Obesity in women is increased by the loss of circulating estrogen after menopause. Shift work, which disrupts circadian rhythms, also increases the risk for obesity. It is not known whether ovarian hormones interact with the circadian system to protect females from obesity. During high-fat feeding, male C57BL/6J mice develop profound obesity and disruption of daily rhythms. Since C57BL/6J female mice did not develop diet-induced obesity (during 8 weeks of high-fat feeding), we first determined if daily rhythms in female mice were resistant to disruption from high-fat diet. We fed female PERIOD2:LUCIFERASE mice 45% high-fat diet for 1 week and measured daily rhythms. Female mice retained robust rhythms of eating behavior and locomotor activity during high-fat feeding that were similar to chow-fed females. In addition, the phase of the liver molecular timekeeping (PER2:LUC) rhythm was not altered by high-fat feeding in females. To determine if ovarian hormones protected daily rhythms in female mice from high-fat feeding, we analyzed rhythms in ovariectomized mice. During high-fat feeding, the amplitudes of the eating behavior and locomotor activity rhythms were reduced in ovariectomized females. Liver PER2:LUC rhythms were also advanced by ~4 h by high-fat feeding, but not chow, in ovariectomized females. Together these data show circulating ovarian hormones protect the integrity of daily rhythms in female mice during high-fat feeding.

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Published in Frontiers in Endocrinology, v. 8, 44, p. 1-11.

© 2017 Palmisano, Stafford and Pendergast.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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This research was supported by National Institutes of Health grants R03DK107851 and K01DK098321 (to JP) and DK058404 (Pilot Award to JP). JP was supported by a Junior Investigator Award from the Center of Research in Obesity and Cardiovascular Disease (P20 GM103527), a Young Investigator Award from the Vanderbilt University Digestive Disease Research Center (National Institutes of Health grant P30 DK058404), and the University of Kentucky. JS was supported by the Center for Integrated Healthcare, U.S. Department of Veterans Affairs (BX002223) and the National Institutes of Health (R01DK109102). BP was supported by the Vanderbilt Medical Scientist Training Program (T32GM07347) and the National Institutes of Health (F30DK104514).

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The Supplementary Material for this article can be found online at http://journal.frontiersin.org/article/10.3389/fendo.2017.00044/ full#supplementary-material.

data sheet 1.pdf (1453 kB)
Data Sheet 1