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Deletion of SIRT1 From Hepatocytes in Mice Disrupts Lipin-1 Signaling and Aggravates Alcoholic Fatty Liver

Deletion of SIRT1 From Hepatocytes in Mice Disrupts Lipin-1 Signaling and Aggravates Alcoholic Fatty Liver
Sirtuin (SIRT1) is a NAD+-dependent protein deacetylase that regulates hepatic lipid metabolism by modifying histones and transcription factors. Ethanol exposure disrupts SIRT1 activity and contributes to alcoholic liver disease (ALD) in rodents, but the exact pathogenic mechanism is not clear. We compared mice with liver-specific deletion of Sirt1 (Sirt1LKO) mice with their LOX littermates (controls).
- University of Barcelona Spain
- Ministry of Health Malaysia
- University of North Carolina at Chapel Hill United States
- National Institutes of Health United States
- National Institute of Environmental Health Sciences United States
Male, Phosphatidate Phosphatase, Nerve Tissue Proteins, Mice, Animals, Humans, Mice, Knockout, Ethanol, Serine-Arginine Splicing Factors, Nuclear Proteins, RNA-Binding Proteins, Endoplasmic Reticulum Stress, Lipid Metabolism, Mice, Inbred C57BL, Disease Models, Animal, Oxidative Stress, Liver, Hepatocytes, Fatty Liver, Alcoholic, Signal Transduction
Male, Phosphatidate Phosphatase, Nerve Tissue Proteins, Mice, Animals, Humans, Mice, Knockout, Ethanol, Serine-Arginine Splicing Factors, Nuclear Proteins, RNA-Binding Proteins, Endoplasmic Reticulum Stress, Lipid Metabolism, Mice, Inbred C57BL, Disease Models, Animal, Oxidative Stress, Liver, Hepatocytes, Fatty Liver, Alcoholic, Signal Transduction
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