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other·endocrinology, preclinical research, biomedical research, nutrition·PMC10445200

Blockade of glucagon increases muscle mass and alters fiber type composition in mice deficient in proglucagon‐derived peptides

Journal of Diabetes Investigation · 16 authors, 13 centres

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TL;DR

This preclinical study used mice genetically deficient in proglucagon-derived peptides (GCGKO mice) to block glucagon action. The central result was that these mice exhibited increased skeletal muscle mass and a shift in muscle fiber composition toward faster type II fibers, mimicking the effects of a high-protein diet.

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This preclinical animal study investigated the effects of blocking glucagon action on skeletal muscle by analyzing muscles from proglucagon-derived peptide-deficient (GCGKO) and control mice for morphology, gene expression, and metabolites.

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other

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endocrinology

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ORIGINAL PAPER

PMC10445200

Blockade of glucagon increases muscle mass and alters fiber type composition in mice deficient in proglucagon‐derived peptides

Journal of Diabetes Investigation

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ABSTRACT

ABSTRACT Aims/Introduction Glucagon is secreted from pancreatic α‐cells and plays an important role in amino acid metabolism in liver. Various animal models deficient in glucagon action show hyper‐amino acidemia and α‐cell hyperplasia, indicating that glucagon contributes to feedback regulation between the liver and the α‐cells. In addition, both insulin and various amino acids, including branched‐chain amino acids and alanine, participate in protein synthesis in skeletal muscle. However, the effect of hyperaminoacidemia on skeletal muscle has not been investigated. In the present study, we examined the effect of blockade of glucagon action on skeletal muscle using mice deficient in proglucagon‐derived peptides (GCGKO mice). Materials and Methods Muscles isolated from GCGKO and control mice were analyzed for their morphology, gene expression and metabolites. Results GCGKO mice showed muscle fiber hypertrophy, and a decreased ratio of type IIA and an increased ratio of type IIB fibers in the tibialis anterior. The expression levels of myosin heavy chain ( Myh ) 7, 2, 1 and myoglobin messenger ribonucleic acid were significantly lower in GCGKO mice than those in control mice in the tibialis anterior. GCGKO mice showed a significantly higher concentration of arginine, asparagine, serine and threonine in the quadriceps femoris muscles, and also alanine, aspartic acid, cysteine, glutamine, glycine and lysine, as well as four amino acids in gastrocnemius muscles. Conclusions These results show that hyperaminoacidemia induced by blockade of glucagon action in mice increases skeletal muscle weight and stimulates slow‐to‐fast transition in type II fibers of skeletal muscle, mimicking the phenotype of a high‐protein diet. Keywords: Amino acid, Glucagon, Skeletal muscle

CITATION EXPORT

Shinji Ueno, Yusuke Seino, Shihomi Hidaka et al.. Blockade of glucagon increases muscle mass and alters fiber type composition in mice deficient in proglucagon‐derived peptides. Journal of Diabetes Investigation. (2023). https://doi.org/10.1111/jdi.14032

AUTHORS

16 · 13 CENTRES

Shinji Ueno, Yusuke Seino, Shihomi Hidaka, Masashi Nakatani, Keisuke Hitachi, Naoya Murao, Yasuhiro Maeda, Haruki Fujisawa, Megumi Shibata, Takeshi Takayanagi, Katsumi Iizuka, Daisuke Yabe, Yoshihisa Sugimura, Kunihiro Tsuchida, Yoshitaka Hayashi, Atsushi Suzuki

1 Departments of Endocrinology, Diabetes and Metabolism, Fujita Health University School of Medicine, Toyoake, Aichi, Japan
2 Yutaka Seino Distinguished Center for Diabetes Research, Kansai Electric Power Medical Research Institute, Kyoto, Kyoto, Japan
3 Faculty of Rehabilitation, Seijoh University, Tokai, Aichi, Japan
4 Institute for Comprehensive Medical Science, Fujita Health University, Toyoake, Aichi, Japan
5 Open Facility Center, Fujita Health University, Toyoake, Aichi, Japan
6 Department of Clinical Nutrition, Fujita Health University, Toyoake, Aichi, Japan
7 Department of Diabetes, Endocrinology and Metabolism, Gifu University Graduate School of Medicine, Gifu, Gifu, Japan
8 Department of Rheumatology and Clinical Immunology, Gifu University Graduate School of Medicine, Gifu, Gifu, Japan
9 Center for One Medicine Innovative Translational Research, Gifu University Graduate School of Medicine, Gifu, Gifu, Japan
10 Center for Healthcare Information Technology, Tokai National Higher Education and Research System, Nagoya, Aichi, Japan
11 Division of Molecular and Metabolic Medicine, Kobe University Graduate School of Medicine, Kobe, Hyogo, Japan
12 Department of Endocrinology, Research Institute of Environmental Medicine, Nagoya University, Nagoya, Aichi, Japan
13 Department of Endocrinology, Nagoya University Graduate School of Medicine, Nagoya, Aichi, Japan