, independent of fatness and fitness. Moderate exercise training did not alter these markers despite improving fitness and whole body insulin sensitivity. This study suggests that additional mechanisms may be involved in improving insulin resistance after exercise training in obese men.

LanguageEnglish
Pages1467-1473
Number of pages7
JournalJournal of Clinical Endocrinology and Metabolism
Volume92
Issue number4
DOIs
Publication statusPublished - 2007
Externally publishedYes

ASJC Scopus subject areas

  • Endocrinology, Diabetes and Metabolism
  • Biochemistry
  • Endocrinology
  • Clinical Biochemistry
  • Biochemistry, medical

Cite this

Heilbronn, Leonie ; Seng, Khee Gan ; Turner, Nigel ; Campbell, Lesley V. ; Chisholm, Donald J. / Markers of mitochondrial biogenesis and metabolism are lower in overweight and obese insulin-resistant subjects. In: Journal of Clinical Endocrinology and Metabolism. 2007 ; Vol. 92, No. 4. pp. 1467-1473.
@article{cdcefcfeb4984dc8965b1b7b95e36ed9,
title = "Markers of mitochondrial biogenesis and metabolism are lower in overweight and obese insulin-resistant subjects",
abstract = "Background: Impaired mitochondrial function in skeletal muscle is implicated in the development of insulin resistance. However, potential differences in fatness and fitness may influence previous results. Methods: Subjects (n =18) were divided into insulin-sensitive (IS) and insulin-resistant (IR) groups by median glucose infusion rate during a hyperinsulinemic euglycemic clamp. Weight, VO2max (maximal aerobic capacity), and percentage body fat were measured before and after 6 continuous weeks of aerobic exercise training at 55-70{\%} VO2max (40 min/session, 4 d/wk). Results: Age, percentage fat, and VO2max were not different between IS and IR groups at baseline. Expression of the nuclear encoded PGC1α and mitochondrial encoded gene COX1 were significantly lower in the IR group (P < 0.05). Citrate synthase activity and protein levels of subunits from complexes I and III of the respiratory chain were also lower in the IR group (P < 0.05). Insulin sensitivity and aerobic fitness were increased after exercise training in both groups (P < 0.001), and the expression of mitochondrial encoded genes CYTB and COX1 was also increased (P < 0.01). However, there was no change in PGC1α expression, mitochondrial enzyme activity, or protein levels of complexes of the respiratory chain in response to exercise in either group. Conclusion: This study confirms that IR men have reduced markers of mitochondrial metabolism, independent of fatness and fitness. Moderate exercise training did not alter these markers despite improving fitness and whole body insulin sensitivity. This study suggests that additional mechanisms may be involved in improving insulin resistance after exercise training in obese men.",
author = "Leonie Heilbronn and Seng, {Khee Gan} and Nigel Turner and Campbell, {Lesley V.} and Chisholm, {Donald J.}",
year = "2007",
doi = "10.1210/jc.2006-2210",
language = "English",
volume = "92",
pages = "1467--1473",
journal = "Journal of Clinical Endocrinology and Metabolism",
issn = "0021-972X",
publisher = "The Endocrine Society",
number = "4",

}

Markers of mitochondrial biogenesis and metabolism are lower in overweight and obese insulin-resistant subjects. / Heilbronn, Leonie; Seng, Khee Gan; Turner, Nigel; Campbell, Lesley V.; Chisholm, Donald J.

In: Journal of Clinical Endocrinology and Metabolism, Vol. 92, No. 4, 2007, p. 1467-1473.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Markers of mitochondrial biogenesis and metabolism are lower in overweight and obese insulin-resistant subjects

AU - Heilbronn, Leonie

AU - Seng, Khee Gan

AU - Turner, Nigel

AU - Campbell, Lesley V.

AU - Chisholm, Donald J.

PY - 2007

Y1 - 2007

N2 - Background: Impaired mitochondrial function in skeletal muscle is implicated in the development of insulin resistance. However, potential differences in fatness and fitness may influence previous results. Methods: Subjects (n =18) were divided into insulin-sensitive (IS) and insulin-resistant (IR) groups by median glucose infusion rate during a hyperinsulinemic euglycemic clamp. Weight, VO2max (maximal aerobic capacity), and percentage body fat were measured before and after 6 continuous weeks of aerobic exercise training at 55-70% VO2max (40 min/session, 4 d/wk). Results: Age, percentage fat, and VO2max were not different between IS and IR groups at baseline. Expression of the nuclear encoded PGC1α and mitochondrial encoded gene COX1 were significantly lower in the IR group (P < 0.05). Citrate synthase activity and protein levels of subunits from complexes I and III of the respiratory chain were also lower in the IR group (P < 0.05). Insulin sensitivity and aerobic fitness were increased after exercise training in both groups (P < 0.001), and the expression of mitochondrial encoded genes CYTB and COX1 was also increased (P < 0.01). However, there was no change in PGC1α expression, mitochondrial enzyme activity, or protein levels of complexes of the respiratory chain in response to exercise in either group. Conclusion: This study confirms that IR men have reduced markers of mitochondrial metabolism, independent of fatness and fitness. Moderate exercise training did not alter these markers despite improving fitness and whole body insulin sensitivity. This study suggests that additional mechanisms may be involved in improving insulin resistance after exercise training in obese men.

AB - Background: Impaired mitochondrial function in skeletal muscle is implicated in the development of insulin resistance. However, potential differences in fatness and fitness may influence previous results. Methods: Subjects (n =18) were divided into insulin-sensitive (IS) and insulin-resistant (IR) groups by median glucose infusion rate during a hyperinsulinemic euglycemic clamp. Weight, VO2max (maximal aerobic capacity), and percentage body fat were measured before and after 6 continuous weeks of aerobic exercise training at 55-70% VO2max (40 min/session, 4 d/wk). Results: Age, percentage fat, and VO2max were not different between IS and IR groups at baseline. Expression of the nuclear encoded PGC1α and mitochondrial encoded gene COX1 were significantly lower in the IR group (P < 0.05). Citrate synthase activity and protein levels of subunits from complexes I and III of the respiratory chain were also lower in the IR group (P < 0.05). Insulin sensitivity and aerobic fitness were increased after exercise training in both groups (P < 0.001), and the expression of mitochondrial encoded genes CYTB and COX1 was also increased (P < 0.01). However, there was no change in PGC1α expression, mitochondrial enzyme activity, or protein levels of complexes of the respiratory chain in response to exercise in either group. Conclusion: This study confirms that IR men have reduced markers of mitochondrial metabolism, independent of fatness and fitness. Moderate exercise training did not alter these markers despite improving fitness and whole body insulin sensitivity. This study suggests that additional mechanisms may be involved in improving insulin resistance after exercise training in obese men.

UR - http://www.scopus.com/inward/record.url?scp=34147175161&partnerID=8YFLogxK

U2 - 10.1210/jc.2006-2210

DO - 10.1210/jc.2006-2210

M3 - Article

VL - 92

SP - 1467

EP - 1473

JO - Journal of Clinical Endocrinology and Metabolism

T2 - Journal of Clinical Endocrinology and Metabolism

JF - Journal of Clinical Endocrinology and Metabolism

SN - 0021-972X

IS - 4

ER -