Hepatic Sdf2l1 controls feeding-induced ER stress and regulates metabolism View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2019-02-27

AUTHORS

Takayoshi Sasako, Mitsuru Ohsugi, Naoto Kubota, Shinsuke Itoh, Yukiko Okazaki, Ai Terai, Tetsuya Kubota, Satoshi Yamashita, Kunio Nakatsukasa, Takumi Kamura, Kaito Iwayama, Kumpei Tokuyama, Hiroshi Kiyonari, Yasuhide Furuta, Junji Shibahara, Masashi Fukayama, Kenichiro Enooku, Kazuya Okushin, Takeya Tsutsumi, Ryosuke Tateishi, Kazuyuki Tobe, Hiroshi Asahara, Kazuhiko Koike, Takashi Kadowaki, Kohjiro Ueki

ABSTRACT

Dynamic metabolic changes occur in the liver during the transition between fasting and feeding. Here we show that transient ER stress responses in the liver following feeding terminated by Sdf2l1 are essential for normal glucose and lipid homeostasis. Sdf2l1 regulates ERAD through interaction with a trafficking protein, TMED10. Suppression of Sdf2l1 expression in the liver results in insulin resistance and increases triglyceride content with sustained ER stress. In obese and diabetic mice, Sdf2l1 is downregulated due to decreased levels of nuclear XBP-1s, whereas restoration of Sdf2l1 expression ameliorates glucose intolerance and fatty liver with decreased ER stress. In diabetic patients, insufficient induction of Sdf2l1 correlates with progression of insulin resistance and steatohepatitis. Therefore, failure to build an ER stress response in the liver may be a causal factor in obesity-related diabetes and nonalcoholic steatohepatitis, for which Sdf2l1 could serve as a therapeutic target and sensitive biomarker. More... »

PAGES

947

Journal

TITLE

Nature Communications

ISSUE

1

VOLUME

10

Author Affiliations

  • Department of Molecular Sciences on Diabetes, Graduate School of Medicine, The University of Tokyo, 113-8655, Tokyo, Japan
  • Department of Diabetes and Metabolic Diseases, Graduate School of Medicine, The University of Tokyo, 113-8655, Tokyo, Japan
  • Department of Clinical Nutrition Therapy, The University of Tokyo Hospital, The University of Tokyo, 113-865, Tokyo, Japan
  • Kowa Company Limited, 460-0003, Nagoya, Japan
  • Department of Molecular Diabetic Medicine, Diabetes Research Center, National Center for Global Health and Medicine, 162-8655, Tokyo, Japan
  • Division of Cardiovascular Medicine, Toho University Ohashi Medical Center, 143-8541, Tokyo, Japan
  • Department of Systems BioMedicine, Tokyo Medical and Dental University, 113-8510, Tokyo, Japan
  • Graduate School of Natural Sciences, Nagoya City University, 464-8601, Nagoya, Japan
  • Division of Biological Sciences, Graduate School of Science, Nagoya University, 464-8601, Nagoya, Japan
  • Graduate School of Comprehensive Human Science, University of Tsukuba, 305-8577, Tsukuba, Japan
  • Genetic Engineering Team, RIKEN Center for Life Science Technologies, 650-0047, Kobe, Japan
  • Department of Pathology, Graduate School of Medicine, The University of Tokyo, 113-8655, Tokyo, Japan
  • Department of Gastroenterology, Graduate School of Medicine, The University of Tokyo, 113-8655, Tokyo, Japan
  • Department of Infectious Disease, Graduate School of Medicine, The University of Tokyo, 113-8655, Tokyo, Japan
  • The First Department of Internal Medicine, Graduate School of Medicine and Pharmaceutical Sciences of Research, The University of Toyama, 930-8555, Toyama, Japan
  • Department of Metabolism and Nutrition, Mizonokuchi Hospital, Faculty of Medicine, Teikyo University, 213-8507, Tokyo, Japan
  • Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1038/s41467-019-08591-6

    DOI

    http://dx.doi.org/10.1038/s41467-019-08591-6

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1112394765

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/30814508


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