Liver Patt1 deficiency protects male mice from age-associated but not high-fat diet-induced hepatic steatosis

Patt1 is a newly identified protein acetyltransferase that is highly expressed in liver. However, the role of Patt1 in liver is still unclear. We generated Patt1 liver-specific knockout (LKO) mice and mainly measured the effect of hepatic Patt1 deficiency on lipid metabolism. Hepatic Patt1 deficienc...

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Main Authors: Yang Liu, Daizhan Zhou, Fang Zhang, Yanyang Tu, Yulei Xia, Hui Wang, Ben Zhou, Yi Zhang, Jingxia Wu, Xiang Gao, Zhishui He, Qiwei Zhai
Format: Article
Language:English
Published: Elsevier 2012-03-01
Series:Journal of Lipid Research
Subjects:
Online Access:http://www.sciencedirect.com/science/article/pii/S0022227520413513
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record_format Article
collection DOAJ
language English
format Article
sources DOAJ
author Yang Liu
Daizhan Zhou
Fang Zhang
Yanyang Tu
Yulei Xia
Hui Wang
Ben Zhou
Yi Zhang
Jingxia Wu
Xiang Gao
Zhishui He
Qiwei Zhai
spellingShingle Yang Liu
Daizhan Zhou
Fang Zhang
Yanyang Tu
Yulei Xia
Hui Wang
Ben Zhou
Yi Zhang
Jingxia Wu
Xiang Gao
Zhishui He
Qiwei Zhai
Liver Patt1 deficiency protects male mice from age-associated but not high-fat diet-induced hepatic steatosis
Journal of Lipid Research
acetyltransferase
liver-specific
lipid metabolism
author_facet Yang Liu
Daizhan Zhou
Fang Zhang
Yanyang Tu
Yulei Xia
Hui Wang
Ben Zhou
Yi Zhang
Jingxia Wu
Xiang Gao
Zhishui He
Qiwei Zhai
author_sort Yang Liu
title Liver Patt1 deficiency protects male mice from age-associated but not high-fat diet-induced hepatic steatosis
title_short Liver Patt1 deficiency protects male mice from age-associated but not high-fat diet-induced hepatic steatosis
title_full Liver Patt1 deficiency protects male mice from age-associated but not high-fat diet-induced hepatic steatosis
title_fullStr Liver Patt1 deficiency protects male mice from age-associated but not high-fat diet-induced hepatic steatosis
title_full_unstemmed Liver Patt1 deficiency protects male mice from age-associated but not high-fat diet-induced hepatic steatosis
title_sort liver patt1 deficiency protects male mice from age-associated but not high-fat diet-induced hepatic steatosis
publisher Elsevier
series Journal of Lipid Research
issn 0022-2275
publishDate 2012-03-01
description Patt1 is a newly identified protein acetyltransferase that is highly expressed in liver. However, the role of Patt1 in liver is still unclear. We generated Patt1 liver-specific knockout (LKO) mice and mainly measured the effect of hepatic Patt1 deficiency on lipid metabolism. Hepatic Patt1 deficiency in male mice markedly decreases fat mass and dramatically alleviates age-associated accumulation of lipid droplets in liver. Moreover, hepatic Patt1 abrogation in male mice significantly reduces the liver triglyceride and free fatty acid levels, but it has no effect on liver cholesterol level, liver weight, and liver function. Consistently, primary cultured Patt1-deficient hepatocytes are resistant to palmitic acid-induced lipid accumulation, but hepatic Patt1 deficiency fails to protect male mice from high-fat diet-induced hepatic steatosis. Further studies show that hepatic Patt1 deficiency decreases fatty acid uptake, reduces lipid synthesis, and enhances fatty acid oxidation, which may contribute to the attenuated hepatic steatosis in Patt1 LKO mice. These results demonstrate that Patt1 plays an important role in hepatic lipid metabolism and have implications toward resolving age-associated hepatic steatosis.
topic acetyltransferase
liver-specific
lipid metabolism
url http://www.sciencedirect.com/science/article/pii/S0022227520413513
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spelling doaj-b47466c170524c96a0a53af4ac4e44732021-04-28T06:04:36ZengElsevierJournal of Lipid Research0022-22752012-03-01533358367Liver Patt1 deficiency protects male mice from age-associated but not high-fat diet-induced hepatic steatosisYang Liu0Daizhan Zhou1Fang Zhang2Yanyang Tu3Yulei Xia4Hui Wang5Ben Zhou6Yi Zhang7Jingxia Wu8Xiang Gao9Zhishui He10Qiwei Zhai11Key Laboratory of Nutrition and Metabolism, Institute for Nutritional Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Science; Graduate School of the Chinese Academy of Science; Shanghai 200031, China; andKey Laboratory of Nutrition and Metabolism, Institute for Nutritional Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Science; Graduate School of the Chinese Academy of Science; Shanghai 200031, China; andKey Laboratory of Nutrition and Metabolism, Institute for Nutritional Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Science; Graduate School of the Chinese Academy of Science; Shanghai 200031, China; andKey Laboratory of Nutrition and Metabolism, Institute for Nutritional Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Science; Graduate School of the Chinese Academy of Science; Shanghai 200031, China; andKey Laboratory of Nutrition and Metabolism, Institute for Nutritional Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Science; Graduate School of the Chinese Academy of Science; Shanghai 200031, China; andKey Laboratory of Nutrition and Metabolism, Institute for Nutritional Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Science; Graduate School of the Chinese Academy of Science; Shanghai 200031, China; andKey Laboratory of Nutrition and Metabolism, Institute for Nutritional Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Science; Graduate School of the Chinese Academy of Science; Shanghai 200031, China; andKey Laboratory of Nutrition and Metabolism, Institute for Nutritional Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Science; Graduate School of the Chinese Academy of Science; Shanghai 200031, China; andKey Laboratory of Nutrition and Metabolism, Institute for Nutritional Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Science; Graduate School of the Chinese Academy of Science; Shanghai 200031, China; andModel Animal Research Center, Nanjing University, Nanjing 210061, ChinaKey Laboratory of Nutrition and Metabolism, Institute for Nutritional Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Science; Graduate School of the Chinese Academy of Science; Shanghai 200031, China; andTo whom correspondence should be addressed; Key Laboratory of Nutrition and Metabolism, Institute for Nutritional Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Science; Graduate School of the Chinese Academy of Science; Shanghai 200031, China; andPatt1 is a newly identified protein acetyltransferase that is highly expressed in liver. However, the role of Patt1 in liver is still unclear. We generated Patt1 liver-specific knockout (LKO) mice and mainly measured the effect of hepatic Patt1 deficiency on lipid metabolism. Hepatic Patt1 deficiency in male mice markedly decreases fat mass and dramatically alleviates age-associated accumulation of lipid droplets in liver. Moreover, hepatic Patt1 abrogation in male mice significantly reduces the liver triglyceride and free fatty acid levels, but it has no effect on liver cholesterol level, liver weight, and liver function. Consistently, primary cultured Patt1-deficient hepatocytes are resistant to palmitic acid-induced lipid accumulation, but hepatic Patt1 deficiency fails to protect male mice from high-fat diet-induced hepatic steatosis. Further studies show that hepatic Patt1 deficiency decreases fatty acid uptake, reduces lipid synthesis, and enhances fatty acid oxidation, which may contribute to the attenuated hepatic steatosis in Patt1 LKO mice. These results demonstrate that Patt1 plays an important role in hepatic lipid metabolism and have implications toward resolving age-associated hepatic steatosis.http://www.sciencedirect.com/science/article/pii/S0022227520413513acetyltransferaseliver-specificlipid metabolism