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Biomedical subjects

N Passariello

Publications and source records attributed to N Passariello.

At least 55 records · Page 3Linked to original sources
PubMed1981

Effects of acetylsalicylic acid on plasma glucose, free fatty acid, betahydroxybutyrate, glucagon and C-peptide responses to salbutamol in insulin-dependent diabetic subjects.

The selective beta 2-adrenergic agonist salbutamol increases plasma glucose concentration and the rate of lipolysis when infused in pregnant diabetic women. The aim of the present study was twofold: (a) to focus on the actions of salbutamol on lipid and carbohydrate metabolism in insulin-dependent diabetics: and (b) to investigate possible interferences of acetylsalicylic acid (ASA) with the metabolic responses to i.v. salbutamol. The results obtained during salbutamol infusion (5 microgram/min) in 6 insulin-dependent diabetic subjects demonstrated that this drug caused sustained increases in plasma glucose, free fatty acid and beta-hydroxybutyrate concentrations, as well as a small and transient rise of plasma glucagon. No change in plasma C-peptide concentration occurred during salbutamol. A concurrent infusion of lysine acetylsalicylate reduced the increase in free fatty acids by half, blunted the weak glucagon response but enhanced the rise in plasma glucose following salbutamol administration. The present data show that salbutamol exerts a potent hyperglycemic, lipolytic and ketogenic effect in insulin-dependent diabetics. We suggest that this beta-adrenergic agent should be used cautiously in human diabetes mellitus.

Adult↗
PubMed1981

Further studies on the significance of circulating platelet aggregates induced by somatostatin in man.

The aim of the present study was to further evaluate the significance of circulating platelet aggregates induced by somatostatin in insulin-dependent diabetic subjects. Eight insulin-dependent diabetics and eight normals were infused with somatostatin at increasing doses (250, 500, and 750 microgram/h), each dose for 30 min. In diabetics, somatostatin induced the appearance in blood of platelet aggregates in a dose-dependent fashion, the highest level being observed with the highest dose (750 microgram/h), p less than 0.005). In normals, circulating platelet aggregates were detected only with the infusion of the highest rate of somatostatin (p less than 0.025). This effect of somatostatin was reversible, since it tended to disappear 30 min after the infusion was stopped. In six additional insulin-dependent diabetics, a previous infusion of phentolamine (0.5 mg/min) completely prevented the appearance of platelet aggregates by somatostatin. No significant variation of the aggregation response to both ADP and collagen and the platelet count was seen in both experiments. Somatostatin, as expected, reduced the basal concentration of plasma glucose, glucagon, and C-peptide in both diabetics and normals. On the basis of these results, we suggest that somatostatin has some proaggregating capacity in vivo, probably by interacting with adrenergic mechanisms.

Adolescent↗
PubMed1981

Calcitonin, a diabetogenic hormone?

The effect of calcitonin on oral glucose tolerance and on insulin, C-peptide, glucagon, and GH secretion has been investigated in man. Eight subjects with normal glucose tolerance and eight with impaired glucose tolerance (IGT) were studied. Each subject received two oral glucose tolerance tests (100 g) in random order, one under basal conditions and the other during the simultaneous in administration of salmon calcitonin (100 Medical Research Council Units). In all subjects, calcitonin exaggerated the rise in plasma glucose after oral sugar. The integrated areas under the plasma glucose curves were 4,400 +/- 840 mg/dl.min (normals) and 8,708 +/- 1,840 mg/dl.min (IGT) without calcitonin, and 8,208 +/- 1,700 mg/dl. min (normals) and 19,500 +/- 3,500 mg/dl. min (IGT) with calcitonin (P less than 0.01). Plasma insulin and C-peptide responses to glucose were significantly reduced (P less than 0.01) by calcitonin at all times after the start of the test in both normal and IGT groups. The inhibitory action of oral glucose on glucagon secretion was partially prevented by calcitonin (P less than 0.01). Moreover, calcitonin completely blunted the GH rebound occurring at the end of the test. These findings demonstrate that calcitonin impairs glucose tolerance in man by both inhibiting glucose-induced insulin secretion (primary effect) and reducing glucose-mediated glucagon suppression (accessory effect). These effects of calcitonin could be explained by a decrease in the cytosolic Ca2+ concentration in both alpha- and beta-cells.

Adult↗
PubMed1981

Colchicine and insulin secretion in man.

The present study is aimed at investigating the effect of acute and chronic colchicine administration on insulin secretion in humans. Acute insulin response to glucose (0.33 g/kg) was significantly decreased by colchicine (3 mg i.v.). In fact, this response (mean change 2-10 min insulin) was 44 +/- 8 microunits/ml before and 32 +/- 6 microunits/ml after colchicine administration (P less than 0.01). As a consequence of this, glucose disappearance rates were reduced (P less than 0.05). Infusion of lysine acetylsalicylate (LAS), an inhibitor of endogenous PG synthesis, completely reversed the inhibitory effect of colchicine upon insulin secretion and also augmented acute insulin response to glucose (response before colchicine + LAS = 45 +/- 8 microunits/ml; response after colchicine + LAS = 51 +/- 9 microunits/ml, P less than 0.05). This effect was associated with an increase in glucose disappearance rates (P less than 0.05). The 10-day treatment with colchicine (2 mg daily) caused a significant suppression of insulin secretion induced by oral glucose (100 g) and significantly increased the plasma glucose concentrations following the test (P less than 0.05). These findings demonstrate that (1) both acute and chronic colchicine administration inhibit glucose-induced insulin secretion and deteriorate glucose tolerance in humans, and (2) LAS completely reverses these negative effects of colchicine. An increased synthesis of endogenous PGE, which are known to inhibit insulin secretion in humans, might account for the inhibiting effect of colchicine on insulin secretion.

Adult↗
PubMed1981

Impaired insulin secretion in human diabetes mellitus III. The effect of the serotonin antagonist metergoline.

The present study was aimed at investigating the effect of metergoline, a powerful and long-lasting antiserotoninergic agent, on insulin responses to glucose and arginine in adult-onset diabetic subjects. The repeated administration of this agent (10 mg daily for two days plus a 4 mg dose 1 hour before the post-treatment test) or placebo did not influence acute insulin response to intravenous glucose (20 g), total insulin secretion or glucose disappearance rates. Similarly, plasma glucose and insulin levels following arginine (30 g perfused over a period of 40 min) were similar before and after metergoline treatment. These results do not support the hypothesis that an endogenous monoamine mechanism plays an important part in defective insulin secretion in human non insulin-dependent diabetes mellitus.

Adult↗
PubMed1980

Somatostatin and insulin secretion in man. III - Lack of interaction with prostaglandins.

In order to asses potential interactions between somatostatin and prostaglandins during regulation of insulin secretion in vivo, in the present investigation we studied the effect of acetylsalicylic acid, an inhibitor of endogenous PG synthesis, on somatostatin-mediated inhibition of glucose-induced insulin secretion in normal man. Acute insulin response (mean change 3'-10') to glucose was almost completely suppressed by somatostatin (500 microgram/h) and glucose utilization was decreased. These somatostatin-induced changes failed to be eliminated by a concurrent infusion of acetylsalicylic acid (40 mg/min). This last drug, when infused alone, increased both the acute insulin response to glucose and glucose tolerance. These results speak against the involvement of PGs in the mediation of somatostatin-induced suppression of insulin secretion.

Aspirin↗
PubMed1979

[Vascular alterations and GH secretion in latent chemical diabetes].

The AA. have investigated the relationship between the secretion of GH and diabetic angiopathy a group of 17 subjects with chemical diabetes during a standard dexamethasone os i.v. glucose test. The results show that functional subclinical microangiopathy was present in the majority of the diabetics studied, who also showed an exaggerated growth hormone response to glucose. Thus, these results suggest that a positive correlation exists between alterations in the secretion of growth hormone and the development of diabetic microangiopathy.

Blood Glucose↗
PubMed1979

Effect of calcitonin on insulin response to arginine in man.

The aim of the present study was to evaluate the effect of calcitonin on insulin response to intravenous arginine in normal humans. For this purpose, eight normal subjects were submitted to an iv arginine tolerance test twice, under basal conditions and during the simultaneous infusion of calcitonin plus arginine. Calcitonin caused a clear inhibition of the insulin response to arginine (p less than 0.01) and also exaggerated the rise in plasma glucose seen with iv arginine (p less than 0.01). Theophylline (250 mg as iv bolus, followed by an iv infusion of 500 mg/h) failed to overcome the inhibitory effect of calcitonin on insulin secretion. It is hypothesized that calcitonin inhibits insulin secretion by changing calcium distribution in the pancreatic beta-cell.

Adolescent↗
PubMed1979

Plasma sorbitol dehydrogenase in diabetic subjects with or without vascular complications.

Plasma Sorbitol Dehydrogenase levels were determined in subjects with diabetes mellitus and normal people. The diabetic subjects had circulating plasma levels of SDH significantly higher (p less than 0.001) than those observed in controls. Moreover, the diabetics with vascular complications presented the highest SDH values. The lack of positive correlation between plasma glucose and SDH levels suggests that SDH, like hemoglobin A1C, reflect the degree of previous metabolic control of diabetes mellitus.

Adolescent↗
PubMedDate not supplied

Effect of Calcitonin on plasma glucose, C-peptide, glucagon and growth hormone responses to arginine in insulin-dependent diabetic subjects.

The present study was aimed at investigating the effect of calcitonin on plasma glucose, C-peptide, glucagon and growth hormone (GH) responses to arginine in insulin-dependent diabetic subjects. For this purpose, 6 insulin-requiring diabetics were submitted to an arginine tolerance test twice, in basal conditions and during the simultaneous infusion of salmon calcitonin (100 MRC) plus arginine in random order. Calcitonin caused a clear inhibition of the plasma glucose rise triggered by the amino acid, without significant modifications of the plasma C-peptide and glucagon responses. A significant rebound of plasma glucose was seen after calcitonin was stopped. Plasma GH rise following arginine administration was significantly inhibited by calcitonin. These findings suggest some positive interferences of calcitonin with the arginine-induced plasma glucose increase in insulin-dependent diabetes.

Adolescent↗
PubMedDate not supplied

Modulation by verapamil of insulin and glucagon secretion in man.

The present investigation was designed to evaluate the effect of acute and protracted verapamil administration on insulin and glucagon secretion in man. For this purpose, 14 normal subjects received two consecutive glucose pulses (5 g.i.v. in less than 20 sec or 20 g.i.v. in less than 1 min, 7 subjects for each group), 70 or 90 min apart, before and during an infusion of verapamil (160 microgram/min). Seven additional normal subjects received two consecutive arginine pulses (5 g i.v.), 70 min apart. In 14 inpatients with coronary heart disease, we investigated the effect of protracted verapamil administration. Seven of these subjects underwent two oral glucose tolerance tests (100 g) and the other 7 two arginine tests (30 g) before and after a 10-day treatment with verapamil, 240 mg/die p.o. divided into three doses; the last dose, 80 mg, was given orally 1 h before the performance of the post-treatment test. Verapamil significantly inhibited the acute insulin response (AIR, mean change from 3-10 min) to glucose (5 g), as well as the AIR and AGR (acute glucagon response) to arginine (5 g). By contrast, verapamil failed to alter significantly the AIR to the higher glucose pulse. There was no significant change of oral glucose tolerance after verapamil, nor was there a change in insulin response to oral glucose. By contrast, insulin and glucagon responses to arginine infusion were significantly reduced by the drug.

Adult↗
PubMedDate not supplied

Effect of human calcitonin (hCT) on glucose- and arginine-stimulated insulin secretion.

Many studies have shown that in normal man salmon and porcine CT administration in bolus inhibits the release of TSH, LH, GH, and glucose- or arginine-induced insulin secretion. In the present study we investigated the effects of human synthetic calcitonin (hCT) on glucose- or arginine-induced insulin secretion in man. Twenty-two subjects were submitted to i.v. administration of hCT during glucose or arginine test. In our opinion, the most interesting results are those observed with arginine plus hCT at two different dosages (25 micrograms and 12.5 micrograms infused in 30 min). In fact arginine plus hCT (25 micrograms in 30 min) administration induced a significant increase of glycemia at 5, 10 and 20 min (p less than 0.01) and at 30 min (p less than 0.05) and a significant decrease of IRI at 5, 10, 20 and 30 min (p less than 0.001) and at 45 min (p less than 0.005). The highest plasma CT levels were observed at 15 and 30 min (490 and 540 pg X ml-1). Arginine plus hCT (12.5 micrograms in 30 min) infusion induced a similar significant increase in plasma glucose at 10, and 20 min (p less than 0.05) and at 30 min (p less than 0.01) and a significant decrease of plasma IRI at 10 min (p less than 0.05) at 20 min and 30 min (p less than 0.005). The highest plasma CT levels were reached at 20 min and 30 min (250 and 270 pg X ml-1, respectively). Our results clearly demonstrate that physiologic doses of hCT are able to inhibit arginine induced insulin secretion in normal man. Since insulin induces hypercalcemia and food ingestion increases both insulin and CT, one could hypothesize that CT inhibits insulin secretion thus controlling post-prandial hypercalcemia by its osteotrophic effect and by its action upon calcium redistributed within the cells.

Arginine↗