Atherogenity of insulin

Clinical studies have demonstrated that those processes linked to hyperinsulinaemia, such as type 2 diabetes or obesity, show a higher mortality due to coronary or cerebral atherosclerosis (Pyorala et al 1985). Furthermore, experimental results show that insulin acts on the vascular wall, either producing hypertension and endothelial changes, or influencing the smooth muscle cells (SMCs) to proliferate. It is well known that endothelial lesions and SMC proliferation are basic steps of atherogenesis (Ross 1993).

For a better understanding of the role of SMCs in atherosclerosis, it is worth mentioning that these cells and collagen represent the main content of the atheroma plaque. SMCs migrate from the media crossing the intima to accumulate and release collagen. Two distinctive phenotypes of SMC are known: contractile and synthetic. Contractile SMCs respond to agents inducing vasomotor changes, whereas the synthetic SMCs are capable of expressing genes for growth regulators and collagen synthesis. Normally, in adult life the vascular wall has only postmitotic SMCs which are contractile. Therefore, muscle cells of atheromas should have changed their differentiated phenotype to a synthetic one, with the capability to proliferate, migrate and finally secrete collagen. At present, it is believed that oxidized low density lipoprotein (LDL) alters the endothelium, producing a cascade of events including SMC migration (for review see, Massy & Keane 1996). The question is whether insulin is able to change the SMC phenotype and, if so, by what mechanism.

Diabetes 2

Diabetes 2

Diabetes is a disease that affects the way your body uses food. Normally, your body converts sugars, starches and other foods into a form of sugar called glucose. Your body uses glucose for fuel. The cells receive the glucose through the bloodstream. They then use insulin a hormone made by the pancreas to absorb the glucose, convert it into energy, and either use it or store it for later use. Learn more...

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