Arteries, inflammation and insulin resistance.

Inflammation plays a role in all stages of atherosclerosis from the formation to the rupture of the plaque. Guided by inflammatory mediators, monocytes bind to an endothelium damaged by cardiovascular risk factors, and then migrate towards the intima where, after incorporating oxidized low-density lipoprotein particles, they are transformed into foam cells. The lipid streak forms and develops as an atherosclerotic plaque, which is susceptible to erosion and rupture. Inflammation fed by excess adipose tissue decreases insulin sensitivity, which is the central feature of the metabolic syndrome. Inflammation therefore appears to be a common factor of atherosclerosis and the metabolic syndrome. The factors triggering this inflammation have yet to be determined. One line of thought would appear to point to diet.

Lower insulin secretory response to glucose induced by artificial nutrition in children: prolonged and total parenteral nutrition.

Long-term parenteral nutrition (TPN) in children is associated with sustained hyperinsulinemia due to a high nutriment infusion flow 12 h/24 h, with plausible lipotoxicity secondary to repeated lipid infusions and with changes in incretin hormone release. The aim of this study was to test whether long-term TPN can lead to an alteration in beta-cell function. Thirteen children (age 9.5 +/- 3.9 y) on total TPN without obvious alternation in glucose tolerance were included. beta-Cell function was quantified with an intravenous glucose tolerance test (IVGTT) and a graded glucose infusion. First phase insulin release (FPIR) was low in five patients. The same demonstrated a lower insulin release under graded glucose infusion, although plasma glucose reached values as high as 15 mM. These data emphasize that metabolic conditions induced by TPN can lead to lower insulin secretory response to glucose. Patients who remain dependent on TPN are at risk of developing glucose tolerance disorders.