Cited by 131Diabetes, Cardiovascular Risks, and LipoproteinsMetabolism, Diabetes, and CancerCardiovascular Function and Risk Factors

Metabolic and molecular basis of insulin resistance

Bajaj, Mandeep, DeFronzo, Ralph A·2003·Journal of Nuclear Cardiology

Integrity signals

Registry

Crossref · 10.1016/s1071-3581(03)00520-8

Cites

92 of 92 references verified0 citation errors · 0 not checkable

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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 [8]

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Authors
Bajaj, M., & DeFronzo, R. A.
Affiliations
The University of Texas at San Antonio Health Science Center (US)
Corresponding author
Bajaj, Mandeep
Venue
Journal of Nuclear Cardiology
Publisher
Elsevier BV
Published
2003-05
Volume
10
Issue
3
Pages
311-323
ISSN
1071-3581 (ISSN-L)
OpenAlex
W2072989847
Cited by
131
References
92
Citations by year
2026: 1 · 2025: 3 · 2024: 2 · 2023: 4 · 2022: 1 · 2021: 10 · 2020: 1 · 2019: 4 · 2018: 2 · 2017: 3 · 2016: 13 · 2015: 10 · 2014: 7 · 2013: 8 · 2012: 6
FWCI
2.86
Type
journal article
Language
en
Open access
closed
Locations
  • Journal of Nuclear Cardiology (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes, Cardiovascular Risks, and Lipoproteins
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiovascular Function and Risk Factors
Keywords
insulin resistance, insulin signaling, glucose metabolism, molecular mechanisms
MeSH terms
Blood Glucose, Diabetes Mellitus, Type 2, Humans, Insulin Resistance, Liver, Monosaccharide Transport Proteins, Muscles, Signal Transduction, Receptor Protein-Tyrosine Kinases

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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.

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