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

. 2023 Apr 3;6:0107. doi: 10.34133/research.0107

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

Exclusive Licensee Science and Technology Review Publishing House. No claim to original U.S. Government Works. Distributed under a Creative Commons Attribution License 4.0 (CC BY 4.0).

PMC Copyright notice

Fig. 2. — The regulatory mechanism of A. muciniphila in obesity. Amuc_1100 promotes p-Akt^thr and Akt^ser expression to enhance insulin sensitivity. Amuc_1100 improves intestinal permeability activation by regulating Cldn3 expression and the Cnr1/CB1 axis in vivo. Cldn3 expression regulated by Amuc_1100 also contributes to the improvement of intestinal permeability. P9 recognizes and binds to the ligand ICAM-2. P9 then induces GLP-1 secretion by promoting p-CREB and p-HSP27 expression levels. P9 promotes thermogenesis and improves obesity and glucose homeostasis in high-fat diet-fed mice by activating the GLP-1R signaling pathway and IL-6. A. muciniphila administration inhibits adipogenesis in adipocytes via the SERPINA3/CTSB axis. It also increases 2-pg and 1-pg levels in circulating blood and activates peroxisome proliferator-activated receptor alpha (PPARα) to regulate lipid metabolism. A. muciniphila reduces carbohydrate absorption by reducing GLUT2, GLUT5, and SGLT1 expression. A. muciniphila reduces the expression levels of the hepatic lipogenesis markers SREBP-1c, ACC, and FAS.