Srebp-1c/Fgf21/Pgc-1α Axis Regulated by Leptin Signaling in Adipocytes-Possible Mechanism of Caloric Restriction-Associated Metabolic Remodeling of White Adipose Tissue.


Journal

Nutrients
ISSN: 2072-6643
Titre abrégé: Nutrients
Pays: Switzerland
ID NLM: 101521595

Informations de publication

Date de publication:
10 Jul 2020
Historique:
received: 06 06 2020
revised: 04 07 2020
accepted: 08 07 2020
entrez: 16 7 2020
pubmed: 16 7 2020
medline: 9 3 2021
Statut: epublish

Résumé

Caloric restriction (CR) improves whole body metabolism, suppresses age-related pathophysiology, and extends lifespan in rodents. Metabolic remodeling, including fatty acid (FA) biosynthesis and mitochondrial biogenesis, in white adipose tissue (WAT) plays an important role in the beneficial effects of CR. We have proposed that CR-induced mitochondrial biogenesis in WAT is mediated by peroxisome proliferator-activated receptor γ coactivator-1α (PGC-1α), which is transcriptionally regulated by sterol regulatory element-binding protein 1c (SREBP-1c), a master regulator of FA biosynthesis. We have also proposed that the CR-associated upregulation of SREBP-1 and PGC-1α might result from the attenuation of leptin signaling and the upregulation of fibroblast growth factor 21 (FGF21) in WAT. However, the detailed molecular mechanisms remain unclear. Here, we interrogate the regulatory mechanisms involving leptin signaling, SREBP-1c, FGF21, and PGC-1α using

Identifiants

pubmed: 32664386
pii: nu12072054
doi: 10.3390/nu12072054
pmc: PMC7400870
pii:
doi:

Substances chimiques

Fatty Acids 0
Leptin 0
Sterol Regulatory Element Binding Protein 1 0
Transcription Factors 0
fibroblast growth factor 21 0
peroxisome-proliferator-activated receptor-gamma coactivator-1 0
Fibroblast Growth Factors 62031-54-3

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Subventions

Organisme : Japan Society for the Promotion of Science
ID : Grants-in-Aid for Scientific Research (B) (No. 17H02179)

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Auteurs

Masaki Kobayashi (M)

Laboratory of Molecular Pathology and Metabolic Disease, Faculty of Pharmaceutical Sciences, Tokyo University of Science, Chiba 278-8510, Japan.

Seira Uta (S)

Laboratory of Molecular Pathology and Metabolic Disease, Faculty of Pharmaceutical Sciences, Tokyo University of Science, Chiba 278-8510, Japan.

Minami Otsubo (M)

Laboratory of Molecular Pathology and Metabolic Disease, Faculty of Pharmaceutical Sciences, Tokyo University of Science, Chiba 278-8510, Japan.

Yusuke Deguchi (Y)

Laboratory of Molecular Pathology and Metabolic Disease, Faculty of Pharmaceutical Sciences, Tokyo University of Science, Chiba 278-8510, Japan.

Ryoma Tagawa (R)

Laboratory of Molecular Pathology and Metabolic Disease, Faculty of Pharmaceutical Sciences, Tokyo University of Science, Chiba 278-8510, Japan.

Yuhei Mizunoe (Y)

Department of Internal Medicine (Endocrinology and Metabolism), Faculty of Medicine, University of Tsukuba, Ibaraki 305-8575, Japan.

Yoshimi Nakagawa (Y)

Division of Complex Biosystem Research, Department of Research and Development, Institute of Natural Medicine, University of Toyama, Toyama 930-0194, Japan.

Hitoshi Shimano (H)

Department of Internal Medicine (Endocrinology and Metabolism), Faculty of Medicine, University of Tsukuba, Ibaraki 305-8575, Japan.
Life Science Center for Survival Dynamics, Tsukuba Advanced Research Alliance (TARA), University of Tsukuba, Ibaraki 305-8575, Japan.
AMED-CREST, Japan Agency for Medical Research and Development (AMED), Tokyo 100-1004, Japan.

Yoshikazu Higami (Y)

Laboratory of Molecular Pathology and Metabolic Disease, Faculty of Pharmaceutical Sciences, Tokyo University of Science, Chiba 278-8510, Japan.
Research Institute for Biomedical Sciences, Tokyo University of Science, Chiba 278-8510, Japan.

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Classifications MeSH