ArticlePloS one2017
Receptor and post-receptor abnormalities contribute to insulin resistance in myotonic dystrophy type 1 and type 2 skeletal muscle.
Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 2 of them syntheses that pooled it.
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Who cites it
29 citing papers in PubMed, 2 syntheses or guidelines pooled it, 38 citations in OpenAlex.
- Protein Phosphorylation Alterations in Myotonic Dystrophy Type 1: A Systematic Review.International journal of molecular sciences · 2023Pooled it
- Dyslipidemia in Muscular Dystrophy: A Systematic Review and Meta-Analysis.Journal of neuromuscular diseases · 2023Pooled it
- Skeletal muscle disorders as risk factors for type 2 diabetes.Molecular and cellular endocrinology · 2025Review
- Proteomic Profiling Towards a Better Understanding of Genetic Based Muscular Diseases: The Current Picture and a Look to the Future.Biomolecules · 2025Review
- Therapeutic advances in type 1 myotonic dystrophy complicated with type 2 diabetes mellitus.Frontiers in neurology · 2025Review
- Recent Progress and Challenges in the Development of Antisense Therapies for Myotonic Dystrophy Type 1.International journal of molecular sciences · 2022Review
- Article
- Molecular Therapies for Myotonic Dystrophy Type 1: From Small Drugs to Gene Editing.International journal of molecular sciences · 2022Review
- Gender effect on onset, prevalence and surgical treatment of cataract in patients with Myotonic Dystrophy type 1.Acta myologica : myopathies and cardiomyopathies : official journal of the Mediterranean Society of Myology · 2022Article
- Current Studies on Molecular Mechanisms of Insulin Resistance.Journal of diabetes research · 2022Review
- Fourier-Transform Infrared Spectroscopy as a Discriminatory Tool for Myotonic Dystrophy Type 1 Metabolism: A Pilot Study.International journal of environmental research and public health · 2021Article
- Metabolic Alterations in Myotonic Dystrophy Type 1 and Their Correlation with Lipin.International journal of environmental research and public health · 2021Review
- Neuromuscular Development and Disease: Learning FromFrontiers in cell and developmental biology · 2021Review
- Impact of Adenosine Analogue, Adenosine-5'-N-Ethyluronamide (NECA), on Insulin Signaling in Skeletal Muscle Cells.BioMed research international · 2021Article
- CTG-Repeat Detection in Primary Human Myoblasts of Myotonic Dystrophy Type 1.Frontiers in neuroscience · 2021Article
- Myotonic dystrophy type 2: the 2020 update.Acta myologica : myopathies and cardiomyopathies : official journal of the Mediterranean Society of Myology · 2020Review
- A CRISPR-Cas13a Based Strategy That Tracks and Degrades Toxic RNA in Myotonic Dystrophy Type 1.Frontiers in genetics · 2020Article
- High Prevalence and Gender-Related Differences of Gastrointestinal Manifestations in a Cohort of DM1 Patients: A Perspective, Cross-Sectional Study.Frontiers in neurology · 2020Article
- MicroRNA-Based Therapeutic Perspectives in Myotonic Dystrophy.International journal of molecular sciences · 2019Review
- Short Tandem Repeat Expansions and RNA-Mediated Pathogenesis in Myotonic Dystrophy.International journal of molecular sciences · 2019Review
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Myotonic dystrophy type 1 (DM1) and type 2 (DM2) are autosomal dominant multisystemic disorders caused by expansion of microsatellite repeats. In both forms, the mutant transcripts accumulate in nuclear foci altering the function of alternative splicing regulators which are necessary for the physiological mRNA processing. Missplicing of insulin receptor (IR) gene (INSR) has been associated with insulin resistance, however, it cannot be excluded that post-receptor signalling abnormalities could also contribute to this feature in DM. We have analysed the insulin pathway in skeletal muscle biopsies and in myotube cultures from DM patients to assess whether downstream metabolism might be dysregulated and to better characterize the mechanism inducing insulin resistance. DM skeletal muscle exhibits alterations of basal phosphorylation levels of Akt/PKB, p70S6K, GSK3β and ERK1/2, suggesting that these changes might be accompanied by a lack of further insulin stimulation. Alterations of insulin pathway have been confirmed on control and DM myotubes expressing fetal INSR isoform (INSR-A). The results indicate that insulin action appears to be lower in DM than in control myotubes in terms of protein activation and glucose uptake. Our data indicate that post-receptor signalling abnormalities might contribute to DM insulin resistance regardless the alteration of INSR splicing.
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Registered trials
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.