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Role of liver PPARγ in high fat diet-induced hepatic steatosis
DC Field | Value | Language |
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dc.contributor.author | 이유정 | - |
dc.date.accessioned | 2015-12-24T08:43:12Z | - |
dc.date.available | 2015-12-24T08:43:12Z | - |
dc.date.issued | 2011 | - |
dc.identifier.uri | https://ir.ymlib.yonsei.ac.kr/handle/22282913/134066 | - |
dc.description | Dept. of Medical Science/박사 | - |
dc.description.abstract | Recently, it has been implied that hepatic peroxisome proliferator activated receptor γ (PPARγ) plays a role in hepatic lipid accumulation. I found that C3H/HeJ mice barely express PPARγ in the liver and are highly resistant to hepatic steatosis in response to a high-fat diet (HFD), as compared to the diet-induced obesity-prone model, C57BL/6 mice. The expression of hepatic PPARγ2 was low in C57BL/6 mice fed a normal chow diet, and was increased robustly when mice were fed a HFD. As a result, hepatic triacylglycerol (TG) and cholesterol levels were significantly increased by HFD, and oil-red O staining demonstrated development of hepatic steatosis. In contrast, the liver of C3H/HeJ mice remained normal without accumulation of lipid droplets on HFD. In addition, C3H/HeJ mice did not develop glucose intolerance, showing a normal glucose tolerance test even after feding HFD. Adenovirus-mediated expression of PPARγ2 in primary hepatocytes isolated from C3H/HeJ mice resulted in increased lipid accumulation, as determined by fatty acid transport and TG contents. Adenoviral overexpression of PPARγ2 in C3H/HeJ mice resulted in a significant accumulation of lipids in the liver as similar as in primary hepatocyte. I also found that hepatic PPARγ2 up-regulated several target genes including aP2/422, FAT/CD36, and monoacylglycerol O-acyltransferase 1 (MGAT1) in the liver. In particular, MGAT1 expression was tightly associated with PPARγ2 expression, indicating that hepatic PPARγ2 is responsible for the fatty liver through an MGAT1-involved pathway in lipid metabolism. Acetylation and methylation analyses of PPARg2 gene showed decreased acetylation status in C3H/HeJ mice but no difference in methylation between C3H/HeJ and C57BL/6 liver. This result suggests that epigenetics and other mechanisms are involved in regulation of the expression of PPARγ in C3H/HeJ mice liver. Taken together, it is suggested that increased PPARg activity on HFD plays a major role in lipid accumulation in liver, by regulating fatty acid transport and the TG incorporation pathway. | - |
dc.description.statementOfResponsibility | restriction | - |
dc.publisher | Graduate School, Yonsei University | - |
dc.rights | CC BY-NC-ND 2.0 KR | - |
dc.rights.uri | https://creativecommons.org/licenses/by-nc-nd/2.0/kr/ | - |
dc.title | Role of liver PPARγ in high fat diet-induced hepatic steatosis | - |
dc.title.alternative | 식이성비만유도와 관련한 PPARγ의 역할 | - |
dc.type | Thesis | - |
dc.identifier.url | https://ymlib.yonsei.ac.kr/catalog/search/book-detail/?cid=CAT000000114005 | - |
dc.contributor.alternativeName | Lee, Yoo Jeong | - |
dc.type.local | Dissertation | - |
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