Key result
Linked insulin effects on glucose transport and NO production may explain endothelial dysfunction in insulin resistance.
Why the study?
The mechanisms underlying endothelial dysfunction in normoglycaemic first-degree relatives and insulin resistant subjects are less well understood and less explained by confounding variables.
Understanding the molecular link between insulin resistance and endothelial nitric oxide production may lead to novel cardiovascular disease prevention strategies in diabetic and non-diabetic subjects.
Answers are grounded in this paper and cite their sources.
No immediate practice change in diabetes care; leaves open whether this molecular link yields new CVD prevention targets.
Dysfunction of the endothelial cell monolayer leads to increased vascular tone and permeability and a prothrombotic environment. Type 2 diabetes is a state of insulin resistance, hyperglycaemia and dyslipidaemia characterised by high cardiovascular risk and accelerated atherosclerosis. Many mechanisms by which hyperglycaemia can result in endothelial dysfunction have now been identified. However, the presence of endothelial dysfunction in normoglycaemic first-degree relatives and insulin resistant subjects is less well understood and less readily explained by `confounding' variables. We suggest that insulin's effects on glucose transport in classical target tissues and nitric oxide production in the endothelium are fundamentally linked at a molecular level. It is expected that greater understanding of these underlying mechanisms will lead to novel approaches to prevention of cardiovascular disease in both diabetic and non-diabetic subjects.
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Storey et al. (2001) conducted a review in Type 2 diabetes and endothelial dysfunction. Insulin's effects on glucose transport and endothelial nitric oxide production may be fundamentally linked at a molecular level, explaining endothelial dysfunction in insulin-resistant states.
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