Steroid receptor coactivator-1 modulates the function of Pomc neurons and energy homeostasis

Hypothalamic neurons expressing the anorectic peptide Pro-opiomelanocortin (Pomc) regulate food intake and body weight. Here, we show that Steroid Receptor Coactivator-1 (SRC-1) interacts with a target of leptin receptor activation, phosphorylated STAT3, to potentiate Pomc transcription. Deletion of...

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Hauptverfasser: Yang, Yongjie (VerfasserIn) , März, Winfried (VerfasserIn)
Dokumenttyp: Article (Journal)
Sprache:Englisch
Veröffentlicht: 12 April 2019
In: Nature Communications
Year: 2019, Jahrgang: 10
ISSN:2041-1723
Online-Zugang: Volltext
Verfasserangaben:Yongjie Yang, Agatha A. van der Klaauw, Liangru Zhu, Tessa M. Cacciottolo, Yanlin He, Lukas K.J. Stadler, Chunmei Wang, Pingwen Xu, Kenji Saito, Antentor Hinton, Xiaofeng Yan, Julia M. Keogh, Elana Henning, Matthew C. Banton, Audrey E. Hendricks, Elena G. Bochukova, Vanisha Mistry, Katherine L. Lawler, Lan Liao, Jianming Xu, Stephen O'Rahilly, Qingchun Tong, UK10K Consortium, Inês Barroso, Bert W. O'Malley, I. Sadaf Farooqi & Yong Xu

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520 |a Hypothalamic neurons expressing the anorectic peptide Pro-opiomelanocortin (Pomc) regulate food intake and body weight. Here, we show that Steroid Receptor Coactivator-1 (SRC-1) interacts with a target of leptin receptor activation, phosphorylated STAT3, to potentiate Pomc transcription. Deletion of SRC-1 in Pomc neurons in mice attenuates their depolarization by leptin, decreases Pomc expression and increases food intake leading to high-fat diet-induced obesity. In humans, fifteen rare heterozygous variants in SRC-1 found in severely obese individuals impair leptin-mediated Pomc reporter activity in cells, whilst four variants found in non-obese controls do not. In a knock-in mouse model of a loss of function human variant (SRC-1L1376P), leptin-induced depolarization of Pomc neurons and Pomc expression are significantly reduced, and food intake and body weight are increased. In summary, we demonstrate that SRC-1 modulates the function of hypothalamic Pomc neurons, and suggest that targeting SRC-1 may represent a useful therapeutic strategy for weight loss. 
650 4 |a Alleles 
650 4 |a Animals 
650 4 |a Body Weight 
650 4 |a Cell Line, Tumor 
650 4 |a Crosses, Genetic 
650 4 |a Gene Deletion 
650 4 |a Gene Knock-In Techniques 
650 4 |a Genetic Variation 
650 4 |a HEK293 Cells 
650 4 |a Heterozygote 
650 4 |a Homeostasis 
650 4 |a Humans 
650 4 |a Hypothalamus 
650 4 |a Leptin 
650 4 |a Male 
650 4 |a Membrane Potentials 
650 4 |a Mice 
650 4 |a Mice, Transgenic 
650 4 |a Mutation, Missense 
650 4 |a Neurons 
650 4 |a Nuclear Receptor Coactivator 1 
650 4 |a Obesity 
650 4 |a Phenotype 
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