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

Kyle L. Hoehn, Nigel Turner, Michael M. Swarbrick, Donna Wilks, Elaine Preston, Yuwei Phua, Himani Joshi, Stuart M. Furler, Mark Larance, Bronwyn D. Hegarty, Simon J. Leslie, Russell Pickford, Andrew J. Hoy, Edward W. Kraegen, David E. James (Lead / Corresponding author), Gregory J. Cooney

    Research output: Contribution to journalArticlepeer-review

    117 Citations (Scopus)

    Abstract

    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.
    Original languageEnglish
    Pages (from-to)70-76
    Number of pages7
    JournalCell Metabolism
    Volume11
    Issue number1
    DOIs
    Publication statusPublished - 6 Jan 2010

    Keywords

    • Oxidation-Reduction
    • Acetyl-CoA Carboxylase
    • Animals
    • Adiposity
    • Fatty Acids
    • Mitochondria
    • Mice
    • Up-Regulation
    • Energy Metabolism
    • AMP-Activated Protein Kinases

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