SENP2 knockdown in human adipocytes reduces glucose metabolism and lipid accumulation, while increases lipid oxidation.
Browning markers
Energy metabolism
Knockdown
Lentivirus
Primary human preadipocytes
SENP2
Journal
Metabolism open
ISSN: 2589-9368
Titre abrégé: Metabol Open
Pays: England
ID NLM: 101767753
Informations de publication
Date de publication:
Jun 2023
Jun 2023
Historique:
received:
07
10
2022
revised:
07
02
2023
accepted:
08
02
2023
medline:
5
4
2023
entrez:
4
4
2023
pubmed:
5
4
2023
Statut:
epublish
Résumé
Adipose tissue is one of the main regulative sites for energy metabolism. Excess lipid storage and expansion of white adipose tissue (WAT) is the primary contributor to obesity, a strong predisposing factor for development of insulin resistance. Sentrin-specific protease (SENP) 2 has been shown to play a role in metabolism in murine fat and skeletal muscle cells, and we have previously demonstrated its role in energy metabolism of human skeletal muscle cells. In the present work, we have investigated the impact of SENP2 on fatty acid and glucose metabolism in primary human fat cells by using cultured primary human adipocytes to knock down the SENP2 gene. Glucose uptake and oxidation, as well as accumulation and distribution of oleic acid into complex lipids were decreased, while oleic acid oxidation was increased in SENP2-knockdown cells compared to control adipocytes. Furthermore, lipogenesis was reduced by SENP2-knockdown in adipocytes. Although TAG accumulation relative to total uptake was unchanged, there was increased mRNA expression of metabolically relevant genes such as
Identifiants
pubmed: 37013149
doi: 10.1016/j.metop.2023.100234
pii: S2589-9368(23)00006-3
pmc: PMC10066554
doi:
Types de publication
Journal Article
Langues
eng
Pagination
100234Informations de copyright
© 2023 The Authors.
Déclaration de conflit d'intérêts
The authors declare the following financial interests/personal relationships which may be considered as potential competing interests: Stefano Bartesaghi and Xiao-Rong Peng are employees at AstraZeneca. The remaining authors have no competing interests to declare.
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