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month download article/chapter potentiates pemetrexed-induced activity taurine-induced nuclear translocation mit/tfe transcription factors amp-activated protein kinase taurine-reduced phosphorylation levels full article pdf transcription factor eb as2o3-induced autophagy privacy choices/manage cookies tfeb links autophagy lysosome-related factors yoshikazu higami erk attenuates autophagy internal medicine research mammalian autophagy research article kaneko taurine-promoted autophagy obesity-related pathology preventing nuclear transport mtor signaling pathway taurine-deficient heart differentiated human adipocytes european economic area improve insulin resistance barbosa-sampaio hc mitochondrial oxidant production ubiquitin-proteasome system adipose tissue macrophages dapk2 downregulation associates reactive oxygen species yuhei mizunoe conditions privacy policy adipocyte characteristics stat-3 signaling pathway placebo-controlled study interheart study investigators case–control study taurine chloramine modulates autophagy fights disease defective hepatic autophagy yuka sudo author correspondence obese malnourished mice electronic supplementary material check access instant access autophagy regulates inflammation accepting optional cookies related subjects

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         headline:Taurine is an amino acid with the ability to activate autophagy in adipocytes
         description:Alterations in adipocyte characteristics are highly implicated in the pathology of obesity. In a recent article, we demonstrated that high-fat diet-induced obesity impairs lysosomal function, thereby suppressing autophagy in mice white adipose tissue. Taurine, an amino acid naturally contained in the normal diet and existing ubiquitously in tissues, has been reported to improve insulin resistance and chronic inflammation in animal models, but underlying mechanisms remain unclear. From these findings, we hypothesized that improvement of obese pathology by taurine may be mediated through recovery of autophagy. In matured 3T3-L1 mouse adipocytes, treatment with taurine-promoted autophagy. Moreover, taurine-induced nuclear translocation of transcription factor EB (TFEB), a master regulator of autophagy- and lysosome-related factors. As this translocation is regulated by several kinase pathways, including extracellular signal-related kinase 1 and 2 (ERK1/2) and mechanistic target of rapamycin protein kinase complex 1 (MTORC1), we examined related signaling elements. Consequently, taurine-reduced phosphorylation levels of ERK1/2 but did not alter the phosphorylation of MTORC1 pathway-associated adenosine monophosphate-activated protein kinase or ribosomal protein S6 kinase. Taken together, these results suggest that taurine may enhance TFEB nuclear translocation through ERK1/2 to accelerate autophagy. The effect discovered in this study may represent a novel mechanism for the improvement of obesity-related pathology by taurine.
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      headline:Taurine is an amino acid with the ability to activate autophagy in adipocytes
      description:Alterations in adipocyte characteristics are highly implicated in the pathology of obesity. In a recent article, we demonstrated that high-fat diet-induced obesity impairs lysosomal function, thereby suppressing autophagy in mice white adipose tissue. Taurine, an amino acid naturally contained in the normal diet and existing ubiquitously in tissues, has been reported to improve insulin resistance and chronic inflammation in animal models, but underlying mechanisms remain unclear. From these findings, we hypothesized that improvement of obese pathology by taurine may be mediated through recovery of autophagy. In matured 3T3-L1 mouse adipocytes, treatment with taurine-promoted autophagy. Moreover, taurine-induced nuclear translocation of transcription factor EB (TFEB), a master regulator of autophagy- and lysosome-related factors. As this translocation is regulated by several kinase pathways, including extracellular signal-related kinase 1 and 2 (ERK1/2) and mechanistic target of rapamycin protein kinase complex 1 (MTORC1), we examined related signaling elements. Consequently, taurine-reduced phosphorylation levels of ERK1/2 but did not alter the phosphorylation of MTORC1 pathway-associated adenosine monophosphate-activated protein kinase or ribosomal protein S6 kinase. Taken together, these results suggest that taurine may enhance TFEB nuclear translocation through ERK1/2 to accelerate autophagy. The effect discovered in this study may represent a novel mechanism for the improvement of obesity-related pathology by taurine.
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            name:Tokyo University of Science
            address:
               name:Translational Research Center, Research Institute of Science and Technology, Tokyo University of Science, Noda, Japan
               type:PostalAddress
            type:Organization
      name:Masato Imae
      affiliation:
            name:Taisho Pharmaceutical Co., Ltd.
            address:
               name:Product Development, Research and Development Headquarters Self-Medication, Taisho Pharmaceutical Co., Ltd., Tokyo, Japan
               type:PostalAddress
            type:Organization
      name:Yoshikazu Higami
      affiliation:
            name:Tokyo University of Science
            address:
               name:Laboratory of Molecular Pathology and Metabolic Disease, Faculty of Pharmaceutical Sciences, Tokyo University of Science, Noda, Japan
               type:PostalAddress
            type:Organization
            name:Tokyo University of Science
            address:
               name:Translational Research Center, Research Institute of Science and Technology, Tokyo University of Science, Noda, Japan
               type:PostalAddress
            type:Organization
      email:[email protected]
PostalAddress:
      name:Laboratory of Molecular Pathology and Metabolic Disease, Faculty of Pharmaceutical Sciences, Tokyo University of Science, Noda, Japan
      name:Laboratory of Molecular Pathology and Metabolic Disease, Faculty of Pharmaceutical Sciences, Tokyo University of Science, Noda, Japan
      name:Translational Research Center, Research Institute of Science and Technology, Tokyo University of Science, Noda, Japan
      name:Laboratory of Molecular Pathology and Metabolic Disease, Faculty of Pharmaceutical Sciences, Tokyo University of Science, Noda, Japan
      name:Translational Research Center, Research Institute of Science and Technology, Tokyo University of Science, Noda, Japan
      name:Laboratory of Molecular Pathology and Metabolic Disease, Faculty of Pharmaceutical Sciences, Tokyo University of Science, Noda, Japan
      name:Laboratory of Molecular Pathology and Metabolic Disease, Faculty of Pharmaceutical Sciences, Tokyo University of Science, Noda, Japan
      name:Laboratory of Molecular Pathology and Metabolic Disease, Faculty of Pharmaceutical Sciences, Tokyo University of Science, Noda, Japan
      name:Translational Research Center, Research Institute of Science and Technology, Tokyo University of Science, Noda, Japan
      name:Laboratory of Molecular Pathology and Metabolic Disease, Faculty of Pharmaceutical Sciences, Tokyo University of Science, Noda, Japan
      name:Laboratory of Molecular Pathology and Metabolic Disease, Faculty of Pharmaceutical Sciences, Tokyo University of Science, Noda, Japan
      name:Translational Research Center, Research Institute of Science and Technology, Tokyo University of Science, Noda, Japan
      name:Department of Internal Medicine Research, Sasaki Institute, Tokyo, Japan
      name:Laboratory of Molecular Pathology and Metabolic Disease, Faculty of Pharmaceutical Sciences, Tokyo University of Science, Noda, Japan
      name:Translational Research Center, Research Institute of Science and Technology, Tokyo University of Science, Noda, Japan
      name:Product Development, Research and Development Headquarters Self-Medication, Taisho Pharmaceutical Co., Ltd., Tokyo, Japan
      name:Laboratory of Molecular Pathology and Metabolic Disease, Faculty of Pharmaceutical Sciences, Tokyo University of Science, Noda, Japan
      name:Translational Research Center, Research Institute of Science and Technology, Tokyo University of Science, Noda, Japan
WebPageElement:
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