Skip to content
DraconiticResearch
Search Sources API
203,203 studies31 sourcesUpdated 1 h ago
Peer-reviewedCC BY-NC-NDProteomics. Clinical applications

Diabetic Polyneuropathy Patients Exhibit an Altered Skeletal Muscle Proteome Phenotype.

  • Frederik Forsberg Thybo1,2
  • Karolina Snopek Khan3
  • Jesper Emil Jakobsgaard4
  • Henning Andersen3
  • Kristian Vissing5
  • Johan Palmfeldt6
6 affiliations
  1. 1Department of Biomedicine, Aarhus University, Aarhus, Denmark.
  2. 2Steno Diabetes Center Aarhus, Aarhus University Hospital, Aarhus, Denmark.
  3. 3Department of Neurology, Aarhus University Hospital, Aarhus, Denmark.
  4. 4NMD Pharma A/S, Aarhus, Denmark.
  5. 5Exercise Biology, Department of Public Health, Aarhus University, Aarhus, Denmark.
  6. 6Research Unit for Molecular Medicine, Department of Clinical Medicine, Aarhus University, Aarhus, Denmark.
Read full textPDFDOICite

Abstract

Purpose

Diabetic polyneuropathy (DPN) is a debilitating complication of diabetes that affects motor nerves and may impair skeletal muscle health. This study investigated skeletal muscle proteomic alterations associated with DPN compared with type 2 diabetes without DPN (T2D) and healthy controls (CON).Experimental design

An exploratory proteomic profiling was performed in 15 participants divided into three groups based on clinical and neurophysiological diagnosis (DPN, n = 5; T2D, n = 5; CON, n = 5). Biopsies from the gastrocnemius lateralis muscle were analyzed using LC-MS/MS-based proteomics and pathway enrichment analyses.Results

A total of 265 and 444 proteins were differentially expressed in DPN compared with T2D and CON, respectively (q < 0.05). Enrichment analyses revealed marked alterations in mitochondrial-related pathways, including cellular respiration, distinguishing DPN from both comparison groups. Differences between T2D and CON were present but less pronounced. DPN was characterized by downregulation of glycogen-regulating proteins (phosphorylase kinase G1 and A1) and upregulation of ferritin light chain (FTL), alpha actin 2, and myosin-binding protein H.Conclusions and clinical relevance

DPN is associated with a distinct and progressive skeletal muscle proteomic phenotype, supporting mitochondrial dysfunction as a key feature and providing a basis for future mechanistic and therapeutic studies.

Related

  1. Combined Teriparatide and Exercise Effects on Diabetic Skeletal Muscle Ultrastructure
    YASUHITO ASAKA, YUJI KASUKAWA, KOJI NOZAKA +10
    In VivoPeer-reviewedCC BY-NC-ND 4.0Full textMolecular biology & gene regulationPMC
  2. Clinical and MEFV variant characteristics of pediatric patients with an FMF-compatible phenotype and PFAPA-compatible features in a Palestinian referral cohort: a retrospective study
    Ahmad K. Abuhammad, Ahmed I. S. Alnatsha, Ibrahim N. Bali +4
    Scientific ReportsPeer-reviewedCC BY-NC-ND 4.0Full textMolecular biology & gene regulationCrossref
  3. Increased Plasma Endogenous Ethanol Correlates with and Discriminates Against Microvascular Complications in Type-2 Diabetic Traditionally Alcohol-Abstinent Saudi Patients: A Biomarker Cross-Sectional Analysis
    Basil Mohammed Alomair, Alaa Abdelhamid Mohamed, Abrar Zayed Ashalan +7
    MetabolitesPeer-reviewedCC BYFull textProteomics & metabolomicsEurope PMC
  4. Microbial and inflammatory features linked to distal sensory polyneuropathy in people with HIV
    Lora Khatib, Mohammadsobhan S. Andalibi, Christophe Vanpouille +14
    Brain, behavior, and immunityPeer-reviewedLicence not statedFull textMolecular biology & gene regulationPMC
  5. Salivary ¹H NMR metabolic profiling of diabetic patients with and without periodontitis: an exploratory pilot study.
    Samaneh Vaziri-Amjad, Bahar Zalei, Nazli Rabienejad +2
    Genomics & informaticsPeer-reviewedCC BYFull textMolecular biology & gene regulationGenetics & genomicsEurope PMC

Cite

BibTeXRIS
BibTeX
@article{thybo2026diabetic,
  title = {{Diabetic Polyneuropathy Patients Exhibit an Altered Skeletal Muscle Proteome Phenotype.}},
  author = {Frederik Forsberg Thybo and Karolina Snopek Khan and Jesper Emil Jakobsgaard and Henning Andersen and Kristian Vissing and Johan Palmfeldt},
  journal = {Proteomics. Clinical applications},
  year = {2026},
  month = oct,
  doi = {10.1002/prca.70060},
  url = {https://europepmc.org/article/MED/42894376},
  note = {CC BY-NC-ND},
}
RIS
TY  - JOUR
TI  - Diabetic Polyneuropathy Patients Exhibit an Altered Skeletal Muscle Proteome Phenotype.
AU  - Frederik Forsberg Thybo
AU  - Karolina Snopek Khan
AU  - Jesper Emil Jakobsgaard
AU  - Henning Andersen
AU  - Kristian Vissing
AU  - Johan Palmfeldt
PY  - 2026
DA  - 2026/10/30
JO  - Proteomics. Clinical applications
DO  - 10.1002/prca.70060
UR  - https://europepmc.org/article/MED/42894376
AB  - Purpose  Diabetic polyneuropathy (DPN) is a debilitating complication of diabetes that affects motor nerves and may impair skeletal muscle health. This study investigated skeletal muscle proteomic alterations associated with DPN compared with type 2 diabetes without DPN (T2D) and healthy controls (CON).Experimental design  An exploratory proteomic profiling was performed in 15 participants divided into three groups based on clinical and neurophysiological diagnosis (DPN, n = 5; T2D, n = 5; CON, n = 5). Biopsies from the gastrocnemius lateralis muscle were analyzed using LC-MS/MS-based proteomics and pathway enrichment analyses.Results  A total of 265 and 444 proteins were differentially expressed in DPN compared with T2D and CON, respectively (q < 0.05). Enrichment analyses revealed marked alterations in mitochondrial-related pathways, including cellular respiration, distinguishing DPN from both comparison groups. Differences between T2D and CON were present but less pronounced. DPN was characterized by downregulation of glycogen-regulating proteins (phosphorylase kinase G1 and A1) and upregulation of ferritin light chain (FTL), alpha actin 2, and myosin-binding protein H.Conclusions and clinical relevance  DPN is associated with a distinct and progressive skeletal muscle proteomic phenotype, supporting mitochondrial dysfunction as a key feature and providing a basis for future mechanistic and therapeutic studies.
SN  - 1862-8346
SN  - 1862-8354
ER  -