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

Seul Gi Lee, Jongbeom Chae, Seon Min Woo, Seung Un Seo, Ha Jeong Kim, Sang Yeob Kim, David D. Schlaepfer, In San Kim, Hee Sae Park, Taeg Kyu Kwon, Ju Ock Nam

Research output: Contribution to journalArticlepeer-review

4 Citations (Scopus)


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.

Original languageEnglish
Pages (from-to)520-531
Number of pages12
JournalExperimental and Molecular Medicine
Issue number3
Publication statusPublished - 2023 Mar

Bibliographical note

Funding Information:
This study was supported by the National Research Foundation of Korea (NRF) funded by the Korean government (NRF-2017R1A2B4011003, NRF-2019R1A2C1090619, 2021R1A6A3A01087252, and NRF-2019R1A2C2005921).

Publisher Copyright:
© 2023, The Author(s).

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Medicine
  • Molecular Biology
  • Clinical Biochemistry


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