Hypoxia and fatty liver

脂肪性肝炎 脂肪肝 生物 肝硬化 缺氧(环境) 内分泌学 脂质代谢 脂肪变性 缺氧诱导因子 肝星状细胞 内科学 化学 医学 生物化学 疾病 基因 有机化学 氧气
作者
Tomohiro Suzuki,Satoko Shinjo,Takatomo Arai,Mai Kanai,Nobuhito Goda
出处
期刊:World Journal of Gastroenterology [Baishideng Publishing Group]
卷期号:20 (41): 15087-15087 被引量:74
标识
DOI:10.3748/wjg.v20.i41.15087
摘要

The liver is a central organ that metabolizes excessive nutrients for storage in the form of glycogen and lipids and supplies energy-producing substrates to the peripheral tissues to maintain their function, even under starved conditions. These processes require a considerable amount of oxygen, which causes a steep oxygen gradient throughout the hepatic lobules. Alcohol consumption and/or excessive food intake can alter the hepatic metabolic balance drastically, which can precipitate fatty liver disease, a major cause of chronic liver diseases worldwide, ranging from simple steatosis, through steatohepatitis and hepatic fibrosis, to liver cirrhosis. Altered hepatic metabolism and tissue remodeling in fatty liver disease further disrupt hepatic oxygen homeostasis, resulting in severe liver hypoxia. As master regulators of adaptive responses to hypoxic stress, hypoxia-inducible factors (HIFs) modulate various cellular and organ functions, including erythropoiesis, angiogenesis, metabolic demand, and cell survival, by activating their target genes during fetal development and also in many disease conditions such as cancer, heart failure, and diabetes. In the past decade, it has become clear that HIFs serve as key factors in the regulation of lipid metabolism and fatty liver formation. This review discusses the molecular mechanisms by which hypoxia and HIFs regulate lipid metabolism in the development and progression of fatty liver disease.
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