| Project/Area Number |
22K20737
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| Research Category |
Grant-in-Aid for Research Activity Start-up
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| Allocation Type | Multi-year Fund |
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| Review Section |
0802:Biomedical structure and function and related fields
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| Research Institution | University of Toyama |
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Principal Investigator |
Bilal Muhammad 富山大学, 学術研究部医学系, 特命助教 (80968529)
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| Project Period (FY) |
2022-08-31 – 2024-03-31
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| Project Status |
Completed (Fiscal Year 2023)
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| Budget Amount *help |
¥2,860,000 (Direct Cost: ¥2,200,000、Indirect Cost: ¥660,000)
Fiscal Year 2023: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2022: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
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| Keywords | adipose tissue / M2 macrophages / insulin resistant / CD206 / M2 macrophage / Nampt / Diabetes / CD206 Macrophages |
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| Outline of Research at the Start |
My current study will provide a new strategy and open-up new field of science, providing piece of evidence that CD206 M2-like macrophages derived-Nampt play important role in macrophages functions and insulin resistance during the development of obesity. The clinical importance of insulin resistance caused by
macrophages dysfunction during the development of obesity is very essential as its value to medical field will be quite beneficial for the patients suffering from obesity related insulin resistance and related disorders.
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| Outline of Final Research Achievements |
My data showed that transgenic lacking Nampt in M2 macrophages were insulin resistant, with blood glucose levels. Then, I utilized another transgenic mouse lacking M2 receptors that were insulin-sensitive with reduced expression of the inflammatory genes in visceral white adipose tissue. This data further suggests that M2 macrophages are actively involved in regulating glucose metabolism through phenotypic switching. 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 other M2-related transgenic mice to knock down the M2 signaling conditionally. This will further help me to explore the underlying regulatory mechanism for the treatment of obesity and type 2 diabetes.
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| Academic Significance and Societal Importance of the Research Achievements |
本研究では、肥満に関連したNAD+の減少とNamptの欠乏が、全身の耐糖能とインスリン感受性を悪化させ、一方で、NAD+の増加が代謝障害を回復させることを示唆している。このメカニズムは、肥満に関連した2型糖尿病の治療に対する新しい戦略を切り開く可能性を持つ。
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