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This version published online on January 23, 2007
Journal of Clinical Endocrinology & Metabolism, doi:10.1210/jc.2006-2210
A more recent version of this article appeared on April 1, 2007
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Submitted on October 10, 2006
Accepted on January 11, 2007

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

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

Diabetes and Obesity Research Program, Garvan Institute of Medical Research, Darlinghurst, NSW; Royal Perth Hospital, School of Medicine & Pharmacology, Perth, WA; School of Health Sciences, University of Wollongong, Wollongong, NSW

* To whom correspondence should be addressed. E-mail: l.heilbronn{at}garvan.org.au.

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 IS and IR groups by median glucose infusion rate during a hyperinsulinemic euglycemic clamp. Weight, VO2max and % body fat were measured before and after 6 continuous weeks of aerobic exercise training at 55-70% VO2max (40 min/session, 4 days/week).

Results: Age, % fat and VO2max were not different between IS and IR groups at baseline. Expression of the nuclear encoded PGC1{alpha} and mitochondrial encoded gene COX1 were significantly lower in the IR group (p<0.05). Citrate synthase activity and protein levels of subunits from complex I and III of the respiratory chain were also lower in the IR group (p<0.05). Insulin sensitivity and aerobic fitness were increased following 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 PGC1{alpha} 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 insulin resistant men have reduced markers of mitochondrial metabolism, independently 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 the improving insulin resistance following exercise training in obese men.
Key words: Mitochondria • oxidative phosphorylation • citrate synthase • insulin sensitivity • obesity • type 2 diabetes




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