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Biomedical subjects

R Torella

Publications and source records attributed to R Torella.

At least 109 records · Page 6Linked to original sources
PubMed1979

Acetylsalicyclic acid restores acute insulin response reduced by furosemide in man.

Prostaglandin E (PGE) infusion in normal man inhibits the acute insulin response to glucose. In order to determine whether endogenously released PGE might also inhibit insulin secretion, glucose-stimulated insulin responses were investigated in normal volunteers after furosemide (40 mg i.v.), a stimulator of endogenous PGE synthesis. Acute insulin response to glucose (20 g i.v.) was significantly reduced by furosemide (response before furosemide: 36 +/- 5 muU/ml; after furosemide: 26 +/- 5 muU/ml, m +/- SE, mean change 3--10 min, N = 8, P less than 0.01), whereas glucose disappearance rates were not modified after furosemide. Infusion of lysine acetylsalicylate (LAS), an inhibitor of endogenous PGE synthesis, completely reversed the inhibitory effect of furosemide on insulin secretion and also augmented acute insulin response to glucose (response before furosemide + LAS: 41 +/- 6 muU/ml; during furosemide + LAS: 50 +/- 7 muU/ml, N = 10, P less than 0.02). This effect was associated with an increase in glucose disappearance rates (P less than 0.05). These findings demonstrate that (1) furosemide inhibits glucose-induced acute insulin responses and (2) LAS completely reverses the inhibitory effect of furosemide and also accelerates glucose disposal. It is suggested that furosemide acts via the release of endogenous PGEs, which are known to inhibit insulin responses in man.

Adult↗
PubMed1979

Arguments for an inhibiting role of prostaglandin E1 on insulin secretion in man.

This study aimed at investigating the effect of exogenous prostaglandin E1 (PGE1) administration on both basal and glucose-stimulated insulin secretion in normal man. For this purpose, six normal subjects were submitted to an infusion of PGE1 (0.2 microgram/kg/min) over a period of 75 min. Plasma glucose exhibited a progressive increase whereas insulin did not show any significant change. In order to exclude the participation of endogenously released catecholamines in these responses to PGE1, six additional subjects received PGE1 60 min after the start of the infusion of the alpha-adrenergic blocking agent phentolamine. Hyperglycemia developed during the combined infusion of phentolamine plus PGE1, but plasma insulin remained essentially unchanged. In other six normal volunteers, PGE1 (0.5 microgram/kg/min) significantly reduced both insulin response to intravenous glucose and glucose tolerance. These results seen to indicate that an intraislet synthesis of prostaglandins is involved in the beta-cell regulation of insulin release.

Adult↗
PubMed1978

The effect of acetylsalicylic acid on insulin response to glucose and arginine in normal man.

In 14 normal subjects, treatment with acetylsalicylic acid (ASA, 3.2 g daily for 3 days) a well known inhibitor of prostaglandin synthesis, caused a slight but significant decrease (p is less than 0.05) in basal plasma glucose levels; by contrast, basal insulin rose from 5 +/- 1 to 8 +/- 1 muU/ml (p is less than 0.01) after ASA. Pretreatment with ASA augmented the early insulin response to a standard IV glucose tolerance test (25 g) in 7 normal subjects (p is less than 0.05 at 2 min; p is less than 0.02 at 5 min; p is less than 0.01 at 10 min). No significant changes were detected in the rate of glucose utilization. 7 additional subjects received a standard arginine test without and with ASA pretreatment. Arginine stimulated insulin levels were increased after ASA (p is less than 0.01 at 15 min; p is less than 0.05 at 30 min; p is less than 0.05 at 45 min), whereas glucose values were lower than under basal conditions at all times, with significant differences at 105 (p is less than 0.02) and 120 (p is less than 0.05) min. A possible role of prostaglandins upon the insulin responses to glucose and arginine is discussed.

Adult↗
PubMed1978

Effects of prostaglandin E1 and prostaglandin F2alpha on insulin and glucagon plasma levels during the intravenous glucose tolerance test in man.

The influence of prostaglandin E1 and prostaglandin F2alpha on circulating concentrations of insulin and glucagon during the intravenous glucose tolerance test has been studied in normal man. Insulin responses to glucose during PGE1 infusion (0.2 microgram/Kg/min) were significantly lower than in control infusions (p less than 0.001 at 2, 5, 10 and 15 min). Moreover, PGE1 caused a clear elevation of basal glucagon (p less than 0.02). PGF2alpha, at the two doses used (0.2 and 0.5 microgram/Kg/min), had no effect on basal glucose, insulin and glucagon levels, nor upon glucose-induced insulin secretion. Neither prostaglandin affected the glucose-induced inhibition of pancreatic alpha-cells. There is thus some evidence that PGs of E series may play some role in modulating the secretion of human pancreatic beta-cells.

Adult↗