# A narrative review on the correlation between diabetic foot and sarcopenia

**Authors:** Yunpeng Sui, Ya Ma, Kai Zhou, Rui Liang, Xiaolei Liu

PMC · DOI: 10.3389/fendo.2026.1711060 · Frontiers in Endocrinology · 2026-02-04

## TL;DR

This review explores how diabetic foot and sarcopenia are linked, worsen each other, and how managing both is crucial for better outcomes in diabetes patients.

## Contribution

The paper highlights the bidirectional relationship between diabetic foot and sarcopenia and emphasizes integrated management strategies.

## Key findings

- Sarcopenia increases the risk of diabetic foot by two to three times and leads to worse outcomes like delayed healing and amputation.
- Diabetic foot accelerates muscle atrophy through reduced mobility and disability.
- Integrated strategies like resistance training and optimized glycemic control are essential to break the cycle.

## Abstract

Diabetic foot (DF) and sarcopenia are common complications in individuals with diabetes and are linked through a bidirectional and mutually reinforcing relationship. From a pathophysiological perspective, insulin resistance disrupts skeletal muscle metabolism, while diabetic neuropathy and peripheral arterial disease compromise muscle function and mobility, increasing susceptibility to DF. Persistent low-grade inflammation further promotes muscle wasting and worsens glycemic dysregulation, establishing a self-perpetuating cycle. The presence of sarcopenia is associated with a two- to three fold increased risk of DF and is linked to poorer outcomes, including delayed wound healing and a higher likelihood of amputation. In turn, disability and reduced mobility caused by DF accelerate muscle disuse and atrophy. Integrated management strategies, encompassing resistance training, adequate protein intake, optimized glycemic control, and proactive foot care, are essential to interrupt this cycle. Although emerging pharmacological agents that enhance muscle anabolism show promise, further clinical validation is required. A multidisciplinary approach is necessary to curb the reciprocal progression of these conditions and to improve clinical outcomes in affected patients.

Infographic illustrating sarcopenia in diabetes, showing observed patient criteria, diagnostic screening, and clinical outcomes. Common risk factors listed are poor glycemic control, nutritional deficiencies, metabolic changes, and sedentary lifestyle. Potential mechanisms include chronic inflammation, oxidative stress, insulin resistance, hormonal imbalances, and neuropathy. Therapeutic strategies include lifestyle changes, omega-3 supplementation, pharmacological therapies, wound dressings, hyperbaric oxygen therapy, and advanced medical resources, visualized with relevant icons and diagrams.

## Linked entities

- **Diseases:** diabetes (MONDO:0005015)

## Full-text entities

- **Genes:** PIK3CB (phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit beta) [NCBI Gene 5291] {aka P110BETA, PI3K, PI3KBETA, PIK3C1}, GHSR (growth hormone secretagogue receptor) [NCBI Gene 2693] {aka GHDP, GHS-R1a, GHSR-1a}, CMPK1 (cytidine/uridine monophosphate kinase 1) [NCBI Gene 51727] {aka CK, CMK, CMPK, UMK, UMP-CMPK, UMPK}, GH1 (growth hormone 1) [NCBI Gene 2688] {aka GH, GH-N, GHB5, GHN, IGHD1A, IGHD1B}, FST (follistatin) [NCBI Gene 10468] {aka FS}, TTN (titin) [NCBI Gene 7273] {aka CMD1G, CMH9, CMPD4, CMYO5, CMYP5, EOMFC}, IL6 (interleukin 6) [NCBI Gene 3569] {aka BSF-2, BSF2, CDF, HGF, HSF, IFN-beta-2}, MSTN (myostatin) [NCBI Gene 2660] {aka GDF8, MSLHP}, PTH (parathyroid hormone) [NCBI Gene 5741] {aka FIH1, PTH1}, CASP3 (caspase 3) [NCBI Gene 836] {aka CPP32, CPP32B, SCA-1}, NFKB1 (nuclear factor kappa B subunit 1) [NCBI Gene 4790] {aka CVID12, EBP-1, KBF1, NF-kB, NF-kB1, NF-kappa-B1}, APLNR (apelin receptor) [NCBI Gene 187] {aka AGTRL1, APJ, APJR, HG11}, GGH (gamma-glutamyl hydrolase) [NCBI Gene 8836] {aka GATD10, GH}, TP53 (tumor protein p53) [NCBI Gene 7157] {aka BCC7, BMFS5, LFS1, P53, TRP53}, APLN (apelin) [NCBI Gene 8862] {aka APEL, XNPEP2}, TNF (tumor necrosis factor) [NCBI Gene 7124] {aka DIF, IMD127, TNF-alpha, TNFA, TNFSF2, TNLG1F}, AKT1 (AKT serine/threonine kinase 1) [NCBI Gene 207] {aka AKT, PKB, PKB-ALPHA, PRKBA, RAC, RAC-ALPHA}, GLP1R (glucagon like peptide 1 receptor) [NCBI Gene 2740] {aka GLP-1, GLP-1-R, GLP-1R}, IGF1 (insulin like growth factor 1) [NCBI Gene 3479] {aka IGF, IGF-I, IGFI, MGF}, AR (androgen receptor) [NCBI Gene 367] {aka AIS, AR8, DHTR, HPCX3, HUMARA, HYSP1}, INS (insulin) [NCBI Gene 3630] {aka IDDM, IDDM1, IDDM2, ILPR, IRDN, MODY10}
- **Diseases:** type 1 diabetes (MESH:D003922), systemic (MESH:D015619), dementia (MESH:D003704), coronary artery disease (MESH:D003324), DPN (MESH:D010523), muscle decline (MESH:D009135), Chronic pain (MESH:D059350), adiposity (MESH:D018205), breast cancer (MESH:D001943), nephropathy (MESH:D007674), muscle degeneration (MESH:D009410), PAD (MESH:D058729), T2DM (MESH:D003924), of lean muscle (MESH:D013851), neuropathic foot (MESH:D005534), Neuropathy (MESH:D009422), tissue damage (MESH:D017695), gangrene (MESH:D005734), foot ulceration (MESH:D016523), necrosis (MESH:D009336), Menopause (MESH:D008594), reduced mobility (MESH:D014086), impaired coordination (MESH:D001259), diabetic complications (MESH:D048909), Nutritional deficiencies (MESH:D044342), Microvascular disease (MESH:D017566), DF (MESH:D017719), amputation (MESH:C565682), neuro-osteoarthropathy (MESH:C536203), Ulcer (MESH:D014456), age (MESH:D019588), Insulin resistance (MESH:D007333), weight loss (MESH:D015431), foot deformities (MESH:D005530), infection (MESH:D007239), Diabetic neuropathy (MESH:D003929), cardiovascular disease (MESH:D002318), retinopathy (MESH:D058437), Vitamin D deficiency (MESH:D014808), wasting (MESH:D019282), hemorrhage (MESH:D006470), falls (MESH:C537863), fatty infiltration (MESH:D017254), hypoxia (MESH:D000860), Loss of muscle mass and strength (MESH:C536030), foot drop (MESH:D020427), glycemic dysregulation (MESH:D021081), metabolic disorder (MESH:D008659), on muscle (MESH:D019042), fractures (MESH:D050723), pain (MESH:D010146), hyperglycemia (MESH:D006943), injuries (MESH:D014947), Neuropathy disease (MESH:D004194), Diabetic sarcopenia (MESH:D055948), muscle atrophy (MESH:D009133), Chronic inflammation (MESH:D007249), muscle disuse (MESH:D020966), atrophy (MESH:D001284), Diabetes mellitus (MESH:D003920)
- **Chemicals:** lipids (MESH:D008055), reactive oxygen species (MESH:D017382), glucose (MESH:D005947), creatinine (MESH:D003404), 25(OH)D (-), phosphocreatine (MESH:D010725), fatty acids (MESH:D005227), amino acids (MESH:D000596), sulfonylureas (MESH:D013453), Testosterone (MESH:D013739), Metformin (MESH:D008687), Leucine (MESH:D007930), glutamic acid (MESH:D018698), O2 (MESH:D010100), chitosan (MESH:D048271), Pi (MESH:D010716), inorganic phosphate (MESH:D010710), Vitamin D (MESH:D014807), cortisol (MESH:D006854), lactic acid (MESH:D019344), omega-3 fatty acids (MESH:D015525)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

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## References

42 references — full list in the complete paper: https://tomesphere.com/paper/PMC12913165/full.md

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Source: https://tomesphere.com/paper/PMC12913165