Insulin resistance in the vasculature
Open accessAbstract
Insulin resistance is typically defined as a reduced ability of insulin to induce glucose uptake by target tissues such as fat and skeletal muscle cells. It accompanies several disease states, including obesity, type 2 diabetes, hepatitis C, and polycystic ovary syndrome, and is a primary feature of metabolic syndrome. Outside of its effects on blood glucose levels, insulin resistance is also associated with a 2- to 3-fold increased risk of cardiovascular mortality. In 1996, Alain Baron, Helmut Steinberg, and colleagues demonstrated that insulin resistance is associated with endothelial dysfunction. This seminal observation led to significant advances in our understanding of insulin's action in health and disease.
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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 [7]
The opening section links insulin resistance to increased cardiovascular mortality and endothelial dysfunction. Figure 1 describes a possible prothrombotic pathway, and the main text associates inflammation with vascular dysfunction. The paper does not support the full proposed list of mediators: it does not identify hypertension, hyperglycemia, hyperinsulinemia, dyslipidemia, or increased platelet reactivity as explanations for the higher vascular risk. (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 [7]
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“Moreover, in the insulin-resistant states of human obesity and type 2 diabetes, this vascular action of insulin was impaired (2).”
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- Authors
- Mather, K. J., Steinberg, H. O., & Baron, A. D.
- Affiliations
- Indiana University School of Medicine (US)
- Merck & Co., Inc., Rahway, NJ, USA (United States) (US)
- ORCID
- Mather, Kieren J.
- Venue
- Journal of Clinical Investigation
- Published
- 2013-03-01
- Volume
- 123
- Issue
- 3
- Pages
- 1003-1004
- ISSN
- 0021-9738 (ISSN-L)
- PMC
- PMC3582147
- OpenAlex
- W1983942577
- Cited by
- 120
- References
- 10
- Citations by year
- 2026: 1 · 2025: 6 · 2024: 5 · 2023: 7 · 2022: 5 · 2021: 8 · 2020: 10 · 2019: 11 · 2018: 9 · 2017: 10 · 2016: 13 · 2015: 17 · 2014: 10 · 2013: 8
- FWCI
- 12.59
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Clinical Investigation (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes, Cardiovascular Risks, and Lipoproteins
- Health Sciences › Medicine › Physiology › Nitric Oxide and Endothelin Effects
- Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
- Keywords
- insulin resistance, endothelial dysfunction, vascular system, cardiovascular risk, metabolic syndrome, type 2 diabetes, obesity, polycystic ovary syndrome, hepatitis C, insulin signaling
- MeSH terms
- Blood Pressure, Body Composition, Diabetes Mellitus, Type 2, Endothelium, Vascular, Glucose, Humans, Insulin, Insulin Resistance, Nitroprusside, Obesity, Regional Blood Flow, Vasodilation, Methacholine Chloride, Muscle, Skeletal
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