Insulin resistance and atherosclerosis
Open accessAbstract
Considerable evidence supports the association between insulin resistance and vascular disease, and this has led to wide acceptance of the clustering of hyperlipidemia, glucose intolerance, hypertension, and obesity as a clinical entity, the metabolic syndrome. While insulin resistance, by promoting dyslipidemia and other metabolic abnormalities, is part of the proatherogenic milieu, it is possible that insulin resistance itself in the vascular wall does not promote atherosclerosis. Recent findings suggest that insulin resistance and atherosclerosis could represent independent and ultimately maladaptive responses to the disruption of cellular homeostasis caused by the excess delivery of fuel.
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The higher vascular risk linked to insulin resistance may be mediated by associated hypertension, hyperglycemia, hyperinsulinemia, dyslipidemia, endothelial dysfunction, hypercoagulability, inflammation, and increased platelet reactivity.
“The presence of insulin resistance increases the risk of vascular disease, possibly because of associated hypertension, hyperglycemia, hyperinsulinemia, dyslipidemia, endothelial dysfunction, hypercoagulability, inflammation, and increased platelet reactivity.7–9”
From Pioglitazone after Ischemic Stroke or Transient Ischemic Attack (2016) · cites this paper as [8]
The Abstract (page unavailable) associates insulin resistance with vascular disease and describes dyslipidemia and other metabolic abnormalities as part of a proatherogenic milieu. The “Hyperglycemia and hypertension” section (page unavailable) discusses elevated glucose and compensatory hyperinsulinemia, while noting that the relationship with hypertension is less clear. Our copy does not support the full proposed list of mediators, particularly hypercoagulability and increased platelet reactivity. (LLM, conf=0.88)
Experimental — accuracy not yet measuredInsulin resistance raises the risk of vascular disease.
“The presence of insulin resistance increases the risk of vascular disease, possibly because of associated hypertension, hyperglycemia, hyperinsulinemia, dyslipidemia, endothelial dysfunction, hypercoagulability, inflammation, and increased platelet reactivity.7–9”
From Pioglitazone after Ischemic Stroke or Transient Ischemic Attack (2016) · cites this paper as [8]
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- Authors
- Semenkovich, C. F.
- Affiliations
- Washington University in St. Louis (US)
- Corresponding author
- Semenkovich, C. F.
- ORCID
- Semenkovich, C. F.
- Venue
- Journal of Clinical Investigation
- Published
- 2006-07-03
- Volume
- 116
- Issue
- 7
- Pages
- 1813-1822
- ISSN
- 0021-9738 (ISSN-L)
- PMC
- PMC1483180
- OpenAlex
- W2797870555
- Cited by
- 481
- References
- 141
- Citations by year
- 2026: 15 · 2025: 28 · 2024: 25 · 2023: 18 · 2022: 18 · 2021: 21 · 2020: 14 · 2019: 19 · 2018: 18 · 2017: 14 · 2016: 22 · 2015: 26 · 2014: 25 · 2013: 22 · 2012: 30
- FWCI
- 4.70
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Clinical Investigation (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Digital Commons@Becker (Washington University School of Medicine) (submittedVersion)
- Funders
- Pfizer
- AstraZeneca
- Topics
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes, Cardiovascular Risks, and Lipoproteins
- Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
- Life Sciences › Immunology and Microbiology › Immunology › Atherosclerosis and Cardiovascular Diseases
- Keywords
- insulin resistance, atherosclerosis, metabolic syndrome, dyslipidemia, impaired glucose tolerance, hypertension, obesity, vascular disease, cellular homeostasis
- MeSH terms
- Animals, Cell Nucleus, Endoplasmic Reticulum, Humans, Hyperglycemia, Hypertension, Insulin Resistance, Mitochondria, Oxidative Stress, Peroxisome Proliferator-Activated Receptors, Dyslipidemias, Atherosclerosis
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.
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