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Endogenous Peroxisome Proliferator-Activated Receptor-gamma Augments Fatty Acid Uptake in Oxidative Muscle
Journal article   Open access   Peer reviewed

Endogenous Peroxisome Proliferator-Activated Receptor-gamma Augments Fatty Acid Uptake in Oxidative Muscle

Andrew W. Norris, Michael F. Hirshman, Jianrong Yao, Niels Jessen, Nicolas Musi, Lihong Chen, William I. Sivitz, Laurie J. Goodyear and C. Ronald Kahn
Endocrinology (Philadelphia), Vol.149(11), pp.5374-5383
11/01/2008
DOI: 10.1210/en.2008-0100
PMCID: PMC2584586
PMID: 18653710
url
https://doi.org/10.1210/en.2008-0100View
Published (Version of record) Open Access

Abstract

In the setting of insulin resistance, agonists of peroxisome proliferator-activated receptor (PPAR)-gamma restore insulin action in muscle and promote lipid redistribution. Mice with muscle-specific knockout of PPAR gamma (MuPPAR gamma KO) develop excess adiposity, despite reduced food intake and normal glucose disposal in muscle. To understand the relation between muscle PPAR gamma and lipid accumulation, we studied the fuel energetics of MuPPAR gamma KO mice. Compared with controls, MuPPAR gamma KO mice exhibited significantly increased ambulatory activity, muscle mitochondrial uncoupling, and respiratory quotient. Fitting with this latter finding, MuPPAR gamma KO animals compared with control siblings exhibited a 25% reduction in the uptake of the fatty acid tracer 2-bromo-palmitate (P < 0.05) and a 13% increase in serum nonesterified fatty acids (P = 0.05). These abnormalities were associated with no change in AMP kinase (AMPK) phosphorylation, AMPK activity, or phosphorylation of acetyl-CoA carboxylase in muscle and occurred despite increased expression of fatty acid transport protein 1. Palmitate oxidation was not significantly altered in MuPPAR gamma KO mice despite the increased expression of several genes promoting lipid oxidation. These data demonstrate that PPAR gamma, even in the absence of exogenous activators, is required for normal rates of fatty acid uptake in oxidative skeletal muscle via mechanisms independent of AMPK and fatty acid transport protein 1. Thus, when PPAR gamma activity in muscle is absent or reduced, there will be decreased fatty acid disposal leading to diminished energy utilization and ultimately adiposity. (Endocrinology 149: 5374-5383, 2008)
Endocrinology & Metabolism Life Sciences & Biomedicine Science & Technology

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