Evidence map›Paper›PMID 40283072›Full record

ArticleLife (Basel, Switzerland)2025

Skeletal Muscle Atrophy Induced by Dexamethasone Is Attenuated by Amino Acid Complex Supplementation in Rats.

So-Jung Lim, Hyun-Jin Kim, Hansik Kim, Heesoo Nam, Kyung-Soo Nam, Inho Kim, Ryun Kang, Inyoung Hwang, Ju-Seop Kang

Abstract read
In one paragraph

Article in Life (Basel, Switzerland), 2025. 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

9 authors.

So-Jung LimDepartment of Pharmacology, College of Medicine, Hanyang University, Seoul 04763, Republic of Korea.ORCID 0009-0009-2590-3218
Hyun-Jin KimDepartment of Pharmacology, College of Medicine, Hanyang University, Seoul 04763, Republic of Korea.ORCID 0000-0002-9742-0508
Hansik KimBogoshinyak Co., Ltd., the Research Institute, 106, Wonbuk 1-gil, Nonsan-si 32925, Republic of Korea.
Heesoo NamBogoshinyak Co., Ltd., the Research Institute, 106, Wonbuk 1-gil, Nonsan-si 32925, Republic of Korea.
Kyung-Soo NamBogoshinyak Co., Ltd., the Research Institute, 106, Wonbuk 1-gil, Nonsan-si 32925, Republic of Korea.
Inho KimThe Korean Food Professional Engineers Association, 127 Beobwon-ro, Songpa-gu, Munjeong-dong, Seoul 05386, Republic of Korea.
Ryun KangDepartment of Medical and Digital Engineering, College of Engineering, Hanyang University, Seoul 04736, Republic of Korea.
Inyoung HwangDepartment of Clinical Pharmacology and Therapeutics, Hanyang University Seoul Hospital, Seoul 04736, Republic of Korea.ORCID 0000-0003-4953-759X
Ju-Seop KangDepartment of Pharmacology, College of Medicine, Hanyang University, Seoul 04763, Republic of Korea.ORCID 0000-0002-5588-8663

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Muscle atrophy, a physiological decline in muscle mass and strength due in ageing, occurs through an imbalance between protein breakdown and synthesis. The purpose of this study was to verify whether amino acid complex supplementation (ACS) can prevent and treat muscle loss in a dexamethasone (Dexa, 800 μg/kg)-induced rat model of sarcopenia. Sprague Dawley rats (6 weeks old) were assigned to seven groups: (i) normal control, (ii) positive control (high-dose ACS, 500 mg), (iii) Dexa only, (iv) Dexa + high-dose ACS (500 mg), (v) Dexa + medium-dose ACS (300 mg), (vi) Dexa + low-dose ACS (100 mg), or (vii) Dexa + liquid amino acid complex formulation (LF, 2 mL), administered orally for 4 weeks. Exercise capacity tests were performed five times using a treadmill test (TT) and forced swimming test (FST). The body weight increase in each group was less than that of the normal group. The blood biochemical indices, AST levels, and AST/ALT ratio significantly increased in the Dexa-treated medium-dose ACS group. The total muscle protein also significantly increased in all ACS groups. In the Dexa-treated LF group, CK decreased below the normal level. Exercise capacity, assessed by TT and FST, increased the most in the positive control and Dexa-treated high-dose ACS groups. In the TT, the Dexa-only group increased by about 18%, but the Dexa-treated high-dose ACS group increased by about 110%. Additionally, in the FST, Dexa-treated rats receiving a high dose of ACS demonstrated significantly increased exercise time and capacity. Electron microscopic (EM) and hematoxylin and eosin (H&E) observations of muscle tissue revealed muscle fiber atrophy in the gastrocnemius muscles of the Dexa-only group. In the EM findings of the Dexa-treated high-dose ACS group, the M-line and Z-line were clearer than in the Dexa-only group, and the mitochondria were partially preserved. In conclusion, the ACS-treated rats showed a clear recovery from muscle damage based on serum indices, total muscle protein mass, and the microscopic findings on muscle tissue. Notably, a high dose of ACS demonstrated the most effective protection and recovery of muscle tissue in the Dexa-induced sarcopenia rat model.

Indexed as

amino acid complex supplementationdexamethasone-induced sarcopeniaforced swimming testM-linetreadmill testZ-line

Identifiers

PMID40283072
PMCPMC12028686

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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.