Research ArticleMetabolism

Skeletal muscle action of estrogen receptor α is critical for the maintenance of mitochondrial function and metabolic homeostasis in females

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Science Translational Medicine  13 Apr 2016:
Vol. 8, Issue 334, pp. 334ra54
DOI: 10.1126/scitranslmed.aad3815

Postmenopausal muscle and mitochondrial mayhem

Menopause ushers in a host of changes that range from unpleasant to undesirable. One undesirable shift is a loss of protection against insulin resistance, which brings with it a constellation of consequences in the form of chronic disease associated with metabolic dysfunction. Now, Ribas et al. investigate the mechanism underlying the postmenopausal chinks in a woman’s energy homeostasis armor.

The estrogen receptor (ER) is known to participate in the preservation of mitochondrial health and insulin sensitivity in mice, but the precise tissue-specific mechanisms remain unclear. Because skeletal muscle is a main tissue responsible for insulin-stimulated glucose disposal, the authors first showed that ERα expression in muscle correlated with metabolic health in human females. They then created a muscle-specific ERα knockout (MERKO) mouse and found that glucose homeostasis was disrupted, fat accumulation increased, and mitochondrial function impaired. These findings imply that ERα action in skeletal muscle helps maintain mitochondrial function and metabolic homeostasis in females.

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