2023 Fiscal Year Annual Research Report
Physiological role of CD206 macrophages and NAD+ metabolism in obesity and insulin resistance.
Project/Area Number |
22K20737
|
Research Institution | University of Toyama |
Principal Investigator |
Bilal Muhammad 富山大学, 学術研究部医学系, 特命助教 (80968529)
|
Project Period (FY) |
2022-08-31 – 2024-03-31
|
Keywords | CD206 / M2 macrophage |
Outline of Annual Research Achievements |
Our data showed that CD206KO mice are insulin-sensitive with reduced expression of the inflammatory genes in visceral white adipose tissue. This data further suggests that CD206 M2 macrophages are actively involved in regulating glucose metabolism. However, how these M2 anti-inflammatory macrophages phenotypically switch to pro-inflammatory M1 type under a high-fat diet is under debate. My focus is to investigate the underlying molecular mechanism that regulates these shifting/switching of macrophages, resulting in insulin resistance under high-fat diet-fed conditions. Furthermore, I am generating CD206 flox mice to knock down the CD206 M2 signaling conditionally. This will further help me to explore the underlying regulatory mechanism for the treatment of obesity and type 2 diabetes.
|