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SF1-specific deletion of the energy sensor AMPKγ2 induces obesity.
Mol. Metab. 92:102091 (2024)
OBJECTIVE: AMP-activated protein kinase (AMPK) is a heterotrimer complex consisting of a catalytic α subunit (α1, α2) with a serine/threonine kinase domain, and two regulatory subunits, β (β1, β2) and γ (γ1, γ2, γ3), encoded by different genes. In the hypothalamus, AMPK plays a crucial role in regulating energy balance, including feeding, energy expenditure, peripheral glucose and lipid metabolism. However, most research on hypothalamic AMPK has concentrated on the catalytic subunits AMPKα1 and AMPKα2, with little focus on the regulatory subunits. METHODS: To fill this gap of knowledge, we investigated the effects of selectively deleting the regulatory isoform AMPKγ2, which is a primary "energy sensor", in steroidogenic factor 1 (SF1) neurons of the ventromedial hypothalamic nucleus (VMH). Complete metabolic phenotyping and molecular analyses in brown adipose tissue (BAT), white adipose tissue (WAT) and liver were carried out. RESULTS: Our findings reveal that, in contrast to the obesity-protective effect of the genetic deletion of AMPKα subunits, the loss of AMPKγ2 leads to a sex-independent and feeding-independent obesity-prone phenotype due to decreased thermogenesis in brown adipose tissue (BAT) and reduced browning of WAT, resulting in lower energy expenditure. Additionally, SF1-Cre AMPKγ2 mice exhibit hepatic lipid accumulation, but surprisingly maintain normal glucose homeostasis. CONCLUSIONS: Overall, these results highlight the distinct roles of AMPK subunits within the hypothalamus.
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Publikationstyp
Artikel: Journalartikel
Dokumenttyp
Wissenschaftlicher Artikel
Schlagwörter
Ampk ; Bat ; Sf1 ; Hypothalamus ; Obesity ; Thermogenesis; Activated Protein-kinase; Adipose-tissue Thermogenesis; Hypothalamic Ampk; Ventromedial Hypothalamus; Thyroid-hormones; Nutrient; Neurons; Glucose; Homeostasis; Expression
ISSN (print) / ISBN
2212-8778
e-ISSN
2212-8778
Zeitschrift
Molecular Metabolism
Quellenangaben
Band: 92,
Artikelnummer: 102091
Verlag
Elsevier
Verlagsort
Amsterdam
Nichtpatentliteratur
Publikationen
Begutachtungsstatus
Peer reviewed
Institut(e)
Institute of Diabetes and Obesity (IDO)
Förderungen
Helmholtz Association-Initiative and Networking Fund (CGC)
European Research Council
La Caixa Foundation
Fundacion Araucaria
Ramon y Cajal from the Ministerio de Ciencia e Innovacion of Spain
German Research Foundation DFG under Germany's Excellence Strategy within the framework of the Munich Cluster for Systems Neurology
FEDER Program of EU
Xunta de Galicia
Ministerio de Ciencia e Innovacion
European Research Council
La Caixa Foundation
Fundacion Araucaria
Ramon y Cajal from the Ministerio de Ciencia e Innovacion of Spain
German Research Foundation DFG under Germany's Excellence Strategy within the framework of the Munich Cluster for Systems Neurology
FEDER Program of EU
Xunta de Galicia
Ministerio de Ciencia e Innovacion