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Start Over Author "Linfei Huang" Journal nature communications
2 results on '"Linfei Huang"'

1. GP73 is a TBC-domain Rab GTPase-activating protein contributing to the pathogenesis of non-alcoholic fatty liver disease without obesity

Author

Yumeng Peng, Qiang Zeng, Luming Wan, Enhao Ma, Huilong Li, Xiaopan Yang, Yanhong Zhang, Linfei Huang, Haotian Lin, Jiangyue Feng, Yixin Xu, Jingfei Li, Muyi Liu, Jing Liu, Changqin Lin, Zhiwei Sun, Gong Cheng, Xuemiao Zhang, Jialong Liu, Dongrui Li, Meng Wei, Yunhai Mo, Xuetao Mu, Xiaowei Deng, Dandan Zhang, Siqing Dong, Hanqing Huang, Yi Fang, Qi Gao, Xiaoli Yang, Feixiang Wu, Hui Zhong, and Congwen Wei

Subjects
Science
Abstract

Dysregulation of lipid metabolism and transport contribute to the pathogenesis of non-alcoholic fatty liver disease (NAFLD). Here the authors identify GP73 as a TBC-domain Rab GTPase-activating protein that regulates very low-density lipoprotein export and promotes NAFLD development in mice.

Published
2021
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2. GP73 is a TBC-domain Rab GTPase-activating protein contributing to the pathogenesis of non-alcoholic fatty liver disease without obesity

Author

Enhao Ma, Yanhong Zhang, Dandan Zhang, Huilong Li, Yunhai Mo, Dongrui Li, Changqin Lin, Jialong Liu, Haotian Lin, Zhiwei Sun, Feixiang Wu, Meng Wei, Luming Wan, Yi Fang, Gong Cheng, Xiaopan Yang, Yixin Xu, Xiaoli Yang, Xuetao Mu, Jingfei Li, Xiaowei Deng, Hanqing Huang, Jiangyue Feng, Siqing Dong, Jing Liu, Congwen Wei, Muyi Liu, Hui Zhong, Qi Gao, Linfei Huang, Yumeng Peng, Qiang Zeng, and Xuemiao Zhang

Subjects
Male, medicine.medical_specialty, Apolipoprotein B, Science, Metabolic disorders, General Physics and Astronomy, Diet, High-Fat, digestive system, General Biochemistry, Genetics and Molecular Biology, Article, Pathogenesis, Mice, Insulin resistance, Non-alcoholic Fatty Liver Disease, Internal medicine, Nonalcoholic fatty liver disease, Medicine, Animals, Obesity, Multidisciplinary, biology, business.industry, Fatty liver, Body Weight, GTPase-Activating Proteins, Membrane Proteins, nutritional and metabolic diseases, Lipid metabolism, General Chemistry, medicine.disease, Phosphoproteins, digestive system diseases, Metformin, Mice, Inbred C57BL, Disease Models, Animal, Endocrinology, Metabolism, Gene Expression Regulation, Liver, Gene Knockdown Techniques, Apolipoprotein B-100, biology.protein, Rab, Insulin Resistance, business, Transcriptome, medicine.drug
Abstract

The prevalence of non-obese nonalcoholic fatty liver disease (NAFLD) is increasing worldwide with unclear etiology and pathogenesis. Here, we show GP73, a Golgi protein upregulated in livers from patients with a variety of liver diseases, exhibits Rab GTPase-activating protein (GAP) activity regulating ApoB export. Upon regular-diet feeding, liver-GP73-high mice display non-obese NAFLD phenotype, characterized by reduced body weight, intrahepatic lipid accumulation, and gradual insulin resistance development, none of which can be recapitulated in liver-GAP inactive GP73-high mice. Common and specific gene expression signatures associated with GP73-induced non-obese NAFLD and high-fat diet (HFD)-induced obese NAFLD are revealed. Notably, metformin inactivates the GAP activity of GP73 and alleviates GP73-induced non-obese NAFLD. GP73 is pathologically elevated in NAFLD individuals without obesity, and GP73 blockade improves whole-body metabolism in non-obese NAFLD mouse model. These findings reveal a pathophysiological role of GP73 in triggering non-obese NAFLD and may offer an opportunity for clinical intervention., Dysregulation of lipid metabolism and transport contribute to the pathogenesis of non-alcoholic fatty liver disease (NAFLD). Here the authors identify GP73 as a TBC-domain Rab GTPase-activating protein that regulates very low-density lipoprotein export and promotes NAFLD development in mice.

Published
2021

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