Type 2 diabetes and atherosclerotic cardiovascular disease: do they share common antecedents?

Abstract

It has been suggested that the association between type 2 diabetes and atherosclerotic cardiovascular disease might result from a shared antecedent — the `common soil' hypothesis. The antecedent could provide a fundamental link between type 2 diabetes and atherosclerosis via the metabolic (or insulin resistance) syndrome. The relative contributions of genes, fetal nutrition and environmental factors to this syndrome remain unclear. Although most patients with type 2 diabetes have insulin resistance, it is uncertain whether the insulin resistance-hyperinsulinaemia complex directly promotes atherogenesis, and whether type 2 diabetes and atheroma are connected via a common mediator such as central obesity, vascular endothelial dysfunction, or disordered lipid metabolism. Insulin sensitivity and cardiovascular risk may be influenced by adipocytokines (e.g. leptin and adiponectin), by excess fatty acids liberated from visceral fat, and inflammatory processes. Disturbances of the neuro-endocrine system, possibly mediated via visceral obesity, are also under investigation. Other putative links between type 2 diabetes and atheroma include polymorphisms in the genes for tumour necrosis factor-α,insulin-like growth factor-1 promoter, and lamin A/C. Trials with certain cardioprotective agents including inhibitors of the renin-angiotensin-aldosterone system and statins can improve cardiovascular outcomes and protect against the development of type 2 diabetes, lending support to the common soil hypothesis.