Role of leptin signal in inflammation-related colorectal carcinogenesis
| Project/Area Number |
23501262
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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 |
Carcinogenesis
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| Research Institution | Kanazawa Medical University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
OYAMA Takeru 金沢大学, 医学系研究科, 助教 (00515314)
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| Project Period (FY) |
2011 – 2013
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2013: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2012: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2011: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | 炎症とがん / レプチン / 発がん / 大腸がん / 高脂血症 / 大腸発がん |
|---|
| Research Abstract |
Leptin is elevated in obesity and may be involved in carcinogenesis including colorectal cancers. The objective of this study was to investigate the role of leptin signal on colitis-related colon carcinogenesis.
In current study, we indicated that Leptin was effective in inhibiting colitis-related colon carcinogenesis through suppression of mucosal inflammation and hyperlipidemia in the ob/ob mice (leptin-deficient obese genetic background). Our results suggest that the leptin might be useful for prevention of inflammation-related colon cancers.
Furthermore, we showed that C57BL/KsJ mice strains are less sensitive to inflammation-related colon carcinogenesis compared with C57BL/6J mice and these differences may be due to the difference in their levels of mucosal inflammation of the colon. These results provided the useful information in the inflammation-related mouse colon carcinogenesis model.
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Report
(4 results)
Research Products
(5 results)
