ArticleDiabetes2010
TBC1D1 regulates insulin- and contraction-induced glucose transport in mouse skeletal muscle.
Article in Diabetes, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 papers.
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Who cites it
79 citing papers in PubMed, 145 citations in OpenAlex.
- 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
- WNK1 Phosphorylation Sites in TBC1D1 and TBC1D4 Modulate Cell-Surface Abundance of GLUT1.Cells · 2026Article
- Insulin Signaling in Alzheimer's Disease: Association with Brain Insulin Resistance.International journal of molecular sciences · 2026Review
- Unilateral electrical stimulation of mice induces transcriptional response in stimulated leg with limited effect on non-stimulated contralateral leg.Experimental physiology · 2025Article
- Single-nucleus transcriptomic profiling of the diaphragm during mechanical ventilation.Scientific reports · 2024Article
- Skeletal muscle from TBC1D4 p.Arg684Ter variant carriers is severely insulin resistant but exhibits normal metabolic responses during exercise.Nature 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
- Novel prognostic biomarker TBC1D1 is associated with immunotherapy resistance in gliomas.Frontiers in immunology · 2024Article
- From Acid Alpha-Glucosidase Deficiency to Autophagy: Understanding the Bases of POMPE Disease.International journal of molecular sciences · 2023Review
- Phosphorylation of AMPKα at Ser485/491 Is Dependent on Muscle Contraction and Not Muscle-Specific IGF-I Overexpression.International journal of molecular sciences · 2023Article
- Liver and muscle circadian clocks cooperate to support glucose tolerance in mice.Cell reports · 2023Article
- Revving the engine: PKB/AKT as a key regulator of cellular glucose metabolism.Frontiers in physiology · 2023Review
- 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
- Article
- Chromatin state distribution of residue-specific histone acetylation in early myoblast differentiation.Journal of big data · 2022Article
- Article
- From leptin to lasers: the past and present of mouse models of obesity.Expert opinion on drug discovery · 2021Article
- Insulin Resistance Is Not Sustained Following Denervation in Glycolytic Skeletal Muscle.International journal of molecular sciences · 2021Article
19 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
objectiveTBC1D1 is a member of the TBC1 Rab-GTPase family of proteins and is highly expressed in skeletal muscle. Insulin and contraction increase TBC1D1 phosphorylation on phospho-Akt substrate motifs (PASs), but the function of TBC1D1 in muscle is not known. Genetic linkage analyses show a TBC1D1 R125W missense variant confers risk for severe obesity in humans. The objective of this study was to determine whether TBC1D1 regulates glucose transport in skeletal muscle. RESEARCH DESIGN AND
methodsIn vivo gene injection and electroporation were used to overexpress wild-type and several mutant TBC1D1 proteins in mouse tibialis anterior muscles, and glucose transport was measured in vivo.
resultsExpression of the obesity-associated R125W mutant significantly decreased insulin-stimulated glucose transport in the absence of changes in TBC1D1 PAS phosphorylation. Simultaneous expression of an inactive Rab-GTPase (GAP) domain of TBC1D1 in the R125W mutant reversed this decrease in glucose transport caused by the R125W mutant. Surprisingly, expression of TBC1D1 mutated to Ala on four conserved Akt and/or AMP-activated protein kinase predicted phosphorylation sites (4P) had no effect on insulin-stimulated glucose transport. In contrast, expression of the TBC1D1 4P mutant decreased contraction-stimulated glucose transport, an effect prevented by concomitant disruption of TBC1D1 Rab-GAP activity. There was no effect of the R125W mutation on contraction-stimulated glucose transport.
conclusionsTBC1D1 regulates both insulin- and contraction-stimulated glucose transport, and this occurs via distinct mechanisms. The R125W mutation of TBC1D1 impairs skeletal muscle glucose transport, which could be a mechanism for the obesity associated with this mutation.
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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.