Hormonal
Insulin resistance promotes atherosclerosis through impaired insulin signaling (specifically reduced PI-3 kinase activation) which decreases nitric oxide production, leading to endothelial dysfunction and accelerated plaque progression, independent of hyperglycemia.
If you have insulin resistance or obesity, your cardiovascular risk is elevated even if your blood sugar is normal. Focus on improving insulin sensitivity through lifestyle changes rather than just monitoring glucose levels, as high insulin itself drives arterial damage.
Insulin resistance promotes a pro-inflammatory state and dyslipidemia in addition to perturbed insulin signaling on important intimal cells... resulting with advanced plaque progression in the setting of hyperinsulinemia... the resultant decrease in nitric oxide production leads to endothelial dysfunction and accelerated atherosclerosis.
Why this rating
The paper cites in vivo trials and established molecular pathways, though it is a commentary/review rather than a primary clinical trial.
Source
Atherosclerosis: Pathophysiology of insulin resistance, hyperglycemia, hyperlipidemia, and inflammation
Joshua Beverly et al. · Journal of Diabetes · 2019
DOI 10.1111/1753-0407.12970
More from this paper
- Atherogenesis is fundamentally driven by the accumulation of oxidatively modified LDL in the arterial intima, facilitated by endothelial dysfunction and scavenger receptor uptake by macrophages to form foam cells.Strong
- Chronic hyperglycemia accelerates atherosclerosis through three distinct mechanisms: formation of advanced glycation end products (AGEs) that modify LDL, increased oxidative stress reducing nitric oxide, and pathologic activation of Protein Kinase C (PKC).Good
- Inflammation is involved in every step of the atherosclerotic process, from initial lipid retention to plaque destabilization, mediated by both innate (macrophages, TLRs) and adaptive (T cells, B cells) immune responses.Good
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