ArticleDiabetes2011
FTO is increased in muscle during type 2 diabetes, and its overexpression in myotubes alters insulin signaling, enhances lipogenesis and ROS production, and induces mitochondrial dysfunction.
Article in Diabetes, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers, 6 of them syntheses that pooled it.
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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.
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Who cites it
58 citing papers in PubMed, 6 syntheses or guidelines pooled it, 124 citations in OpenAlex.
- Replication of FTO Gene associated with lean mass in a Meta-Analysis of Genome-Wide Association Studies.Scientific reports · 2020Pooled it
- Replication of FTO Gene associated with lean mass in a Meta-Analysis of Genome-Wide Association Studies.Scientific reports · 2020Pooled it
- Associations of genetic variants in/near body mass index-associated genes with type 2 diabetes: a systematic meta-analysis.Clinical endocrinology · 2014Pooled it
- Genetic variant in fat mass and obesity-associated gene associated with type 2 diabetes risk in Han Chinese.BMC genetics · 2013Pooled it
- Association of genetic variation in FTO with risk of obesity and type 2 diabetes with data from 96,551 East and South Asians.Diabetologia · 2012Pooled it
- Pooled it
- Dietary Fat Modifies the Effects of FTO Genotype on Changes in Insulin Sensitivity.The Journal of nutrition · 2015Trial
- Grape polyphenols prevent fructose-induced oxidative stress and insulin resistance in first-degree relatives of type 2 diabetic patients.Diabetes care · 2013Trial
- The role of mNaunyn-Schmiedeberg's archives of pharmacology · 2026Review
- m6A RNA modification and its emerging roles in diseases: recent advances and therapeutic implications.Journal of translational medicine · 2026Review
- The CommonNutrients · 2026Article
- Insulin signaling pathway related mNutrition & metabolism · 2026Article
- METTL16-mBMC biology · 2026Article
- NBiomolecules · 2026Review
- Regulation of m6A methylation in the immune microenvironment in the development of diabetes mellitus.Journal of translational medicine · 2025Review
- Insulin Resistance in Type 1 Diabetes: Pathophysiological, Clinical, and Therapeutic Relevance.Endocrine reviews · 2025Review
- Alteration of methylation pattern and gene expression of FTO, PPARγ and Slc2a4 on pre-diabetes-induced BALB/c mice.Molecular and cellular biochemistry · 2025Article
- Review
- Risk of Fat Mass- and Obesity-Associated Gene-Dependent Obesogenic Programming by Formula Feeding Compared to Breastfeeding.Nutrients · 2024Review
- N6-methyladenosine (m6A) modification in inflammation: a bibliometric analysis and literature review.PeerJ · 2024Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveA strong association between genetic variants and obesity was found for the fat mass and obesity-associated gene (FTO). However, few details are known concerning the expression and function of FTO in skeletal muscle of patients with metabolic diseases. RESEARCH DESIGN AND
methodsWe investigated basal FTO expression in skeletal muscle from obese nondiabetic subjects and type 1 and type 2 diabetic patients, compared with age-matched control subjects, and its regulation in vivo by insulin, glucose, or rosiglitazone. The function of FTO was further studied in myotubes by overexpression experiments.
resultsWe found a significant increase of FTO mRNA and protein levels in muscle from type 2 diabetic patients, whereas its expression was unchanged in obese or type 1 diabetic patients. Moreover, insulin or glucose infusion during specific clamps did not regulate FTO expression in skeletal muscle from control or type 2 diabetic patients. Interestingly, rosiglitazone treatment improved insulin sensitivity and reduced FTO expression in muscle from type 2 diabetic patients. In myotubes, adenoviral FTO overexpression increased basal protein kinase B phosphorylation, enhanced lipogenesis and oxidative stress, and reduced mitochondrial oxidative function, a cluster of metabolic defects associated with type 2 diabetes.
conclusionsThis study demonstrates increased FTO expression in skeletal muscle from type 2 diabetic patients, which can be normalized by thiazolidinedione treatment. Furthermore, in vitro data support a potential implication of FTO in oxidative metabolism, lipogenesis and oxidative stress in muscle, suggesting that it could be involved in the muscle defects that characterize type 2 diabetes.
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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 Socratic graph.