Ventromedial Hypothalamic Nucleus Subset Stimulates Tissue Thermogenesis via Preoptic Area Outputs.

Energy expenditure obesity pituitary adenylate cyclase activating peptide preoptic area thermogenesis ventromedial hypothalamic nucleus

Journal

Molecular metabolism
ISSN: 2212-8778
Titre abrégé: Mol Metab
Pays: Germany
ID NLM: 101605730

Informations de publication

Date de publication:
08 May 2024
Historique:
received: 29 12 2023
revised: 20 04 2024
accepted: 27 04 2024
medline: 11 5 2024
pubmed: 11 5 2024
entrez: 10 5 2024
Statut: aheadofprint

Résumé

Hypothalamic signals potently stimulate energy expenditure by engaging peripheral mechanisms to restore energy homeostasis. Previous studies have identified several critical hypothalamic sites (e.g. preoptic area (POA) and ventromedial hypothalamic nucleus (VMN)) that could be part of an interconnected neurocircuit that controls tissue thermogenesis and essential for body weight control. However, the key neurocircuit that can stimulate energy expenditure has not yet been established. Here, we investigated the downstream mechanisms by which VMN neurons stimulate adipose tissue thermogenesis. We manipulated subsets of VMN neurons acutely as well as chronically and studied its effect on tissue thermogenesis and body weight control, using Sf1 Activation of the VMN neurons that express the steroidogenic factor 1 (Sf1; VMN These data indicate that VMN

Identifiants

pubmed: 38729241
pii: S2212-8778(24)00082-6
doi: 10.1016/j.molmet.2024.101951
pii:
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

101951

Informations de copyright

Copyright © 2024 The Author(s). Published by Elsevier GmbH.. All rights reserved.

Auteurs

Rashmita Basu (R)

Department of Pharmacology and Toxicology, Indiana University School of Medicine, Indianapolis, IN, USA; Lilly Diabetes Research Center, Indiana Biosciences Research Institute, Indianapolis, IN, USA.

Andrew J Elmendorf (AJ)

Department of Pharmacology and Toxicology, Indiana University School of Medicine, Indianapolis, IN, USA; Lilly Diabetes Research Center, Indiana Biosciences Research Institute, Indianapolis, IN, USA.

Betty Lorentz (B)

Lilly Diabetes Research Center, Indiana Biosciences Research Institute, Indianapolis, IN, USA.

Connor A Mahler (CA)

Lilly Diabetes Research Center, Indiana Biosciences Research Institute, Indianapolis, IN, USA.

Olivia Lazzaro (O)

Lilly Diabetes Research Center, Indiana Biosciences Research Institute, Indianapolis, IN, USA.

Britany App (B)

Lilly Diabetes Research Center, Indiana Biosciences Research Institute, Indianapolis, IN, USA.

Shudi Zhou (S)

Department of Medical Neuroscience, Indiana University School of Medicine, Indianapolis, IN, USA.

Yura Yamamoto (Y)

Lilly Diabetes Research Center, Indiana Biosciences Research Institute, Indianapolis, IN, USA.

Mya Suber (M)

Lilly Diabetes Research Center, Indiana Biosciences Research Institute, Indianapolis, IN, USA.

Jamie C Wann (JC)

Department of Biochemistry and Molecular Biology, Indiana University School of Medicine, Indianapolis, IN, USA.

Hyun Cheol Roh (HC)

Department of Biochemistry and Molecular Biology, Indiana University School of Medicine, Indianapolis, IN, USA.

Patrick L Sheets (PL)

Department of Medical Neuroscience, Indiana University School of Medicine, Indianapolis, IN, USA.

Travis S Johnson (TS)

Lilly Diabetes Research Center, Indiana Biosciences Research Institute, Indianapolis, IN, USA; Department of Biostatistics and Health Data Science, Indiana University School of Medicine, Indianapolis, IN, USA; Melvin and Bren Simon Comprehensive Cancer Centre, Indiana University School of Medicine, Indianapolis, IN, USA.

Jonathan N Flak (JN)

Department of Pharmacology and Toxicology, Indiana University School of Medicine, Indianapolis, IN, USA; Lilly Diabetes Research Center, Indiana Biosciences Research Institute, Indianapolis, IN, USA. Electronic address: jflak@indianabiosciences.org.

Classifications MeSH