Reduction of stearoyl-CoA desaturase (SCD) contributes muscle atrophy through the excess endoplasmic reticulum stress in chronic kidney disease

Yuki Niida; Masashi Masuda; Yuichiro Adachi; Aika Yoshizawa; Hirokazu Ohminami; Yuki Mori; Kohta Ohnishi; Hisami Yamanaka-Okumura; Takayuki Uchida; Takeshi Nikawa; Hironori Yamamoto; Makoto Miyazaki; Yutaka Taketani

doi:10.3164/jcbn.20-24

Original Articles

Reduction of stearoyl-CoA desaturase (SCD) contributes muscle atrophy through the excess endoplasmic reticulum stress in chronic kidney disease

Yuki Niida, Masashi Masuda, Yuichiro Adachi, Aika Yoshizawa, Hirokazu Ohminami, Yuki Mori, Kohta Ohnishi, Hisami Yamanaka-Okumura, Takayuki Uchida, Takeshi Nikawa, Hironori Yamamoto, Makoto Miyazaki, Yutaka Taketani

Author information

Yuki Niida
Department of Clinical Nutrition and Food Management, Institute of Biomedical Sciences, Tokushima University Graduate School
Masashi Masuda
Department of Clinical Nutrition and Food Management, Institute of Biomedical Sciences, Tokushima University Graduate School
Yuichiro Adachi
Department of Clinical Nutrition and Food Management, Institute of Biomedical Sciences, Tokushima University Graduate School
Aika Yoshizawa
Department of Clinical Nutrition and Food Management, Institute of Biomedical Sciences, Tokushima University Graduate School
Hirokazu Ohminami
Department of Clinical Nutrition and Food Management, Institute of Biomedical Sciences, Tokushima University Graduate School
Yuki Mori
Department of Clinical Nutrition and Food Management, Institute of Biomedical Sciences, Tokushima University Graduate School
Kohta Ohnishi
Department of Clinical Nutrition and Food Management, Institute of Biomedical Sciences, Tokushima University Graduate School
Hisami Yamanaka-Okumura
Department of Clinical Nutrition and Food Management, Institute of Biomedical Sciences, Tokushima University Graduate School
Takayuki Uchida
Department of Nutritional Physiology, Institute of Biomedical Sciences, Tokushima University Graduate School
Takeshi Nikawa
Department of Nutritional Physiology, Institute of Biomedical Sciences, Tokushima University Graduate School
Hironori Yamamoto
Department of Clinical Nutrition and Food Management, Institute of Biomedical Sciences, Tokushima University Graduate School
Department of Health and Nutrition, Faculty of Human Life, Jin-ai University
Department of Nephrology, Faculty of Medical Sciences, University of Fukui
Makoto Miyazaki
Division of Renal Diseases and Hypertension, Department of Medicine, University of Colorado Denver
Yutaka Taketani
Department of Clinical Nutrition and Food Management, Institute of Biomedical Sciences, Tokushima University Graduate School

Keywords: skeletal muscle atrophy, endoplasmic reticulum stress, chronic kidney disease, stearoyl-CoA desaturase, saturated fatty acid

JOURNAL FREE ACCESS

2020 Volume 67 Issue 2 Pages 179-187

DOI https://doi.org/10.3164/jcbn.20-24

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Details

Abstract

Skeletal muscle atrophy is associated with mortality and poor prognosis in patients with chronic kidney disease (CKD). However, underlying mechanism by which CKD causes muscle atrophy has not been completely understood. The quality of lipids (lipoquality), which is defined as the functional features of diverse lipid species, has recently been recognized as the pathology of various diseases. In this study, we investigated the roles of the stearoyl-CoA desaturase (SCD), which catalyzes the conversion of saturated fatty acids into monounsaturated fatty acids, in skeletal muscle on muscle atrophy in CKD model animals. In comparison to control rats, CKD rats decreased the SCD activity and its gene expression in atrophic gastrocnemius muscle. Next, oleic acid blocked the reduction of the thickness of C2C12 myotubes and the increase of the endoplasmic reticulum stress induced by SCD inhibitor. Furthermore, endoplasmic reticulum stress inhibitor ameliorated CKD-induced muscle atrophy (the weakness of grip strength and the decrease of muscle fiber size of gastrocnemius muscle) in mice and the reduction of the thickness of C2C12 myotubes by SCD inhibitor. These results suggest that the repression of SCD activity causes muscle atrophy through excessive endoplasmic reticulum stress in CKD.

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