ArticleDiabetes2013
Deletion of skeletal muscle SOCS3 prevents insulin resistance in obesity.
Article in Diabetes, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 84 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
84 citing papers in PubMed, 144 citations in OpenAlex.
- Review
- The multifaceted role of SOCS3 in colorectal cancer: molecular mechanisms and clinical implications.Molecular biology reports · 2026Review
- GV-971 remodels the gut microbiota-bile acid-FXR axis to ameliorate obesity and metabolic dysfunction.Cell discovery · 2026Article
- Skeletal muscle expression of the genes associated with glycoprotein 130 signaling in relation to obesity and insulin sensitivity.Journal of endocrinological investigation · 2026Article
- Integrated miRNAs, Transcriptome, and Metabolome Uncover Underlying Mechanisms for Breast Muscle Metabolic Regulation in Liancheng White and Cherry Valley Ducks.Animals : an open access journal from MDPI · 2026Article
- The miR-30c-5p/SOCS3 axis is a potential driver of inflammation and metabolic imbalance in Duchenne muscular dystrophy.Frontiers in cell and developmental biology · 2026Article
- Spatial-Bioenergetic-Immune Axis in Type 2 Diabetes Mellitus-Associated Sarcopenia: A Review from Pathogenesis to Targeted Reconstruction.Journal of inflammation research · 2026Review
- Association between metabolic syndrome, diabetes mellitus, inflammation and cognitive dysfunctions in schizophrenia: a cross-sectional analysis.Schizophrenia (Heidelberg, Germany) · 2025Article
- Thyrotropin exacerbates insulin resistance by triggering macrophage inflammation in subclinical hypothyroidism.Experimental & molecular medicine · 2025Article
- Frozen Shoulder as a Metabolic and Immune Disorder: Potential Roles of Leptin Resistance, JAK-STAT Dysregulation, and Fibrosis.Journal of clinical medicine · 2025Review
- Pharmacological advances in multi-targeted strategies for type 2 diabetes mellitus: a systematic perspective based on traditional Chinese medicine.Frontiers in pharmacology · 2025Review
- Endothelial c-Myc knockout disrupts metabolic homeostasis and triggers the development of obesity.Frontiers in cell and developmental biology · 2024Article
- Differential Roles of Interleukin-6 in Severe Acute Respiratory Syndrome-Coronavirus-2 Infection and Cardiometabolic Diseases.Cardiology discovery · 2023Article
- Higher pNRF2, SOCS3, IRF3, and RIG1 Tissue Protein Expression in NASH Patients versus NAFL Patients: pNRF2 Expression Is Concomitantly Associated with Elevated Fasting Glucose Levels.Journal of personalized medicine · 2023Article
- Molecular Mechanisms for the Vicious Cycle between Insulin Resistance and the Inflammatory Response in Obesity.International journal of molecular sciences · 2023Review
- Article
- Paternal phthalate exposure-elicited offspring metabolic disorders are associated with altered sperm small RNAs in mice.Environment international · 2023Article
- Serotonin transporter-deficient mice display enhanced adipose tissue inflammation after chronic high-fat diet feeding.Frontiers in immunology · 2023Article
- Retinoic acid and RARγ maintain satellite cell quiescence through regulation of translation initiation.Cell death & disease · 2022Article
- Article
24 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
15 authors at 5 institutions in 4 countries.
Funding
Abstract
Obesity is associated with chronic low-grade inflammation that contributes to defects in energy metabolism and insulin resistance. Suppressor of cytokine signaling (SOCS)-3 expression is increased in skeletal muscle of obese humans. SOCS3 inhibits leptin signaling in the hypothalamus and insulin signal transduction in adipose tissue and the liver. Skeletal muscle is an important tissue for controlling energy expenditure and whole-body insulin sensitivity; however, the physiological importance of SOCS3 in this tissue has not been examined. Therefore, we generated mice that had SOCS3 specifically deleted in skeletal muscle (SOCS MKO). The SOCS3 MKO mice had normal muscle development, body mass, adiposity, appetite, and energy expenditure compared with wild-type (WT) littermates. Despite similar degrees of obesity when fed a high-fat diet, SOCS3 MKO mice were protected against the development of hyperinsulinemia and insulin resistance because of enhanced skeletal muscle insulin receptor substrate 1 (IRS1) and Akt phosphorylation that resulted in increased skeletal muscle glucose uptake. These data indicate that skeletal muscle SOCS3 does not play a critical role in regulating muscle development or energy expenditure, but it is an important contributing factor for inhibiting insulin sensitivity in obesity. Therapies aimed at inhibiting SOCS3 in skeletal muscle may be effective in reversing obesity-related glucose intolerance and insulin resistance.
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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.