Differences in betaine-homocysteine methyltransferase expression, endoplasmic reticulum stress response, and liver injury between alcohol-fed mice and rats.
Differences in betaine-homocysteine methyltransferase expression, endoplasmic reticulum stress response, and liver injury between alcohol-fed mice and rats.
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DOI：
10.1002/hep.23391
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发表时间：
2010-03
期刊：
影响因子：
13.5
通讯作者：
Kaplowitz, Neil
中科院分区：
文献类型：
--
作者：
Shinohara, Masao;Ji, Cheng;Kaplowitz, Neil
Chronic ethanol infusion resulted in greater serum ALT elevation, lipid accumulation, necroinflammation, and focal hepatic cell death in mice than rats. Mice exhibited a remarkable hyperhomocysteinemia but no increase was seen in rats. Similarly, a high methionine low folate diet (HMLF) induced less steatosis, serum ALT increase, and hyperhomocysteinemia in rats than in mice. Western blot analysis of betaine homocysteine methyltransferase (BHMT) expression showed that rats fed either ethanol or HMLF had significantly increased BHMT expression which did not occur in mice. Nuclear NFκB p65 was increased in mouse in response to alcohol feeding. The human BHMT promoter was repressed by homocysteine in mouse hepatocytes but not rat hepatocytes. BHMT induction was faster and greater in primary rat hepatocytes than mouse hepatocytes in response to exogenous homocysteine exposure. Mice fed ethanol i.g. exhibited an increase in GRP78 and IRE1 which was not seen in the rat and SREBP-1 was increased to a greater extent in mice than rats. Thus, rats are more resistant to ethanol induced steatosis, ER stress and hyperhomocysteinemia and this correlates with induction of BHMT in rats. These findings support the hypothesis that a critical factor in the pathogenesis of alcoholic liver injury is the enhanced ability of rat or impaired ability of mouse to up-regulate BHMT which prevents hyperhomocysteinemia, ER stress and liver injury.
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