Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

. 2022 Feb 19;298(4):101748. doi: 10.1016/j.jbc.2022.101748

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

© 2022 The Authors

This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/).

PMC Copyright notice

Graphical summary. Feeding-related insulin activity induces TGF-β1 expression in adipocytes. Autocrine action activates the TGFBR–SMAD3 axis, which even enhances the expression of TGF-β1 as a positive feedback loop. Moreover, it induces ECM remodeling with the induction of related genes such as collagen, MMPs, and ADAMs, which triggers intracellular FAK–AKT signaling and enhances lipogenesis. Cell-autonomous TGF-β1 activity plays an important role in linking the ECM to intracellular processes, which allows adipocytes to adapt to physiological feeding events and harmonizes extracellular and intracellular environments for lipid homeostasis. ADAM, a disintegrin and metalloproteinase; ECM, extracellular matrix; FAK, focal adhesion kinase; MMP, matrix metalloproteinase; SMAD3, SMAD family member 3; TGF-β1, transforming growth factor β1; TGFBR, transforming growth factor β receptor.