E M Lasché | Search PubMed

PubMed1984

The effect of high insulin concentrations on prostacyclin production as measured by 6-keto PGF1 alpha determination.

The effect of insulin in varied concentrations on the production of 6-keto PGF1 alpha, the metabolite of prostacyclin, by rat aortic tissue in vitro was assessed by radioimmunoassay. An insulin concentration of 50 microU/ml produced no change in 6-keto PGF1 alpha from the control samples, but concentrations of 100 microU/ml and 250 microU/ml reduced production from a control value of 0.326 +/- 0.031 ng/mg to 0.253 +/- .018 ng/mg (P less than .05) and 0.226 +/- 0.015 ng/mg (P less than .025) respectively. These results suggest that the suppression of PGI2 production may occur in states associated with insulin levels above those normally found in the postprandial state and might be one mechanism by which hyperinsulinemia might favor macrovascular disease.

6-Ketoprostaglandin F1 alpha↗

PubMed1982

Interaction of insulin and prostacyclin production in the rat.

The effects of hyperinsulinemia on production of prostacyclin (PGI2), a potent inhibitor of platelet aggregation, was studied in vitro in the rat. Aortic rings following 1-h preincubation at 37 degrees C and 1 h at 4 degrees C were incubated with and without purified porcine insulin in Krebs' glucose at 37 degrees C for 5 min and immediately percent inhibition of platelet aggregation was determined. PGI2 production in ng/mg aorta was estimated from a curve using PGI2 standard. The mean PGI2 production was significantly decreased in those rings incubated with insulin in concentration of 2500, 500, and 250 microunits/ml. Likewise, incubation of rings at 22 degrees C for 30 min resulted in at least ten times less PGI2 with insulin. Since PGI2 appears to exert its antiaggregatory effect through cyclic AMP, theophylline was added to the incubation medium resulting in potentiation of inhibition of aggregation which was decreased to control levels when insulin was also added to the medium. Pancreatic slices yielded no significant change in insulin obtained when incubated with and without 5 ng of PGI2 in 2 ml of 2.8 mM glucose, but in a high glucose medium (28 mM) the PGI2-treated slices yielded significantly less insulin. Since PGI2 may play a role in the formation of atherosclerotic plaques, these results suggest a possible deleterious effect of elevated insulin levels in type II and in insulin-treated type I diabetics with regard to macrovascular disease. Suppression of insulin production in presence of PGI2 in high glucose medium resembles the action of other prostaglandins and suggests it may inhibit insulin secretion after a glucose load.

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The diabetic driver.

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Accidents, Traffic↗