Insulin action on glucose transport and plasma membrane GLUT4 content in skeletal muscle from patients with NIDDM
Abstract
We investigated the response of the glucose transport system to insulin, in the presence of ambient glucose concentrations, in isolated skeletal muscle from seven patients with non-insulin-dependent diabetes mellitus (NIDDM) (age, 55 +/- 3 years, BMI 27.4 +/- 1.8 kg/m2) and seven healthy control subjects (age, 54 +/- 3 years, BMI 26.5 +/- 1.1 kg/m2). Insulin-mediated whole body glucose utilization was similar between the groups when studied in the presence of ambient glucose concentrations (approximately 10 mmol/l for the NIDDM patients and 5 mmol/l for the control subjects). Samples were obtained from the vastus lateralis muscle, by means of an open muscle biopsy procedure, before and after a 40-min insulin infusion. An increase in serum insulin levels from 54 +/- 12 to 588 +/- 42 pmol/l, induced a 1.6 +/- 0.2-fold increase in glucose transporter protein (GLUT4) in skeletal muscle plasma membranes obtained from the control subjects (p < 0.05), whereas no significant increase was noted in plasma membrane fractions prepared from NIDDM muscles, despite a similar increase in serum insulin levels. At concentrations of 5 mmol/l 3-O-methylglucose in vitro, insulin (600 pmol/l) induced a 2.2-fold (p < 0.05) increase in glucose transport in NIDDM muscles and a 3.4-fold (p < 0.001) increase in the control muscles. Insulin-stimulated 3-O-methylglucose transport was positively correlated with whole body insulin-mediated glucose uptake in all participants (r = 0.78, p < 0.001) and negatively correlated with fasting plasma glucose levels in the NIDDM subjects (r = 0.93, p < 0.001). Muscle fibre type distribution and capillarization were similar between the groups. Our results suggest that insulin-stimulated glucose transport in skeletal muscle from patients with NIDDM is down-regulated in the presence of hyperglycaemia. The increased flux of glucose as a consequence of hyperglycaemia may result in resistance to any further insulin-induced gain of GLUT4 at the level of the plasma membrane.
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In insulin-resistant individuals with T2DM, glucose transport activity is severely impaired.
“In insulin resistant individuals with T2DM, glucose transport activity is severely impaired [156, 181, 182, 187–189].”
From Pathogenesis of insulin resistance in skeletal muscle (2010) · cites this paper as [188]
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- Authors
- Zierath, J. R., He, L., Gumà, A., Wahlström, E. O., Klip, A., & Wallberg-Henriksson, H.
- Affiliations
- Karolinska Institutet (SE)
- Great Ormond Street Hospital (GB)
- Venue
- Diabetologia
- Published
- 1996-10
- Volume
- 39
- Issue
- 10
- Pages
- 1180-9
- ISSN
- 0012-186X (ISSN-L)
- 1432-0428
- OpenAlex
- W2068205637
- Cited by
- 402
- References
- 50
- Citations by year
- 2026: 1 · 2025: 12 · 2024: 8 · 2023: 14 · 2022: 6 · 2021: 6 · 2020: 16 · 2019: 14 · 2018: 14 · 2017: 14 · 2016: 11 · 2015: 16 · 2014: 10 · 2013: 13 · 2012: 21
- FWCI
- 4.04
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Diabetologia (publishedVersion)
- PubMed (publishedVersion)
- 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
- insulin action, glucose transport, GLUT4, skeletal muscle, type 2 diabetes, hyperglycemia, insulin resistance, plasma membrane, 3-O-methylglucose, vastus lateralis, muscle biopsy
- MeSH terms
- Analysis of Variance, Biological Transport, Biopsy, C-Peptide, Cell Membrane, Diabetes Mellitus, Type 2, Glucose, Humans, Hyperinsulinism, Insulin, Kinetics, Male, Middle Aged, Monosaccharide Transport Proteins, Muscle Proteins, Oxygen Consumption, Reference Values, Glucose Clamp Technique, Body Mass Index, Muscle, Skeletal, 3-O-Methylglucose, Glucose Transporter Type 4, In Vitro Techniques
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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