Targeting Peroxisome Proliferator-Activated Receptor-β/δ (PPARβ/δ) for the Treatment or Prevention of Alcoholic Liver Disease

被引:0
|
作者
Koga, Takayuki [1 ]
Peters, Jeffrey M. [2 ,3 ]
机构
[1] Daiichi Univ Pharm, Lab Hygien Chem, Dept Hlth Sci & Hyg, Minami Ku, 22-1 Tamagawa Cho, Fukuoka 8158511, Japan
[2] Penn State Univ, Dept Vet & Biomed Sci, University Pk, PA 16802 USA
[3] Penn State Univ, Ctr Mol Toxicol & Carcinogenesis, University Pk, PA 16802 USA
关键词
alcoholic liver disease; lipid accumulation; insulin resistance; peroxisome proliferator-activated receptor (PPAR); xenobiotic-metabolizing enzyme; HEPATIC INSULIN-RESISTANCE; CONSTITUTIVE ANDROSTANE RECEPTOR; ENDOPLASMIC-RETICULUM STRESS; INDUCED OXIDANT STRESS; FATTY-ACID SYNTHESIS; ADIPOSE-TISSUE; GLUCOSE-METABOLISM; ETHANOL-METABOLISM; NUCLEAR RECEPTORS; OXIDATIVE STRESS;
D O I
暂无
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
Excessive, chronic alcohol consumption can lead to alcoholic liver disease. The etiology of alcoholic liver disease is multifactorial and is influenced by alterations in gene expression and changes in fatty acid metabolism, oxidative stress, and insulin resistance. These events can lead to steatosis, fibrosis, and eventually to cirrhosis and liver cancer. Many of these functions are regulated by peroxisome proliferator-activated receptors (PPARs). Thus, it is not surprising that PPARs can modulate the mechanisms that cause alcoholic liver disease. While the roles of PPAR alpha and PPAR gamma are clearer, the role of PPAR beta/delta in alcoholic liver disease requires further clarification. This review summarizes the current understanding based on recent studies that indicate that PPAR beta/delta can likely be targeted for the treatment and/or the prevention of alcoholic liver disease.
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页码:1598 / 1606
页数:9
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