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Regulation of Adipose Tissue Inflammation and Insulin Resistance by MAPK Phosphatase 5.
Zhang, Yongliang; Nguyen, Thang; Tang, Peng; Kennedy, Norman J; Jiao, Huipeng; Zhang, Mingliang; Reynolds, Joseph M; Jaeschke, Anja; Martin-Orozco, Natalia; Chung, Yeonseok; He, Wei-min; Wang, Chen; Jia, Weiping; Ge, Baoxue; Davis, Roger J; Flavell, Richard A; Dong, Chen.
Afiliación
  • Zhang Y; From the Department of Microbiology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore 117597, Singapore, the Immunology Programme, Life Science Institute, National University of Singapore, Singapore 117597, Singapore.
  • Nguyen T; the Department of Immunology, University of Washington, Seattle, Washington 98195.
  • Tang P; From the Department of Microbiology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore 117597, Singapore, the Immunology Programme, Life Science Institute, National University of Singapore, Singapore 117597, Singapore.
  • Kennedy NJ; the Howard Hughes Medical Institute, University of Massachusetts, Worcester, Massachusetts 01606.
  • Jiao H; From the Department of Microbiology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore 117597, Singapore, the Immunology Programme, Life Science Institute, National University of Singapore, Singapore 117597, Singapore.
  • Zhang M; the Department of Endocrinology and Metabolism, Shanghai Jiaotong University Affiliated Sixth People's Hospital, Shanghai Diabetes Institute, Shanghai Clinical Center of Diabetes, Shanghai 200233, China.
  • Reynolds JM; the Department of Immunology, MD Anderson Cancer Center, Houston, Texas 77054.
  • Jaeschke A; the Pathobiology and Molecular Medicine Graduate Program, University of Cincinnati, Ohio 45215.
  • Martin-Orozco N; the Department of Immunology, MD Anderson Cancer Center, Houston, Texas 77054.
  • Chung Y; the Department of Immunology, MD Anderson Cancer Center, Houston, Texas 77054.
  • He WM; the Center for Environmental and Genetic Medicine, Institute of Biosciences and Technology, Texas A&M University System Health Sciences Center, Houston, Texas 77030.
  • Wang C; the Department of Endocrinology and Metabolism, Shanghai Jiaotong University Affiliated Sixth People's Hospital, Shanghai Diabetes Institute, Shanghai Clinical Center of Diabetes, Shanghai 200233, China.
  • Jia W; the Department of Endocrinology and Metabolism, Shanghai Jiaotong University Affiliated Sixth People's Hospital, Shanghai Diabetes Institute, Shanghai Clinical Center of Diabetes, Shanghai 200233, China.
  • Ge B; the Laboratory of Signal Transduction, Institute of Health Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences and Shanghai Jiao-Tong University School of Medicine, Shanghai 200025, China.
  • Davis RJ; the Howard Hughes Medical Institute, University of Massachusetts, Worcester, Massachusetts 01606.
  • Flavell RA; the Department of Immunology, Howard Hughes Medical Institute, Yale University, New Haven, Connecticut 06520, and Richard.flavell@yale.edu.
  • Dong C; the Institute for Immunology, Tsinghua University, Beijing 100084, China chendong@tsinghua.edu.cn.
J Biol Chem ; 290(24): 14875-83, 2015 Jun 12.
Article en En | MEDLINE | ID: mdl-25922079
Obesity and metabolic disorders such as insulin resistance and type 2 diabetes have become a major threat to public health globally. The mechanisms that lead to insulin resistance in type 2 diabetes have not been well understood. In this study, we show that mice deficient in MAPK phosphatase 5 (MKP5) develop insulin resistance spontaneously at an early stage of life and glucose intolerance at a later age. Increased macrophage infiltration in white adipose tissue of young MKP5-deficient mice correlates with the development of insulin resistance. Glucose intolerance in MKP5-deficient mice is accompanied by significantly increased visceral adipose weight, reduced AKT activation, enhanced p38 activity, and increased inflammation in visceral adipose tissue when compared with wild-type (WT) mice. Deficiency of MKP5 resulted in increased inflammatory activation in macrophages. These findings thus demonstrate that MKP5 critically controls inflammation in white adipose tissue and the development of metabolic disorders.
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Texto completo: 1 Colección: 01-internacional Banco de datos: MEDLINE Asunto principal: Resistencia a la Insulina / Tejido Adiposo / Fosfatasas de la Proteína Quinasa Activada por Mitógenos / Inflamación Límite: Animals Idioma: En Revista: J Biol Chem Año: 2015 Tipo del documento: Article País de afiliación: Singapur
Texto completo
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Texto completo: 1 Colección: 01-internacional Banco de datos: MEDLINE Asunto principal: Resistencia a la Insulina / Tejido Adiposo / Fosfatasas de la Proteína Quinasa Activada por Mitógenos / Inflamación Límite: Animals Idioma: En Revista: J Biol Chem Año: 2015 Tipo del documento: Article País de afiliación: Singapur