Hepatic Sdf2l1 controls feeding-induced ER stress and regulates metabolism
Endoplasmic reticulum (ER) stress has been proposed to play a role in metabolic diseases. Here, Sasako and colleagues identify stromal cell-derived factor 2 like 1 (Sdf2l1) as a regulator of the ER stress response to feeding in the liver, and suggest that its downregulation may promote diabetes and...
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| Format: | Article |
| Language: | English |
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Nature Publishing Group
2019-02-01
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| Series: | Nature Communications |
| Online Access: | https://doi.org/10.1038/s41467-019-08591-6 |
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doaj-c07e772286d14098b0891e96575742172021-05-11T12:25:13ZengNature Publishing GroupNature Communications2041-17232019-02-0110111610.1038/s41467-019-08591-6Hepatic Sdf2l1 controls feeding-induced ER stress and regulates metabolismTakayoshi Sasako0Mitsuru Ohsugi1Naoto Kubota2Shinsuke Itoh3Yukiko Okazaki4Ai Terai5Tetsuya Kubota6Satoshi Yamashita7Kunio Nakatsukasa8Takumi Kamura9Kaito Iwayama10Kumpei Tokuyama11Hiroshi Kiyonari12Yasuhide Furuta13Junji Shibahara14Masashi Fukayama15Kenichiro Enooku16Kazuya Okushin17Takeya Tsutsumi18Ryosuke Tateishi19Kazuyuki Tobe20Hiroshi Asahara21Kazuhiko Koike22Takashi Kadowaki23Kohjiro Ueki24Department of Diabetes and Metabolic Diseases, Graduate School of Medicine, The University of TokyoDepartment of Diabetes and Metabolic Diseases, Graduate School of Medicine, The University of TokyoDepartment of Diabetes and Metabolic Diseases, Graduate School of Medicine, The University of TokyoDepartment of Diabetes and Metabolic Diseases, Graduate School of Medicine, The University of TokyoDepartment of Diabetes and Metabolic Diseases, Graduate School of Medicine, The University of TokyoDepartment of Diabetes and Metabolic Diseases, Graduate School of Medicine, The University of TokyoDepartment of Diabetes and Metabolic Diseases, Graduate School of Medicine, The University of TokyoDepartment of Systems BioMedicine, Tokyo Medical and Dental UniversityDivision of Biological Sciences, Graduate School of Science, Nagoya UniversityDivision of Biological Sciences, Graduate School of Science, Nagoya UniversityGraduate School of Comprehensive Human Science, University of TsukubaGraduate School of Comprehensive Human Science, University of TsukubaAnimal Resource Development Unit, RIKEN Center for Life Science TechnologiesAnimal Resource Development Unit, RIKEN Center for Life Science TechnologiesDepartment of Pathology, Graduate School of Medicine, The University of TokyoDepartment of Pathology, Graduate School of Medicine, The University of TokyoDepartment of Gastroenterology, Graduate School of Medicine, The University of TokyoDepartment of Gastroenterology, Graduate School of Medicine, The University of TokyoDepartment of Infectious Disease, Graduate School of Medicine, The University of TokyoDepartment of Gastroenterology, Graduate School of Medicine, The University of TokyoThe First Department of Internal Medicine, Graduate School of Medicine and Pharmaceutical Sciences of Research, The University of ToyamaDepartment of Systems BioMedicine, Tokyo Medical and Dental UniversityDepartment of Gastroenterology, Graduate School of Medicine, The University of TokyoDepartment of Diabetes and Metabolic Diseases, Graduate School of Medicine, The University of TokyoDepartment of Diabetes and Metabolic Diseases, Graduate School of Medicine, The University of TokyoEndoplasmic reticulum (ER) stress has been proposed to play a role in metabolic diseases. Here, Sasako and colleagues identify stromal cell-derived factor 2 like 1 (Sdf2l1) as a regulator of the ER stress response to feeding in the liver, and suggest that its downregulation may promote diabetes and hepatic steatosis in humans.https://doi.org/10.1038/s41467-019-08591-6 |
| collection |
DOAJ |
| language |
English |
| format |
Article |
| sources |
DOAJ |
| author |
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 |
| spellingShingle |
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 Hepatic Sdf2l1 controls feeding-induced ER stress and regulates metabolism Nature Communications |
| author_facet |
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 |
| author_sort |
Takayoshi Sasako |
| title |
Hepatic Sdf2l1 controls feeding-induced ER stress and regulates metabolism |
| title_short |
Hepatic Sdf2l1 controls feeding-induced ER stress and regulates metabolism |
| title_full |
Hepatic Sdf2l1 controls feeding-induced ER stress and regulates metabolism |
| title_fullStr |
Hepatic Sdf2l1 controls feeding-induced ER stress and regulates metabolism |
| title_full_unstemmed |
Hepatic Sdf2l1 controls feeding-induced ER stress and regulates metabolism |
| title_sort |
hepatic sdf2l1 controls feeding-induced er stress and regulates metabolism |
| publisher |
Nature Publishing Group |
| series |
Nature Communications |
| issn |
2041-1723 |
| publishDate |
2019-02-01 |
| description |
Endoplasmic reticulum (ER) stress has been proposed to play a role in metabolic diseases. Here, Sasako and colleagues identify stromal cell-derived factor 2 like 1 (Sdf2l1) as a regulator of the ER stress response to feeding in the liver, and suggest that its downregulation may promote diabetes and hepatic steatosis in humans. |
| url |
https://doi.org/10.1038/s41467-019-08591-6 |
| work_keys_str_mv |
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