Cited by 107Metabolism, Diabetes, and CancerDiabetes, Cardiovascular Risks, and LipoproteinsAdipose Tissue and Metabolism

Molecular Mechanisms of Skeletal Muscle Insulin Resistance in Type 2 Diabetes

Bouzakri, Karim, Koistinen, Heikki, Zierath, Juleen·2005·Current Diabetes Reviews

Abstract

Type 2 (non-insulin-dependent) diabetes mellitus afflicts millions of people worldwide and is one of the main causes of morbidity and mortality. Current therapeutic agents to treat Type 2 diabetes are insufficient and thus, newer approaches are desperately needed. Type 2 diabetes is manifested by progressive metabolic impairments in tissues such as skeletal muscle, adipose tissue and liver, such that these tissues become less responsive to insulin. Skeletal muscle is quantitatively the most important tissue involved in maintaining glucose homeostasis under insulin-stimulated conditions, and is a major site of insulin resistance in Type 2 diabetic patients. At the cellular level, glucose transport into skeletal muscle is the rate-limiting step for whole body glucose uptake and a primary site of insulin resistance in Type 2 diabetes. Thus, skeletal muscle is a key insulin target tissue that harbours intrinsic defects that impinges upon whole body glucose homeostasis. Here, we review the current knowledge of signalling events that regulate glucose transport in human skeletal muscle.

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Crossref · 10.2174/1573399054022785

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  • Skeletal muscle insulin resistance involves reduced insulin-stimulated glucose uptake and arises from impaired insulin signalling plus several post-receptor defects, including defective glucose transport and phosphorylation and lower glucose oxidation and glycogen synthesis.

    “Insulin resistance in skeletal muscle is manifested by decreased insulin-stimulated glucose uptake and results from impaired insulin signaling and multiple post-receptor intracellular defects including impaired glucose transport, glucose phosphorylation, and reduced glucose oxidation and glycogen synthesis.”

    From Pathogenesis of insulin resistance in skeletal muscle (2010) · cites this paper as [9]

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Authors
Bouzakri, K., Koistinen, H., & Zierath, J.
Affiliations
  • Karolinska Institutet (SE)
  • Helsinki University Hospital (FI)
Venue
Current Diabetes Reviews
Published
2005-06-01
Volume
1
Issue
2
Pages
167-174
ISSN
1573-3998 (ISSN-L)
OpenAlex
W2168469188
Cited by
106
References
0
Citations by year
2026: 1 · 2025: 3 · 2024: 7 · 2023: 9 · 2022: 5 · 2021: 4 · 2020: 5 · 2019: 5 · 2018: 14 · 2017: 2 · 2016: 6 · 2015: 3 · 2014: 5 · 2013: 8 · 2012: 8
FWCI
0.37
Type
journal article
Language
en
Open access
closed
Locations
  • Current Diabetes Reviews (publishedVersion)
  • PubMed (publishedVersion)
  • HAL (submittedVersion)
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
type 2 diabetes, insulin resistance, skeletal muscle, glucose transport, glucose homeostasis, insulin signaling, glucose uptake, insulin target tissues
MeSH terms
Adipose Tissue, Biological Transport, Diabetes Mellitus, Type 2, Glucose, Homeostasis, Humans, Hypoglycemic Agents, Insulin, Insulin Resistance, Liver, Receptor, Insulin, Muscle, Skeletal, Phosphatidylinositol 3-Kinases, Glucose Transporter Type 4

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