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Biomedical subjects

R Torella

Publications and source records attributed to R Torella.

At least 91 records · Page 5Linked 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

Prostaglandins and the alpha-cell.

Experimental evidence has recently accumulated indicating that administration of some prostaglandins (PGs), particularly those of the E series, can evoke release of glucagon by the pancreatic alpha-cells. Virtually, all the in vitro studies (isolated perfused rat pancreas, isolated guinea-pig islets) agree that PGs can increase both basal and stimulated glucagon release. On the other hand, inhibition of PG synthesis with indomethacin blocks glucagon release. In rats and in normal humans, PGE1, but not PGA2 or PGF2a, causes a progressive rise of plasma glucagon levels. While in the rat this response seems independent of the adrenergic nervous system, in man the hyperglucagonemia induced by PGE1 is easily suppressed by propranolol, suggesting an interaction between the prostaglandin and the beta-receptors of the alpha-cell. Studies with inhibitors of PG synthesis in vivo have yielded conflicting results, depending on the particular experimental protocol used and on the type of inhibitor tested. In normal humans, it seems that acetylsalicylic acid (ASA) has no effect on glucagon response to arginine, tolbutamide and insulin-induced hypoglycemia. Conversely, a stimulator of PG synthesis, such as furosemide, increases glucagon response to an arginine pulse in man. In insulin-dependent diabetics, who present an exaggerated glucagon response to stimulants, ASA fails to alter glucagon response to arginine, but completely blunts the glucagon response to salbutamol, a weak beta-2 receptor agonist. In conclusion, these observations provide evidence in support to a role for PGs, at least PGE, in the contro of glucagon release.

Albuterol↗
PubMed1981

Impaired insulin secretion in human diabetes mellitus. II. A possible role for prostaglandins.

Human diabetes mellitus is characterized by impaired insulin response to intravenous glucose. In search of possible endogenous factors which impair insulin release, we have investigated the effect of lysine acetylsalicylate (LAS), an inhibitor of endogenous prostaglandin (PGs) synthesis, upon insulin responses to glucose and arginine in subjects with type II (adult-on-set) diabetes mellitus. Acute insulin response to glucose (20 g) was significantly increased by LAS (response before LAS=26 +/- 10%; during LAS=77+15%, mean+/-SEM, mean change 3-10 min insulin, % basal, n=8, p 0.01), as well as second phase insulin secretion (before LAS=1437+/-316%; during LAS=3960+/-550%, change 10-60 min, uU/ml-min, % basal, p less than 0.01). This effect was associated with an increase in glucose disappearance rates (p less than 0.01). Acute insulin response to arginine (5 g iv) was also increased by LAS infusion. These results suggest that endogenous PGs may be one of the factors which impair insulin secretion in human diabetes.

Adult↗
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↗
PubMed1980

[Thromboelastographic patterns in patients suffering from chronic obstructive lung disease after hyperventilation].

In an our previous study we studied the influence of O2 therapy administration on the thromboelastographic pattern of patients suffering from chronic obstructive lung disease. We showed that basal hypocoagulability of our patients became normal after O2 administration. In this study we refer the thromboelastographic pattern observed in patients suffering from the same disease before and after hyperventilation. We don't find any changes about total coagulability either in patients or in healthy subjects after hyperventilation. Therefore we suggest that the absence of any changes is due to PCO2 and pH variations that occur at the same time of PO2 modification during hyperventilation; PCO2 and pH variations may influence the haemoglobin oxygen affinity and annul the effect of the increase PO2 on the tissue oxygenation. We suppose that the increase of patients suffering from chronic obstructive lung disease, is due to decreased fibrinolysis or to increased production of prostacycline induced by hyperventilation.

Adult↗
PubMed1980

[Effect of circulating insulin on liver damage by CCl4 in the rat. I. Biochemical studies].

The authors have studied the damaging effects of CCl4 (0.05ml/Kg) in healthy rats, in alloxan-diabetic rats, and in rats treated with tolbutamide per os (100mg/Kg) for twenty days. Biochemical studies in these animals demonstrated that actually hyperinsulinemia has a preventive effect in relation to the damage produced by CCl4 as demonstrated by a decrease in bilirubinemia and transaminasemia.

Animals↗
PubMed1980

Effect of furosemide on insulin and glucagon responses to arginine in normal subjects.

This study aimed at evaluating the influence of furosemide upon insulin and glucagon responses to arginine in healthy subjects. For this purpose, six normal subjects received two consecutive arginine pulses (3 g), 60 min apart, before and after the administration of furosemide (40 mg, IV). The acute insulin response (mean change from 3-10 min) to the second arginine pulse was significantly inhibited by furosemide (mean increase: 14.8 +/- 3.0 microU/ml versus 11.7 +/- 2.5 microU/ml, p < 0.01). By contrast, the acute glucagon response was significantly increased (mean increase: 77 +/- 18 pg/ml versus 105 +/- 21 pg/ml, p < 0.01). No significant changes in plasma glucose levels occurred. In control experiments, in which saline rather than furosemide was administered, the acute insulin and glucagon response to the first arginine pulse did not differ from that observed with the second pulse. The effect of furosemide on insulin and glucagon secretion might be mediated through enhanced release of endogenous prostaglandin E.

Adult↗
PubMed1980

Impairment of insulin secretion in man by nifedipine.

The effect of nifedipine, a calcium antagonist, on carbohydrate metabolism and insulin secretion was evaluated in patients who required treatment with this drug. 20 subjects underwent two oral glucose tolerance tests (100 g), one under basal conditions, and the other after ten days of treatment with nifedipine 30 mg/day by mouth, in three divided doses. 10 subjects had normal glucose tolerance; in them nifedipine administration reduced the insulin response to oral glucose in the first 60 min, but improved glucose tolerance. The other 10 subjects had impaired glucose tolerance and nifedipine treatment resulted in a further reduction both of insulin secretion and glucose tolerance. No such effects were seen in the placebo (weight- and disease-matched) group. The mechanism by which nifedipine influences carbohydrate metabolism and insulin secretion is discussed.

Adult↗
PubMed1980

Somatostatin and insulin secretion in man. IV. The role of calcium.

In this study we evaluated the influence of changes in serum calcium concentration upon somatostatin-mediated inhibition of insulin secretion in man. For this purpose, we investigated the effect of somatostatin in a group of subjects with hypoparathyroidism before and after correction of hypocalcemia and in normal subjects made hypercalcemic by exogenous calcium administration. In the presence of hypocalcemia, somatostatin caused an almost total inhibition of glucose-induced insulin secretion. In addition, somatostatin significantly decreased glucose tolerance in those hypocalcemic patients who exhibited normal tolerance under basal conditions [glucose utilization (kG), 1.44 +/- 0.13 before vs. 0.68 +/- 0.14 during somatostatin; P < 0.02]. Glucose tolerance was unaltered in those subjects who had a decreased glucose tolerance under basal conditions (kG, 1.01 +/- 0.1 before vs. 0.88 +/- 0.16 during somatostatin; P = NS). Under normocalcemic conditions, the insulin response to glucose and glucose tolerance were significantly greater than values measured during hypocalcemia. However, somatostatin blunted the insulin response to glucose and significantly decreased glucose utilization. These inhibitory effects of somatostatin upon insulin secretion and glucose tolerance were not reversed by a concurrent infusion of calcium (serum calcium, 6.9 +/- 0.3 meq/liter) in a group of normal subjects. Our data confirm the reduced insulin secretion and glucose tolerance in hypoparathyroidism and demonstrate that the suppressive effect of somatostatin upon glucose-stimulated insulin secretion is independent of changes in serum calcium concentration over a wide range.

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

[Acetylsalicylic acid and hormonal response in insulin induced hypoglycemia].

The influence of a short-term treatment with acetylsalicylic acid (ASA 3,2 g/daily), an inhibitor of endogenous prostaglandin synthesis, on plasma glucose, glucagon and growth hormone responses to insulin-induced hypoglycemia, has been investigated in seven subjects. ASA caused a slight but significant reduction in basal glucose levels, but did not alter the pattern of glucagon and growth hormone secretion following hypoglycemia. On the basis of these results, it is hypothesized that endogenous prostaglandins are not implicated in the response of pancreatic alfa-cell to hypoglycemia.

Adult↗
PubMed1979

Influence of acetylsalicylic acid on plasma glucose, insulin, glucagon, and growth hormone levels following tolbutamide stimulation in man.

The effects of acetylsalicylic acid (ASA), a known inhibitor of prostaglandin (PG) synthesis, on plasma glucose, insulin, glucagon and growth hormone (GH) responses to tolbutamide were examined in ten normal volunteers. Treatment with 3.2 g ASA daily for 3 days caused a significant reduction in basal plasma glucose levels (p less than 0.05); by contrast, basal insulin rose from 23 +/- 2 to 31 +/- 2 microU/ml (p less than 0.01). No significant changes in the basal concentrations of glucagon and GH were found after ASA. Insulin response to tolbutamide was significantly augmented after ASA (p less than 0.01) while GH response to hypoglycemia was reduced (p less than 0.05). The pattern of plasma glucose and glucagon was not significantly modified by the treatment. Since ASA seems to have an action opposite to PGE on insulin and GH secretion, it is possible that the ASA may work through inhibition of PG synthesis.

Adult↗