Evidence map›Paper›PMID 37300240›Full record

ArticleJournal of diabetes investigation2023

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

Shinji Ueno, Yusuke Seino, Shihomi Hidaka, Masashi Nakatani, Keisuke Hitachi, Naoya Murao, Yasuhiro Maeda, Haruki Fujisawa, Megumi Shibata, Takeshi Takayanagi and 6 more

Open access · goldAbstract read
In one paragraph

Article in Journal of diabetes investigation, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
8.3field-weighted citation impact, top 2% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

9 citing papers in PubMed, 26 citations in OpenAlex.

  1. Article
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  4. Nutrients · 2025
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

16 authors at 4 institutions in 1 country.

Shinji UenoDepartments of Endocrinology, Diabetes and Metabolism, Fujita Health University School of Medicine, Toyoake, Aichi, Japan.
Yusuke SeinoDepartments of Endocrinology, Diabetes and Metabolism, Fujita Health University School of Medicine, Toyoake, Aichi, Japan.ORCID https://orcid.org/0000-0002-9099-3493
Shihomi HidakaDepartments of Endocrinology, Diabetes and Metabolism, Fujita Health University School of Medicine, Toyoake, Aichi, Japan.
Masashi NakataniFaculty of Rehabilitation, Seijoh University, Tokai, Aichi, Japan.
Keisuke HitachiInstitute for Comprehensive Medical Science, Fujita Health University, Toyoake, Aichi, Japan.ORCID https://orcid.org/0000-0002-7300-5238
Naoya MuraoDepartments of Endocrinology, Diabetes and Metabolism, Fujita Health University School of Medicine, Toyoake, Aichi, Japan.ORCID https://orcid.org/0000-0002-7424-4476
Yasuhiro MaedaOpen Facility Center, Fujita Health University, Toyoake, Aichi, Japan.
Haruki FujisawaDepartments of Endocrinology, Diabetes and Metabolism, Fujita Health University School of Medicine, Toyoake, Aichi, Japan.
Megumi ShibataDepartments of Endocrinology, Diabetes and Metabolism, Fujita Health University School of Medicine, Toyoake, Aichi, Japan.
Takeshi TakayanagiDepartments of Endocrinology, Diabetes and Metabolism, Fujita Health University School of Medicine, Toyoake, Aichi, Japan.ORCID https://orcid.org/0000-0002-9507-6993
Katsumi IizukaDepartment of Clinical Nutrition, Fujita Health University, Toyoake, Aichi, Japan.ORCID https://orcid.org/0000-0002-9837-6238
Daisuke YabeYutaka Seino Distinguished Center for Diabetes Research, Kansai Electric Power Medical Research Institute, Kyoto, Kyoto, Japan.ORCID https://orcid.org/0000-0002-5334-7687
Yoshihisa SugimuraDepartments of Endocrinology, Diabetes and Metabolism, Fujita Health University School of Medicine, Toyoake, Aichi, Japan.
Kunihiro TsuchidaInstitute for Comprehensive Medical Science, Fujita Health University, Toyoake, Aichi, Japan.ORCID https://orcid.org/0000-0002-3983-5756
Yoshitaka HayashiDepartment of Endocrinology, Research Institute of Environmental Medicine, Nagoya University, Nagoya, Aichi, Japan.ORCID https://orcid.org/0000-0002-7557-4303
Atsushi SuzukiDepartments of Endocrinology, Diabetes and Metabolism, Fujita Health University School of Medicine, Toyoake, Aichi, Japan.
Fujita Health University · JPNagoya University · JPSeijoh University · JPTokai Gakuen University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

AIMS/

introductionGlucagon 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

methodsMuscles isolated from GCGKO and control mice were analyzed for their morphology, gene expression and metabolites.

resultsGCGKO 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.

conclusionsThese 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.

Indexed as

GlucagonMuscle, SkeletalProglucagonAmino AcidsAnimalsMiceAmino AcidsGlucagonProglucagonAmino acidGlucagonSkeletal muscle

Identifiers

PMID37300240
PMCPMC10445200
OpenAlexW4380077443

What OpenQuestion holds

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LicenceCC BY-NC
Read underepoch 390

Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.