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

التفاصيل البيبلوغرافية
العنوان: Blockade of glucagon increases muscle mass and alters fiber type composition in mice deficient in proglucagon-derived peptides.
المؤلفون: Ueno S; Departments of Endocrinology, Diabetes and Metabolism, Fujita Health University School of Medicine, Toyoake, Aichi, Japan., Seino Y; Departments of Endocrinology, Diabetes and Metabolism, Fujita Health University School of Medicine, Toyoake, Aichi, Japan.; Yutaka Seino Distinguished Center for Diabetes Research, Kansai Electric Power Medical Research Institute, Kyoto, Kyoto, Japan., Hidaka S; Departments of Endocrinology, Diabetes and Metabolism, Fujita Health University School of Medicine, Toyoake, Aichi, Japan., Nakatani M; Faculty of Rehabilitation, Seijoh University, Tokai, Aichi, Japan.; Institute for Comprehensive Medical Science, Fujita Health University, Toyoake, Aichi, Japan., Hitachi K; Institute for Comprehensive Medical Science, Fujita Health University, Toyoake, Aichi, Japan., Murao N; Departments of Endocrinology, Diabetes and Metabolism, Fujita Health University School of Medicine, Toyoake, Aichi, Japan.; Yutaka Seino Distinguished Center for Diabetes Research, Kansai Electric Power Medical Research Institute, Kyoto, Kyoto, Japan., Maeda Y; Open Facility Center, Fujita Health University, Toyoake, Aichi, Japan., Fujisawa H; Departments of Endocrinology, Diabetes and Metabolism, Fujita Health University School of Medicine, Toyoake, Aichi, Japan., Shibata M; Departments of Endocrinology, Diabetes and Metabolism, Fujita Health University School of Medicine, Toyoake, Aichi, Japan., Takayanagi T; Departments of Endocrinology, Diabetes and Metabolism, Fujita Health University School of Medicine, Toyoake, Aichi, Japan., Iizuka K; Department of Clinical Nutrition, Fujita Health University, Toyoake, Aichi, Japan., Yabe D; Yutaka Seino Distinguished Center for Diabetes Research, Kansai Electric Power Medical Research Institute, Kyoto, Kyoto, Japan.; Department of Diabetes, Endocrinology and Metabolism, Gifu University Graduate School of Medicine, Gifu, Gifu, Japan.; Department of Rheumatology and Clinical Immunology, Gifu University Graduate School of Medicine, Gifu, Gifu, Japan.; Center for One Medicine Innovative Translational Research, Gifu University Graduate School of Medicine, Gifu, Gifu, Japan.; Center for Healthcare Information Technology, Tokai National Higher Education and Research System, Nagoya, Aichi, Japan.; Division of Molecular and Metabolic Medicine, Kobe University Graduate School of Medicine, Kobe, Hyogo, Japan., Sugimura Y; Departments of Endocrinology, Diabetes and Metabolism, Fujita Health University School of Medicine, Toyoake, Aichi, Japan., Tsuchida K; Institute for Comprehensive Medical Science, Fujita Health University, Toyoake, Aichi, Japan., Hayashi Y; Department of Endocrinology, Research Institute of Environmental Medicine, Nagoya University, Nagoya, Aichi, Japan.; Department of Endocrinology, Nagoya University Graduate School of Medicine, Nagoya, Aichi, Japan., Suzuki A; Departments of Endocrinology, Diabetes and Metabolism, Fujita Health University School of Medicine, Toyoake, Aichi, Japan.
المصدر: Journal of diabetes investigation [J Diabetes Investig] 2023 Sep; Vol. 14 (9), pp. 1045-1055. Date of Electronic Publication: 2023 Jun 09.
نوع المنشور: Journal Article
اللغة: English
بيانات الدورية: Publisher: Asian Association for the Study of Diabetes and Blackwell Pub. Asia Country of Publication: Japan NLM ID: 101520702 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 2040-1124 (Electronic) Linking ISSN: 20401116 NLM ISO Abbreviation: J Diabetes Investig Subsets: MEDLINE
أسماء مطبوعة: Original Publication: Tokyo : Asian Association for the Study of Diabetes and Blackwell Pub. Asia
مواضيع طبية MeSH: Glucagon*/metabolism , Muscle, Skeletal*/metabolism , Proglucagon*/genetics , Proglucagon*/metabolism, Animals ; Mice ; Amino Acids
مستخلص: 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.
(© 2023 The Authors. Journal of Diabetes Investigation published by Asian Association for the Study of Diabetes (AASD) and John Wiley & Sons Australia, Ltd.)
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فهرسة مساهمة: Keywords: Amino acid; Glucagon; Skeletal muscle
المشرفين على المادة: 0 (Amino Acids)
9007-92-5 (Glucagon)
55963-74-1 (Proglucagon)
تواريخ الأحداث: Date Created: 20230610 Date Completed: 20230829 Latest Revision: 20230829
رمز التحديث: 20240628
مُعرف محوري في PubMed: PMC10445200
DOI: 10.1111/jdi.14032
PMID: 37300240
قاعدة البيانات: MEDLINE
الوصف
تدمد:2040-1124
DOI:10.1111/jdi.14032