Impaired insulin-induced site-specific phosphorylation of TBC1 domain family, member 4 (TBC1D4) in skeletal muscle of type 2 diabetes patients is restored by endurance exercise-training.
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Aims/hypothesis Insulin-mediated glucose disposal rates (R(d)) are reduced in type 2 diabetic patients, a process in which intrinsic signalling defects are thought to be involved. Phosphorylation of TBC1 domain family, member 4 (TBC1D4) is at present the most distal insulin receptor signalling event linked to glucose transport. In this study, we examined insulin action on site-specific phosphorylation of TBC1D4 and the effect of exercise training on insulin action and signalling to TBC1D4 in skeletal muscle from type 2 diabetic patients.Methods During a 3 h euglycaemic-hyperinsulinaemic (80 mU min⁻¹ m⁻²) clamp, we obtained M. vastus lateralis biopsies from 13 obese type 2 diabetic and 13 obese, non-diabetic control individuals before and after 10 weeks of endurance exercise-training.Results Before training, reductions in insulin-stimulated R (d), together with impaired insulin-stimulated glycogen synthase fractional velocity, Akt Thr³⁰⁸ phosphorylation and phosphorylation of TBC1D4 at Ser³¹⁸, Ser⁵⁸⁸ and Ser⁷⁵¹ were observed in skeletal muscle from diabetic patients. Interestingly, exercise-training normalised insulin-induced TBC1D4 phosphorylation in diabetic patients. This happened independently of increased TBC1D4 protein content, but exercise-training did not normalise Akt phosphorylation in diabetic patients. In both groups, training-induced improvements in insulin-stimulated R(d) (~20%) were associated with increased muscle protein content of Akt, TBC1D4, α2-AMP-activated kinase (AMPK), glycogen synthase, hexokinase II and GLUT4 (20-75%).Conclusions/interpretation Impaired insulin-induced site-specific TBC1D4 phosphorylation may contribute to skeletal muscle insulin resistance in type 2 diabetes. The mechanisms by which exercise-training improves insulin sensitivity in type 2 diabetes may involve augmented signalling of TBC1D4 and increased skeletal muscle content of key insulin signalling and effector proteins, e.g., Akt, TBC1D4, AMPK, glycogen synthase, GLUT4 and hexokinase II.
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Obese people have reduced cardiorespiratory fitness and their VO2max may be reduced to 20 mL/(kg·min) or less.
“Obese people have reduced cardiorespiratory fitness and their VO2max may be reduced to 20 mL/(kg⋅min–1) or less (Christ-Roberts et al., 2004; Vind et al., 2011); however, this is not necessarily solely due to low cardiorespiratory fitness but may also result from an increase in body weight.”
From Effect of Exercise Training on Fat Loss—Energetic Perspectives and the Role of Improved Adipose Tissue Function and Body Fat Distribution (2021) · cites this paper as Vind et al., 2011
The Participants section identifies the study groups as obese, and Table 1 reports their pre-training VO₂peak values. Training increased VO₂peak (Metabolic characteristics), but the reported pre-training group means were 27.8 and 26.7 mL/(kg·min), not 20 or less. The paper also does not compare obese participants with non-obese people to establish that obesity is associated with reduced fitness. (LLM, conf=0.82)
Experimental — accuracy not yet measuredImproved insulin sensitivity in skeletal muscle in response to exercise training can be in part explained by upregulation of proteins involved in glucose metabolism and the insulin signaling pathway, including GLUT4, hexokinase II, AKT2, glycogen synthase, AMPK, and mitochondrial proteins.
“The improved insulin sensitivity in skeletal muscle in response to exercise training can be in part explained by the upregulation of proteins involved in glucose metabolism and the insulin signaling pathway, including the insulin-sensitive glucose transporter 4 (GLUT4), hexokinase II, AKT2, glycogen synthase, and AMP-activated protein kinase (AMPK), as well as mitochondrial proteins”
From Effect of Exercise Training on Fat Loss—Energetic Perspectives and the Role of Improved Adipose Tissue Function and Body Fat Distribution (2021) · cites this paper as Vind et al., 2011
The Discussion (page unavailable) links improved insulin-mediated glucose disposal after endurance training to increased muscle content of Akt2, GLUT4, hexokinase II and AMPK; it also reports increased glycogen synthase protein. Our copy does not report an increase in mitochondrial proteins as part of this explanation. Its mitochondrial references concern other studies, not the claimed protein upregulation. (LLM, conf=0.88)
Experimental — accuracy not yet measuredTBC1D4 phosphorylation (S318, 341, 588, 642, and 751) is reduced in skeletal muscle from obese type 2 diabetics under basal conditions, but can be restored to comparable levels of nondiabetics by 10 weeks of endurance training.
“TBC1D4 phosphorylation (S318, 341, 588, 642, and 751) is reduced in skeletal muscle from obese type 2 diabetics under basal conditions, but can be restored to comparable levels of nondiabetics by 10 weeks of endurance training [81].”
From AMPK and Exercise: Glucose Uptake and Insulin Sensitivity (2013) · cites this paper as [81]
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Self-citation
- Authors
- Vind, B. F., Pehmøller, C., Treebak, J. T., Birk, J. B., Hey-Mogensen, M., Beck-Nielsen, H., Zierath, J. R., Wojtaszewski, J. F. P., & Højlund, K.
- Affiliations
- Odense University Hospital (DK)
- University of Copenhagen (DK)
- Karolinska Institutet (SE)
- Corresponding author
- Højlund, K.
- Venue
- Diabetologia
- Published
- 2010-10-13
- Volume
- 54
- Issue
- 1
- Pages
- 157-167
- ISSN
- 0012-186X (ISSN-L)
- 1432-0428
- OpenAlex
- W2010367429
- Cited by
- 129
- References
- 49
- Citations by year
- 2026: 3 · 2025: 7 · 2024: 8 · 2023: 8 · 2022: 10 · 2021: 10 · 2020: 9 · 2019: 5 · 2018: 5 · 2017: 4 · 2016: 11 · 2015: 11 · 2014: 8 · 2013: 11 · 2012: 11
- FWCI
- 3.91
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Diabetologia (publishedVersion)
- PubMed (publishedVersion)
- University of Southern Denmark Research Portal (University of Southern Denmark) (publishedVersion)
- Research at the University of Copenhagen (University of Copenhagen) (submittedVersion)
- Funders
- Sundhed og Sygdom, Det Frie Forskningsråd (LSHM-CT-2004-005272)
- University of Dundee
- European Commission (LSHMCT-2004-005272)
- Ministério da Ciência, Tecnologia e Inovação
- Lundbeckfonden
- Novo Nordisk
- Syddansk Universitet
- Copenhagen Graduate School for Nanoscience and Nanotechnology
- H. Lundbeck A/S
- Diabetesforeningen
- Medical Research Council
- Klinisk Institut, Syddansk Universitet
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes, Cardiovascular Risks, and Lipoproteins
- Health Sciences › Medicine › Physiology › Adipose Tissue and Metabolism
- Keywords
- TBC1D4, insulin resistance, type 2 diabetes, skeletal muscle, endurance training, insulin signaling, site-specific phosphorylation, glucose transport, glucose disposal, Akt, AMPK, glycogen synthase, GLUT4, hexokinase 2, insulin receptor substrate
- MeSH terms
- Blood Glucose, C-Peptide, Diabetes Mellitus, Type 2, Electrophoresis, Polyacrylamide Gel, Glycogen Synthase, Glycated Hemoglobin, Humans, Insulin, Male, Middle Aged, Phosphorylation, Blotting, Western, Glucose Clamp Technique, Exercise, Muscle, Skeletal, GTPase-Activating Proteins
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