期刊
BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR AND CELL BIOLOGY OF LIPIDS
卷 1821, 期 5, 页码 762-769出版社
ELSEVIER
DOI: 10.1016/j.bbalip.2011.09.007
关键词
Lipase; Hepatic steatosis; Triacylglycerol; Carboxylesterase; Arylacetamide deacetylase; Autophagy; Lipophagy
资金
- Canadian Institutes of Health Research
- Heart and Stroke Foundation of Canada
The hallmark of obesity and one of the key contributing factors to insulin resistance, type 2 diabetes and cardiovascular disease is excess triacylglycerol (TG) storage. In hepatocytes, excessive accumulation of TG is the common denominator of a wide range of clinicopathological entities known as nonalcoholic fatty liver disease, which can eventually progress to cirrhosis and associated complications including hepatic failure, hepatocellular carcinoma and death. A tight regulation between TG synthesis, hydrolysis, secretion and fatty acid oxidation is required to prevent lipid accumulation as well as lipid depletion from hepatocytes. Therefore, understanding the pathways that regulate hepatic TG metabolism is crucial for development of therapies to ameliorate pathophysiological conditions associated with excessive hepatic TG accumulation, including dyslipidemias, viral infection and atherosclerosis. This review highlights the physiological roles of liver lipases that degrade TG in cytosolic lipid droplets, endoplasmic reticulum, late endosomes/lysosomes and along the secretory route. This article is part of a Special Issue entitled Triglyceride Metabolism and Disease. (C) 2011 Elsevier B.V. All rights reserved.
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