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頁籤選單縮合
題名 | An Adipocentric View of Liver Fibrosis and Cirrhosis=從脂肪代謝觀點談肝臟纖維化及硬化 |
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作者姓名(中文) | 莊錦豪; 王佩文; 戴明泓; | 書刊名 | 長庚醫學 |
卷期 | 27:12 2004.12[民93.12] |
頁次 | 頁855-868 |
分類號 | 415.534 |
關鍵詞 | 肝臟; 纖維化; 肝硬化; 肥胖; 非酒精性脂肪肝病; 細胞素; 瘦體素; Adipocytokine/Adipokine; Adiponectin; Cirrhosis; Hepatic stellate cells; Insulin; Insulin-like growth factor; Leptin; Liver fibrosis; Nonalcoholic fatty liver disease; Obesity; Preadipocyte factor1/delta-like protein1; |
語文 | 英文(English) |
中文摘要 | 肝臟因慢性或反覆性傷害,如酒精中毒,肝炎病毒,免疫或先天代謝異常,而致纖維化或硬化。因肥胖導致之非酒精性脂肪肝病,可能是最近才發現可導致肝硬化的病因。肥胖也提供沃土,使本來因酒精或病毒引起之肝病,更容易走向硬化。胰島素,IGF-1,PPAR,leptin,adiponectin及Pref-1/dlk 1是脂肪代謝相關的荷爾蒙,生長因子,細胞核受體及細胞素。但它們在肝纖維化的病程中也插一腳,主要藉由調控共同的目標-即肝臟星狀細胞HSC。HSC的活化增生,導致肝臟纖維化相關蛋白質如膠原的生成,催化肝纖維化的進行。胰島素及IGF-1在體外可活化HSC並生成膠原。但在體內,IGF-1的作用卻在減輕肝纖維化。PPARγ之配體(ligand)在體外可抑制HSC活化及膠原的生成,與其體內抑制肝纖維化吻合,但與PPARβ之作用相反。瘦體素leptin是促纖維化的因子,因此缺leptin或其受體的小白鼠,反而較不容易因毒性肝損傷導致肝臟的纖維化。Adiponectin是抑制肝纖維化的細胞素,因此剔除adiponectin基因的小白鼠,容易產生厲害的肝纖維化,而補充重組adiponectin後,情形即好轉。Pref-1/dlk 1可在人體內調控HSC而影響肝纖維化的進展。應用活躍於脂肪代謝的分子,如PPARγ之配體或adiponectin,雖不一定能達到減肥的目的,但在減輕代謝徵候群或肝硬化上,或有不容忽視的潛力。有利於減代謝徵候群的減重,也同樣可能減少肥胖相關之肝硬化。 |
英文摘要 | Liver fibrosis is the consequence of chronic or repeated liver injury caused by hepatotoxic agents like alcohol and viruses, as well as immune and congenital metabolic disorders. Nonalcoholic fatty liver disease (NAFLD), caused by obesity and abnormal lipid metabolism, may be the latest known cause of liver fibrosis and cirrhosis. Furthermore, NAFLD with obesity can provide a terrain in which alcoholic and viral liver diseases, such as chronic hepatitis C, are prone to cause liver cirrhosis. Insulin, insulin-like growth factor (IGF)-1, peroxisome proliferators-activated receptors (PPARs), leptin, adiponectin, and preadipocyte factor-1/delta-like 1 (Pref-1/dlk 1) are hormones, growth factors, nuclear receptors, and cytokines that are actively involved in lipid metabolism. They share common target cells important in liver fibrosis, i.e., hepatic stellate cells (HSCs). Activation of HSCs is known to initiate and perpetuate liver fibrosis. Insulin and IGF-1 stimulate HSC activation and collagen production in vitro. However, IGF-1 alleviates liver fibrosis in vivo. Ligands of PPARγ inhibit HSC activation and collagen synthesis in viro and in vitro, and are helpful in decreasing liver fibrosis. But ligands of PPARβ enhance proliferation of HSCs. Leptin is profibrogenic, and liver fibrosis is decreased in leptin- or leptin receptor-deficient mice. Adiponectin is, on the contrary, anti-fibrogenic. Extensive liver fibrosis may develop in adiponectin-knockout mice and is alleviated by administration of recombinant adiponectin. Pref-1/dlk 1 is implicated in fibrogenesis of the liver through its modulation of HSCs. The use of such biologically active molecules in lipid metabolism as ligands of PPARγ and adiponectin might not help slim down a patient on the whole, but can potentially be used to halt the progression of liver fibrosis. Weight reduction, a strategy for controlling obesity and metabolic syndromes, may also be a tool for decreasing NAFLD and alleviating liver corrjpsos. |
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