Secretin-dependent signals in the ventromedial hypothalamus regulate energy metabolism and bone homeostasis in mice.


Journal

Nature communications
ISSN: 2041-1723
Titre abrégé: Nat Commun
Pays: England
ID NLM: 101528555

Informations de publication

Date de publication:
03 Feb 2024
Historique:
received: 05 04 2023
accepted: 22 01 2024
medline: 4 2 2024
pubmed: 4 2 2024
entrez: 3 2 2024
Statut: epublish

Résumé

Secretin, though originally discovered as a gut-derived hormone, is recently found to be abundantly expressed in the ventromedial hypothalamus, from which the central neural system controls satiety, energy metabolism, and bone homeostasis. However, the functional significance of secretin in the ventromedial hypothalamus remains unclear. Here we show that the loss of ventromedial hypothalamus-derived secretin leads to osteopenia in male and female mice, which is primarily induced by diminished cAMP response element-binding protein phosphorylation and upregulation in peripheral sympathetic activity. Moreover, the ventromedial hypothalamus-secretin inhibition also contributes to hyperphagia, dysregulated lipogenesis, and impaired thermogenesis, resulting in obesity in male and female mice. Conversely, overexpression of secretin in the ventromedial hypothalamus promotes bone mass accrual in mice of both sexes. Collectively, our findings identify an unappreciated secretin signaling in the central neural system for the regulation of energy and bone metabolism, which may serve as a new target for the clinical management of obesity and osteoporosis.

Identifiants

pubmed: 38310104
doi: 10.1038/s41467-024-45436-3
pii: 10.1038/s41467-024-45436-3
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

1030

Subventions

Organisme : Research Grants Council, University Grants Committee (RGC, UGC)
ID : 17126222
Organisme : Research Grants Council, University Grants Committee (RGC, UGC)
ID : 17113120
Organisme : Research Grants Council, University Grants Committee (RGC, UGC)
ID : 17115923

Informations de copyright

© 2024. The Author(s).

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Auteurs

Fengwei Zhang (F)

School of Biological Sciences, the University of Hong Kong, Hong Kong, China.

Wei Qiao (W)

Applied Oral Sciences & Community Dental Care, Faculty of Dentistry, the University of Hong Kong, Hong Kong, China. drqiao@hku.hk.
Shenzhen Key Laboratory for Innovative Technology in Orthopaedic Trauma, the University of Hong Kong-Shenzhen Hospital, Shenzhen, China. drqiao@hku.hk.

Ji-An Wei (JA)

School of Biological Sciences, the University of Hong Kong, Hong Kong, China.
Key Laboratory of CNS Regeneration (Ministry of Education), GHM Institute of CNS Regeneration, Jinan University, Guangzhou, China.

Zhengyi Tao (Z)

School of Biological Sciences, the University of Hong Kong, Hong Kong, China.

Congjia Chen (C)

School of Biological Sciences, the University of Hong Kong, Hong Kong, China.

Yefeng Wu (Y)

Applied Oral Sciences & Community Dental Care, Faculty of Dentistry, the University of Hong Kong, Hong Kong, China.

Minghui Lin (M)

School of Biological Sciences, the University of Hong Kong, Hong Kong, China.

Ka Man Carmen Ng (KMC)

School of Biological Sciences, the University of Hong Kong, Hong Kong, China.

Li Zhang (L)

Key Laboratory of CNS Regeneration (Ministry of Education), GHM Institute of CNS Regeneration, Jinan University, Guangzhou, China.
Neuroscience and Neurorehabilitation Institute, University of Health and Rehabilitation Sciences, Qingdao, China.

Kelvin Wai-Kwok Yeung (KW)

Shenzhen Key Laboratory for Innovative Technology in Orthopaedic Trauma, the University of Hong Kong-Shenzhen Hospital, Shenzhen, China. wkkyeung@hku.hk.
Department of Orthopaedics and Traumatology, School of Clinical Medicine, Li Ka Shing Faculty of Medicine, the University of Hong Kong, Hong Kong, China. wkkyeung@hku.hk.

Billy Kwok Chong Chow (BKC)

School of Biological Sciences, the University of Hong Kong, Hong Kong, China. bkcc@hku.hk.

Classifications MeSH