ArticleDiabetologia2009
Potential role of TBC1D4 in enhanced post-exercise insulin action in human skeletal muscle.
Article in Diabetologia, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers.
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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.
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Who cites it
65 citing papers in PubMed, 119 citations in OpenAlex.
- The effect of exercise-intensity on skeletal muscle stress kinase and insulin protein signaling.PloS one · 2017Trial
- Trial
- Insulin resistance after a 72-h fast is associated with impaired AS160 phosphorylation and accumulation of lipid and glycogen in human skeletal muscle.American journal of physiology. Endocrinology and metabolism · 2012Trial
- Exercise increases TBC1D1 phosphorylation in human skeletal muscle.American journal of physiology. Endocrinology and metabolism · 2011Trial
- Intramuscular neutrophil-derived immunometabolic niches locally boost insulin-responsive GLUT4 translocation after muscle contraction.The Journal of physiology · 2026Article
- Insulin- and exercise-induced phosphoproteomics of human skeletal muscle identify REPS1 as a regulator of muscle glucose uptake.Cell reports. Medicine · 2025Article
- Skeletal muscle from TBC1D4 p.Arg684Ter variant carriers is severely insulin resistant but exhibits normal metabolic responses during exercise.Nature metabolism · 2024Article
- Phosphorylation of AS160-serine 704 is not essential for exercise-increase in insulin-stimulated glucose uptake by skeletal muscles from female or male rats.American journal of physiology. Endocrinology and metabolism · 2024Article
- Effects of swimming training in hot and cold temperatures combined with cinnamon supplementation on HbA1C levels, TBC1D1, and TBC1D4 in diabetic rats.Nutrition & diabetes · 2024Article
- AS160 expression, but not AS160 Serine-588, Threonine-642, and Serine-704 phosphorylation, is essential for elevated insulin-stimulated glucose uptake by skeletal muscle from female rats after acute exercise.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2023Article
- Improving Mitochondrial Function in Skeletal Muscle Contributes to the Amelioration of Insulin Resistance by Nicotinamide Riboside.International journal of molecular sciences · 2023Article
- Microtubule-mediated GLUT4 trafficking is disrupted in insulin-resistant skeletal muscle.eLife · 2023Article
- Skeletal muscle mechanisms contributing to improved glycemic control following intense interval exercise and training.Sports medicine and health science · 2023Review
- Electrical stimulated GLUT4 signalling attenuates critical illness-associated muscle wasting.Journal of cachexia, sarcopenia and muscle · 2022Article
- Post-translational Modifications: The Signals at the Intersection of Exercise, Glucose Uptake, and Insulin Sensitivity.Endocrine reviews · 2022Review
- Illumination of the Endogenous Insulin-Regulated TBC1D4 Interactome in Human Skeletal Muscle.Diabetes · 2022Article
- Impact of pre-exercise feeding status on metabolic adaptations to endurance-type exercise training.The Journal of physiology · 2022Article
- Article
- Exercise effects on γ3-AMPK activity, Akt substrate of 160 kDa phosphorylation, and glucose uptake in muscle of normal and insulin-resistant female rats.Journal of applied physiology (Bethesda, Md. : 1985) · 2022Article
- No evidence for change in expression ofAdipocyte · 2021Article
5 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
13 authors at 3 institutions in 3 countries.
Funding
Abstract
aims/hypothesisTBC1 domain family, member 4 (TBC1D4; also known as AS160) is a cellular signalling intermediate to glucose transport regulated by insulin-dependent and -independent mechanisms. Skeletal muscle insulin sensitivity is increased after acute exercise by an unknown mechanism that does not involve modulation at proximal insulin signalling intermediates. We hypothesised that signalling through TBC1D4 is involved in this effect of exercise as it is a common signalling element for insulin and exercise.
methodsInsulin-regulated glucose metabolism was evaluated in 12 healthy moderately trained young men 4 h after one-legged exercise at basal and during a euglycaemic-hyperinsulinaemic clamp. Vastus lateralis biopsies were taken before and immediately after the clamp.
resultsInsulin stimulation increased glucose uptake in both legs, with greater effects (approximately 80%, p < 0.01) in the previously exercised leg. TBC1D4 phosphorylation, assessed using the phospho-AKT (protein kinase B)substrate antibody and phospho- and site-specific antibodies targeting six phosphorylation sites on TBC1D4, increased at similar degrees to insulin stimulation in the previously exercised and rested legs (p < 0.01). However, TBC1D4 phosphorylation on Ser-318, Ser-341, Ser-588 and Ser-751 was higher in the previously exercised leg, both in the absence and in the presence of insulin (p < 0.01; Ser-588, p = 0.09; observed power = 0.39). 14-3-3 binding capacity for TBC1D4 increased equally (p < 0.01) in both legs during insulin stimulation. CONCLUSION/
interpretationWe provide evidence for site-specific phosphorylation of TBC1D4 in human skeletal muscle in response to physiological hyperinsulinaemia. The data support the idea that TBC1D4 is a nexus for insulin- and exercise-responsive signals that may mediate increased insulin action after exercise.
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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.