Role of CD206 surface antigen on M2 macrophages in the development of insulin resistance in the diet-induced obese mice model

• Project/Area Number: 24K19282
• Research Category: Grant-in-Aid for Early-Career Scientists
• Allocation Type: Multi-year Fund
• Review Section: Basic Section 54040:Metabolism and endocrinology-related
• 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): 2024-04-01 – 2027-03-31
• Project Status: Granted (Fiscal Year 2024)
• Budget Amount: ¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000); Fiscal Year 2026: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000); Fiscal Year 2025: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000); Fiscal Year 2024: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
• Keywords: Mrc1 / M2 macrophage

Outline of Research at the Start

My current research data clearly showed LAMs formation in CD206 M2-like macrophages depleted or CD206KO mice (mice lacking CD206 antigen in M2 macrophages) mice are significantly downregulated with improved metabolism.
Furthermore, I will evaluate the underlying mechanism of how CD206 deficient macrophages are challenging to develop LAMs, how CD206+ M2-like macrophages uptake free fatty acids (FFA) to become LAMs, and how miRNAs derived from LAMs-exosome suppress metabolic favorable genes to develop insulin resistance.