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Our research focuses on the mechanisms by which nutrient sensors regulate nutrient metabolism and energy homeostasis. We seek to identify new molecular targets that could be leveraged in the management of obesity, type 2 diabetes, fatty liver disease, and other age-related metabolic diseases. Our research goals are:
To characterize novel nutrient-sensing pathways involved in the regulation of lipid metabolism and energy homeostasis using nutritionally challenged models, metabolic disease mouse models, genetically modified mouse models, pharmacologically treated mouse models, as well as cell/molecular biology. Current efforts are focused on the molecular mechanism(s) by which vitamin A-related retinoic acid receptors and the hepatocyte-derived hormone, FGF21, regulate metabolic homeostasis and how this regulation affects the progression of Type 2 diabetes and age-related metabolic disease.
To identify the regulation and function of nutrient sensing and to characterize its therapeutic potential on non-alcoholic fatty liver disease. Current efforts are focused on the role of SIRT1 and AMP-activated protein kinase in the regulation of lipid metabolism in non-alcoholic fatty liver disease.
To define the molecular mechanisms underlying the pathogenesis of alcoholic liver disease. Current efforts are focused on the role of the nutrient sensing network in the development of alcoholic fatty liver and liver injury.
To investigate the role of nutrient sensing in adipose tissue metabolism and dysfunction. Although adipose tissue fibrosis impairs adipocyte plasticity, little is known about how aberrant extracellular matrix remodeling of fat tissue is initiated during the development of obesity. Our recent studies demonstrate the critical role of AMPK and TGFβ1 in adipocytes in the regulation of extracellular matrix homeostasis and systemic glucose metabolism in obese mice and humans. Targeting the AMPK pathway, like the action of metformin, may provide an exciting new approach for treatment of obesity-induced adipose tissue fibrosis and other tissue fibrosis.
Our research focuses on the mechanisms by which nutrient sensors regulate nutrient metabolism and energy homeostasis. We seek to identify new molecular targets that could be leveraged in the management of obesity, type 2 diabetes, fatty liver disease, and other age-related metabolic diseases. Our research goals are:
To characterize novel nutrient-sensing pathways involved in the regulation of lipid metabolism and energy homeostasis using nutritionally challenged models, metabolic disease mouse models, genetically modified mouse models, pharmacologically treated mouse models, as well as cell/molecular biology. Current efforts are focused on the molecular mechanism(s) by which vitamin A-related retinoic acid receptors and the hepatocyte-derived hormone, FGF21, regulate metabolic homeostasis and how this regulation affects the progression of Type 2 diabetes and age-related metabolic disease.
To identify the regulation and function of nutrient sensing and to characterize its therapeutic potential on non-alcoholic fatty liver disease. Current efforts are focused on the role of SIRT1 and AMP-activated protein kinase in the regulation of lipid metabolism in non-alcoholic fatty liver disease.
To define the molecular mechanisms underlying the pathogenesis of alcoholic liver disease. Current efforts are focused on the role of the nutrient sensing network in the development of alcoholic fatty liver and liver injury.
To investigate the role of nutrient sensing in adipose tissue metabolism and dysfunction. Although adipose tissue fibrosis impairs adipocyte plasticity, little is known about how aberrant extracellular matrix remodeling of fat tissue is initiated during the development of obesity. Our recent studies demonstrate the critical role of AMPK and TGFβ1 in adipocytes in the regulation of extracellular matrix homeostasis and systemic glucose metabolism in obese mice and humans. Targeting the AMPK pathway, like the action of metformin, may provide an exciting new approach for treatment of obesity-induced adipose tissue fibrosis and other tissue fibrosis.
研究兴趣
论文共 85 篇作者统计合作学者相似作者
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Jennifer Adjei‐Mosi, Qing Sun, Steven Blake Smithson, Gavyn Lee Shealy, Krupa Dhruvitha Amerineni,Zerong Liang,Hanqing Chen, Mei Wang, Qinggong Ping,Jingyan Han,Masahiro Morita,Amrita Kamat,
Aging Cellno. 5 (2023)
Jennifer Adjei-Mosi, Qing Sun, Steven Blake Smithson,Gavyn Lee Shealy, Krupa Dhruvitha Amerineni,Zerong Liang,Hanqing Chen, Mei Wang, Qinggong Ping,Jingyan Han,Masahiro Morita,Amrita Kamat,
Aging cell (2023)
Guannan Li,Hanqing Chen,Feng Shen, Steven Blake Smithson,Gavyn Lee Shealy, Qinggong Ping,Zerong Liang,Jingyan Han,Andrew C. Adams,Yu Li,Dechun Feng,Bin Gao,
Hepatology (Baltimore, Md.)no. 5 (2023): 1506-1524
ALCOHOLISM-CLINICAL AND EXPERIMENTAL RESEARCH (2023): 121-121
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Trends in Endocrinology & Metabolismno. 12 (2022): 801-803
Journal of Clinical Investigationno. 24 (2021)
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