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Acute or chronic upregulation of mitochondrial fatty acid oxidation has no net effect on whole-body energy expenditure or adiposity


Activation of AMP-activated protein kinase (AMPK) is thought to convey many of the beneficial effects of exercise via its inhibitory effect on acetyl-CoA carboxylase 2 (ACC2) and promotion of fatty acid oxidation. Hence, AMPK and ACC have become major drug targets for weight loss and improved insulin action. However, it remains unclear whether or how activation of the fatty acid oxidation pathway without a concomitant increase in energy expenditure could be beneficial. Here, we have used either pharmacological (administration of the AMPK agonist 5(') aminoimidazole-4-carboxamide-riboside) or genetic means (mutation of the ACC2 gene in mice) to manipulate fatty acid oxidation to determine whether this is sufficient to promote leanness. Both of these strategies increased whole-body fatty acid oxidation without altering energy expenditure or adiposity. We conclude that negative energy balance is a prerequisite for weight reduction, and increased fatty acid oxidation per se has little, if any, effect to reduce adiposity.

Type Journal
ISBN 1932-7420 (Electronic)
Authors Hoehn, K. L.; Turner, N.; Swarbrick, M. M.; Wilks, D.; Preston, E.; Phua, Y.; Joshi, H.; Furler, S. M.; Larance, M.; Hegarty, B. D.; Leslie, S. J.; Pickford, R.; Hoy, A. J.; Kraegen, E. W.; James, D. E.; Cooney, G. J.;
Garvan Authors Prof Gregory Cooney
Publisher Name CELL METAB
Published Date 2010-01-01 00:00:00
Published Volume 11
Published Issue 1
Published Pages 70-6
Status Published In-print
OpenAccess Link Hoehn CM.pdf