Prostaglandins and prostaglandin synthesis inhibitors are known to influence the secretion of a number of hormones. More specifically, sodium salicylate is known to increase insulin secretion in Type II diabetics in response to a glucose stimulus. To challenge the hypothesis that prostaglandins may be instrumental in a generalized defect of glucose recognition in Type II diabetics, the effect of sodium salicylate on the hormonal counter-regulatory response to insulin-induced hypoglycaemia was examined. Before salicylate treatment, seven Type II diabetics had brisk increases (mean ± SEM) in circulating adrenaline (time 0 = 50 ± 7 pg/ml; peak = 1630 ± 330 pg/ml), noradrenaline (time 0 = 260 ± 46 pg/ml; peak = 770 ± 140 pg/ml), glucagon (time 0 = 38 ± 6 pg/ml; peak = 75 ± 10 pg/ml) and pancreatic polypeptide (time 0 = 149 ± 30 pg/ml; peak = 1170 ± 180 pg/ml) in response to insulin-induced hypoglycaemia. In contrast to previous studies in normal subjects, treatment with sodium salicylate failed to augment hypoglycaemia-induced secretion of adrenaline, noradrenaline or pancreatic polypeptide in Type II diabetics. The glucagon response to hypoglycaemia was augmented by sodium salicylate when the data were expressed as the incremental area under the glucagon vs. time curve, but not when peak response was used for analysis. These results are inconsistent with a prostaglandin-related generalized defect in glucose recognition in Type II diabetics and suggest that augmentation of hormone secretion in these patients by sodium salicylate may be specific for glucose-induced insulin secretion.
|Original language||English (US)|
|Number of pages||7|
|State||Published - 1984|