# Therapeutic effect of traditional Chinese medicine on diabetic sarcopenia: a systematic review and meta-analysis of preclinical studies

**Authors:** Ruiting Zhang, Yingzhe Liu, Lin Zhu, Dongxia Li, Xiangbin Pan

PMC · DOI: 10.3389/fendo.2025.1647271 · Frontiers in Endocrinology · 2026-01-12

## TL;DR

This study reviews preclinical evidence showing that traditional Chinese medicine may help treat diabetic sarcopenia by improving muscle mass and strength in animal models.

## Contribution

The study provides a systematic review and meta-analysis of preclinical TCM interventions for diabetic sarcopenia, highlighting their potential therapeutic effects and mechanisms.

## Key findings

- TCM significantly increased gastrocnemius muscle weight and cross-sectional area in animal models.
- TCM improved grip strength and reduced blood glucose levels in diabetic sarcopenia models.
- TCM showed bidirectional regulation of body weight in different sarcopenia contexts.

## Abstract

Diabetic sarcopenia (DS) is an emerging complication of diabetes. Although clinical treatment options remain inadequate, preliminary evidence suggests that Traditional Chinese Medicine (TCM) holds therapeutic promise. This study aims to systematically evaluate the existing preclinical evidence for TCM treatments in diabetic sarcopenia.

We conducted a meta-analysis of animal studies investigating TCM interventions for DS. The initial literature search cutoff date was June 2024, with an updated search conducted during manuscript revision in November 2025. The search covered all records from seven databases from their inception to November 2025. Data analysis is performed using Review Manager 5.3 software. A fixed-effect model was selected when heterogeneity among studies was insignificant (P ≥ 0.1 or I² ≤ 50%); otherwise, a random-effects model was used. The robustness of the primary outcomes was assessed through sensitivity analysis. Publication bias was evaluated using Egger’s test and funnel plots. Additionally, meta-regression was employed to explore potential sources of heterogeneity.This study has been registered on the PROSPERO platform (Registration Number: CRD42024596404).

The meta-analysis demonstrated that TCM intervention significantly increased gastrocnemius muscle weight [SMD = 1.85, 95% CI (1.07, 2.63), P < 0.00001] and muscle cross-sectional area [SMD = 2.68, 95% CI (1.63, 3.73), P < 0.00001], while improving muscle tissue morphology and grip strength [SMD = 1.57, 95% CI (0.49, 2.65), P = 0.004]. Notably, TCM exerted a bidirectional regulatory effect on body weight: significantly increasing it in diabetic cachexia models [SMD = 0.73, P = 0.02] while reducing it in obesity with sarcopenia models [SMD = -1.97, P < 0.00001]. A significant reduction in blood glucose levels was also observed [SMD = -3.13, P < 0.00001]. Mechanistically, preclinical evidence suggests that specific TCM interventions may modulate protein turnover homeostasis, potentially by activating the IGF1-PI3K-Akt-mTOR synthetic pathway and inhibiting the FoxO/Ubiquitin-Proteasome degradation pathway, alongside optimizing the pathological microenvironment.

Current preclinical evidence suggests that specific TCM interventions may show potential in alleviating Diabetic Sarcopenia in animal models by improving muscle mass, strength, and metabolic function. Certain formulations appeared to exhibit a bidirectional regulation of body weight, which may reflect a context-dependent metabolic impact. However, due to the prevalent lack of blinding and allocation concealment in the included studies, the reported efficacy may be systematically overestimated. Consequently, current evidence remains preliminary. Future research must strictly adhere to ARRIVE guidelines and standardize interventions to generate robust preclinical data, paving the way for high-quality clinical trials.

https://www.crd.york.ac.uk/prospero/, identifier CRD4202459640.

## Linked entities

- **Proteins:** IGF1 (insulin like growth factor 1), PIK3CA (phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha), AKT1 (AKT serine/threonine kinase 1), MTOR (mechanistic target of rapamycin kinase), foxo (forkhead box, sub-group O)
- **Diseases:** diabetes (MONDO:0005015)

## Full-text entities

- **Genes:** MTOR (mechanistic target of rapamycin kinase) [NCBI Gene 2475] {aka FRAP, FRAP1, FRAP2, RAFT1, RAPT1, SKS}, IGF1 (insulin like growth factor 1) [NCBI Gene 3479] {aka IGF, IGF-I, IGFI, MGF}, PIK3CB (phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit beta) [NCBI Gene 5291] {aka P110BETA, PI3K, PI3KBETA, PIK3C1}, AKT1 (AKT serine/threonine kinase 1) [NCBI Gene 207] {aka AKT, PKB, PKB-ALPHA, PRKBA, RAC, RAC-ALPHA}
- **Diseases:** diabetes (MESH:D003920), diabetic cachexia (MESH:D002100), DS (MESH:D055948), obesity (MESH:D009765)
- **Chemicals:** glucose (MESH:D005947)

## Full text

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## Figures

8 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12832245/full.md

## References

57 references — full list in the complete paper: https://tomesphere.com/paper/PMC12832245/full.md

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Source: https://tomesphere.com/paper/PMC12832245