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TGFBI remodels adipose metabolism by regulating the Notch-1 signaling pathway

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Author(s)
Seul Gi LeeJongbeom ChaeSeon Min WooSeung Un SeoHa-Jeong KimSang-Yeob KimDavid D SchlaepferIn-San KimHee-Sae ParkTaeg Kyu KwonJu-Ock Nam
Keimyung Author(s)
Kwon, Taeg Kyu
Department
Dept. of Immunology (면역학)
Journal Title
Exp Mol Med
Issued Date
2023
Volume
55
Issue
3
Abstract
Extracellular matrix proteins are associated with metabolically healthy adipose tissue and regulate inflammation, fibrosis, angiogenesis, and subsequent metabolic deterioration. In this study, we demonstrated that transforming growth factor-beta (TGFBI), an extracellular matrix (ECM) component, plays an important role in adipose metabolism and browning during high-fat diet-induced obesity. TGFBI KO mice were resistant to adipose tissue hypertrophy, liver steatosis, and insulin resistance. Furthermore, adipose tissue from TGFBI KO mice contained a large population of CD11b+ and CD206+ M2 macrophages, which possibly control adipokine secretion through paracrine mechanisms. Mechanistically, we showed that inhibiting TGFBI-stimulated release of adipsin by Notch-1-dependent signaling resulted in adipocyte browning. TGFBI was physiologically bound to Notch-1 and stimulated its activation in adipocytes. Our findings revealed a novel protective effect of TGFBI deficiency in obesity that is realized via the activation of the Notch-1 signaling pathway.
Keimyung Author(s)(Kor)
권택규
Publisher
School of Medicine (의과대학)
Type
Article
ISSN
2092-6413
Source
https://www.nature.com/articles/s12276-023-00947-9
DOI
10.1038/s12276-023-00947-9
URI
https://kumel.medlib.dsmc.or.kr/handle/2015.oak/44974
Appears in Collections:
1. School of Medicine (의과대학) > Dept. of Immunology (면역학)
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