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    17 beta-Estradiol Directly Lowers Mitochondrial Membrane Microviscosity and Improves Bioenergetic Function in Skeletal Muscle

    Year: 2018

    Journal: Cell Metab., Volume 27, JAN 9, page 167

    Authors: Torres, Maria J.; Kew, Kim A.; Ryan, Terence E.; Pennington, Edward Ross; Lin, Chien-Te; Buddo, Katherine A.; Fix, Amy M.; Smith, Cheryl A.; Gilliam, Laura A.; Karvinen, Sira; Lowe, Dawn A.; Spangenburg, Espen E.; Zeczycki, Tonya N.; Shaikh, Saame Raza; Neufer, P. Darrell

    Organizations: U.S. Public Health Services [R01 HL123647, R01 AT008375, ADA BS-1-15-170, R01 AG031743, R01 DK096907, R01 DK110656]

    Menopause results in a progressive decline in 17 beta-estradiol (E2) levels, increased adiposity, decreased insulin sensitivity, and a higher risk for type 2 diabetes. Estrogen therapies can help reverse these effects, but the mechanism(s) by which E2 modulates susceptibility to metabolic disease is not well understood. In young C57BL/6N mice, short-term ovariectomy decreased-whereas E2 therapy restored-mitochondrial respiratory function, cellular redox state (GSH/GSSG), and insulin sensitivity in skeletal muscle. E2 was detected by liquid chromatography-mass spectrometry in mitochondrial membranes and varied according to whole-body E2 status independently of ER alpha. Loss of E2 increased mitochondrial membrane microviscosity and H2O2 emitting potential, whereas E2 administration in vivo and in vitro restored membrane E2 content, microviscosity, complex I and I + III activities, H2O2 emitting potential, and submaximal OXPHOS responsiveness. These findings demonstrate that E2 directly modulates membrane biophysical properties and bioenergetic function in mitochondria, offering a direct mechanism by which E2 status broadly influences energy homeostasis.
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