2014 Fiscal Year Final Research Report
Role of the immunoproteasome in the pathogenesis of metabolic syndrome
| Project/Area Number |
23591359
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Endocrinology
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| Research Institution | Jichi Medical University |
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Principal Investigator |
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| Co-Investigator(Renkei-kenkyūsha) |
TAKAHASHI Masafumi 自治医科大学, 医学部, 教授 (40296108)
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| Project Period (FY) |
2011-04-28 – 2015-03-31
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| Keywords | 免疫プロテアソーム / 肥満 / 高脂肪食 / 炎症 / マクロファージ |
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| Outline of Final Research Achievements |
Obesity increases the risk of developing metabolic disorders. The detailed pathogenic mechanism of inflammation in obesity is not fully understood. Low-molecular-mass polypeptide-7 (LMP7) is a proteolytic subunit of the immunoproteasome that plays a fundamental role in the immune system, and has been involved in the pathogenesis of several autoimmune diseases. We investigated the role of LMP7 in obesity using LMP7-deficient mice. LMP7 deficiency showed resistance to obesity, suppressed macrophage accumulation in adipose tissue, improved glucose tolerance, and suppressed serum triglyceride level elevation induced by high-fat diet (HFD) feeding, which increased fecal lipid contents. Using bone-marrow-transferred chimeric mice, we found that LMP7 in both hematopoietic and non-hematopoietic cells had critical roles in HFD-induced obesity development. These findings demonstrate that LMP7 in both hematopoietic and non-hematopoietic cells contributes to the pathogenesis of obesity.
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| Free Research Field |
免疫学・内分泌学
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