Dietary and sex-specific factors regulate hypothalamic neurogenesis in young adult mice
Abstract
The hypothalamus is the central regulator of a broad range of homeostatic and instinctive physiological processes, such as the sleep-wake cycle, food intake, and sexually dimorphic behaviors. These behaviors can be modified by various environmental and physiological cues, although the molecular and cellular mechanisms that mediate these effects remain poorly understood. Recently, it has become clear that both the juvenile and adult hypothalamus exhibit ongoing neurogenesis, which serve to modify homeostatic neural circuitry. In this report, we share new findings on the contributions of sex-specific and dietary factors to regulating neurogenesis in the hypothalamic mediobasal hypothalamus, a recently identified neurogenic niche. We report that high fat diet (HFD) selectively activates neurogenesis in the median eminence (ME) of young adult female but not male mice, and that focal irradiation of the ME in HFD-fed mice reduces weight gain in females but not males. These results suggest that some physiological effects of high fat diet are mediated by the stimulation of ME neurogenesis in a sexually dimorphic manner. We discuss these results in the context of recent advances in understanding the cellular and molecular mechanisms that regulate neurogenesis in postnatal and adult hypothalamus.
Additional Information
© 2014 Lee, Yoo, Pak, Salvatierra, Velarde, Aja and Blackshaw. 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. Received: 19 March 2014; Accepted: 26 May 2014; Published online: 13 June 2014. We would like to thank W. Yap, B. Clark and J. Bedont for their insightful comments on the manuscript. This work was supported by a Diabetes Research Center Training and Feasibility grant to Seth Blackshaw. Seth Blackshaw was a W. M. Keck Distinguished Young Scholar in Medical Research. Conflict of Interest Statement: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.Attached Files
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Additional details
- PMCID
- PMC4056383
- Eprint ID
- 46876
- Resolver ID
- CaltechAUTHORS:20140707-102340431
- Diabetes Research Center Training and Feasibility Grant
- W. M. Keck Foundation
- Created
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2014-07-07Created from EPrint's datestamp field
- Updated
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2021-11-10Created from EPrint's last_modified field