Evidence map›Paper›PMID 39256892›Full record

ArticlePhysiological reports2024

Akt1 deficiency does not affect fiber type composition or mitochondrial protein expression in skeletal muscle of male mice.

Tatsuya Miyaji, Ryuichi Kasuya, Atsushi Sawada, Daisuke Sawamura, Yu Kitaoka, Mitsunori Miyazaki

Abstract read
In one paragraph

Article in Physiological reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

1 citing paper in PubMed.

  1. Article
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

6 authors.

Tatsuya MiyajiDepartment of Integrative Physiology, Graduate School of Biomedical and Health Sciences, Hiroshima University, Higashihiroshima, Japan.
Ryuichi KasuyaDepartment of Integrative Physiology, Graduate School of Biomedical and Health Sciences, Hiroshima University, Higashihiroshima, Japan.
Atsushi SawadaDepartment of Physical Therapy, School of Rehabilitation Sciences, Health Sciences University of Hokkaido, Tobetsu, Japan.ORCID 0009-0003-3392-0102
Daisuke SawamuraDepartment of Rehabilitation Science, Faculty of Health Sciences, Hokkaido University, Sapporo, Japan.
Yu KitaokaDepartment of Human Sciences, Kanagawa University, Yokohama, Japan.ORCID 0000-0001-6932-2735
Mitsunori MiyazakiDepartment of Integrative Physiology, Graduate School of Biomedical and Health Sciences, Hiroshima University, Higashihiroshima, Japan.ORCID 0000-0001-7824-2091

Funding

MEXT | Japan Society for the Promotion of Science (JSPS) JP17K18040MEXT | Japan Society for the Promotion of Science (JSPS) JP22H03439MEXT | Japan Society for the Promotion of Science (JSPS) JP23K18432MEXT | Japan Society for the Promotion of Science (JSPS) JP25702041
6 · The paper itself

Abstract

Insulin-like growth factor-1-induced activation of ATP citrate lyase (ACLY) improves muscle mitochondrial function through an Akt-dependent mechanism. In this study, we examined whether Akt1 deficiency alters skeletal muscle fiber type and mitochondrial function by regulating ACLY-dependent signaling in male Akt1 knockout (KO) mice (12-16 weeks old). Akt1 KO mice exhibited decreased body weight and muscle wet weight, with reduced cross-sectional areas of slow- and fast-type muscle fibers. Loss of Akt1 did not affect the phosphorylation status of ACLY in skeletal muscle. The skeletal muscle fiber type and expression of mitochondrial oxidative phosphorylation complex proteins were unchanged in Akt1 KO mice compared with the wild-type control. These observations indicate that Akt1 is important for the regulation of skeletal muscle fiber size, whereas the regulation of muscle fiber type and muscle mitochondrial content occurs independently of Akt1 activity.

Indexed as

Mice, KnockoutProto-Oncogene Proteins c-aktAnimalsATP Citrate (pro-S)-LyaseMaleMiceMice, Inbred C57BLMitochondrial ProteinsMitochondria, MuscleMuscle Fibers, SkeletalMuscle, SkeletalAkt1 protein, mouseATP Citrate (pro-S)-LyaseMitochondrial ProteinsProto-Oncogene Proteins c-aktAkt1glycolysismitochondriaskeletal muscle

Identifiers

PMID39256892
PMCPMC11387151

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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.