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Fibroblast growth factor 21 increases hepatic oxidative capacity but not physical activity or energy expenditure in hepatic peroxisome proliferator‐activated receptor γ coactivator‐1α‐deficient mice

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What is the central question of this study? Does a reduction in hepatic peroxisome proliferator‐activated receptor γ coactivator‐1α (PGC‐1α), which has been observed in an insulin‐resistant obese state, impair the… Click to show full abstract

What is the central question of this study? Does a reduction in hepatic peroxisome proliferator‐activated receptor γ coactivator‐1α (PGC‐1α), which has been observed in an insulin‐resistant obese state, impair the ability of fibroblast growth factor 21 (FGF21) to modulate metabolism? What is the main finding and its importance? A deficit in hepatic PGC‐1α does not compromise the ability of FGF21 to increase hepatic fatty acid oxidation; however, the effects of FGF21 to regulate whole‐body metabolism (i.e. total and resting energy expenditure), as well as ambulatory activity, were altered when hepatic PGC‐1α was reduced.

Keywords: peroxisome proliferator; proliferator activated; fibroblast growth; hepatic peroxisome; activated receptor; receptor coactivator

Journal Title: Experimental Physiology
Year Published: 2018

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