Format

Send to

Choose Destination
Nat Commun. 2018 Apr 18;9(1):1544. doi: 10.1038/s41467-018-03796-7.

TAp63 contributes to sexual dimorphism in POMC neuron functions and energy homeostasis.

Author information

1
Children's Nutrition Research Center, Department of Pediatrics, Baylor College of Medicine, Houston, TX, 77030, USA.
2
Molecular Physiology and Biophysics, Baylor College of Medicine, Houston, TX, 77030, USA.
3
Brown Foundation Institute of Molecular Medicine, University of Texas Health Science Center at Houston, Houston, TX, 77030, USA.
4
Department of Molecular Oncology, Cancer Biology and Evolution Program, Department of Cutaneous Oncology, H. Lee Moffitt Cancer Center, Tampa, FL, 33612, USA.
5
Children's Nutrition Research Center, Department of Pediatrics, Baylor College of Medicine, Houston, TX, 77030, USA. yongx@bcm.edu.
6
Department of Molecular and Cellular Biology, Baylor College of Medicine, Houston, TX, 77030, USA. yongx@bcm.edu.

Abstract

Sexual dimorphism exists in energy balance, but the underlying mechanisms remain unclear. Here we show that the female mice have more pro-opiomelanocortin (POMC) neurons in the arcuate nucleus of hypothalamus than males, and female POMC neurons display higher neural activities, compared to male counterparts. Strikingly, deletion of the transcription factor, TAp63, in POMC neurons confers "male-like" diet-induced obesity (DIO) in female mice associated with decreased POMC neural activities; but the same deletion does not affect male mice. Our results indicate that TAp63 in female POMC neurons contributes to the enhanced POMC neuron functions and resistance to obesity in females. Thus, TAp63 in POMC neurons is one key molecular driver for the sexual dimorphism in energy homeostasis.

PMID:
29670083
PMCID:
PMC5906443
DOI:
10.1038/s41467-018-03796-7
[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for Nature Publishing Group Icon for PubMed Central
Loading ...
Support Center