Molecular Mechanisms of Alcoholic Fatty Liver
| Autor: | Byoung-Joon Song, Bin Gao, Vishnudutt Purohit |
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| Rok vydání: | 2009 |
| Předmět: |
medicine.medical_specialty
Cirrhosis Medicine (miscellaneous) Peroxisome proliferator-activated receptor Toxicology Article Internal medicine medicine Animals Humans PPAR alpha adipocyte protein 2 Sterol Regulatory Element Binding Proteins chemistry.chemical_classification biology Adiponectin Tumor Necrosis Factor-alpha Fatty liver Complement C3 Peroxisome NAD medicine.disease Psychiatry and Mental health Endocrinology chemistry biology.protein lipids (amino acids peptides and proteins) Alcoholic fatty liver Steatohepatitis Fatty Liver Alcoholic |
| Zdroj: | Alcoholism: Clinical and Experimental Research. 33:191-205 |
| ISSN: | 1530-0277 0145-6008 |
| DOI: | 10.1111/j.1530-0277.2008.00827.x |
| Popis: | Alcoholic fatty liver is a potentially pathologic condition which can progress to steatohepatitis, fibrosis, and cirrhosis if alcohol consumption is continued. Alcohol exposure may induce fatty liver by increasing NADH/NAD(+) ratio, increasing sterol regulatory element-binding protein-1 (SREBP-1) activity, decreasing peroxisome proliferator-activated receptor-alpha (PPAR-alpha) activity, and increasing complement C3 hepatic levels. Alcohol may increase SREBP-1 activity by decreasing the activities of AMP-activated protein kinase and sirtuin-1. Tumor necrosis factor-alpha (TNF-alpha) produced in response to alcohol exposure may cause fatty liver by up-regulating SREBP-1 activity, whereas betaine and pioglitazone may attenuate fatty liver by down-regulating SREBP-1 activity. PPAR-alpha agonists have potentials to attenuate alcoholic fatty liver. Adiponectin and interleukin-6 may attenuate alcoholic fatty liver by up-regulating PPAR-alpha and insulin signaling pathways while down-regulating SREBP-1 activity and suppressing TNF-alpha production. Recent studies show that paracrine activation of hepatic cannabinoid receptor 1 by hepatic stellate cell-derived endocannabinoids also contributes to the development of alcoholic fatty liver. Furthermore, oxidative modifications and inactivation of the enzymes involved in the mitochondrial and/or peroxisomal beta-oxidation of fatty acids could contribute to fat accumulation in the liver. |
| Databáze: | OpenAIRE |
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