Investigation of the regulatory mechanism for fat accumulation via the bioactive peptides derived from macrophages

2015 Fiscal Year Final Research Report

• Project/Area Number: 26840038
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: Functional biochemistry
• Research Institution: University of Miyazaki
• Principal Investigator: AKIEDA SAYAKA 宮崎大学, フロンティア科学実験総合センター, 助教 (20549076)
• Co-Investigator(Renkei-kenkyūsha): DATE YUKARI 宮崎大学, 理事 (70381100)
• Project Period (FY): 2014-04-01 – 2016-03-31
• Keywords: マクロファージ / 肥満 / 生理活性物質 / エネルギー代謝調節 / グアニリン / 脂肪細胞

Outline of Final Research Achievements

Recently, we showed that double-transgenic (dTg) rats overexpressing guanylin (Gn) and its receptor, GC-C, specifically in macrophages did not become obese even when fed a high-fat diet. In this study, to characterize macrophages expressing Gn and GC-C, we analyzed the expression of the M1 markers of macrophages isolated from dTg and wild type (WT) rats. The expression of proinflammatory cytokines and M1 macrophage markers were expressed at a significantly lower level in the macrophages of dTg rats than in those of WT rats. We also found that the chemotaxis of Gn/GC-C macrophages incubated with fatty acids significantly increases compared to the macrophages of WT rats. Our results suggest that the low levels of proinflammatory markers in Gn/GC-C macrophages at least in part contribute to the anti-obese phenotype of dTg rats. In addition, the accelerated chemotaxis of Gn/GC-C macrophages in response to fatty acids suggests that these macrophages can uniquely react to excess fatty acids.

Free Research Field

内分泌学、代謝学