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Biomedical subjects

R Torella

Publications and source records attributed to R Torella.

At least 73 records · Page 4Linked to original sources
PubMed1987

Impaired glucose metabolism in heroin and methadone users.

Plasma glucose and insulin responses to both oral and intravenous glucose stimulation were evaluated in heroin and methadone addicts, compared to healthy control subjects. Both groups of addicts had an altered response to oral and intravenous glucose load. These phenomena were linked to a reduced insulin response. Moreover, increased fasting insulin levels in both groups of addicts were observed. These data show that both heroin and methadone addiction may alter glucose metabolism, and, furthermore, stress the findings of similarities between opiate addicts and non-insulin dependent diabetics.

Adult↗
PubMed1987

Hyperglycemia and obesity as determinants of glucose, insulin, and glucagon responses to beta-endorphin in human diabetes mellitus.

The effect of human beta-endorphin on plasma glucose, insulin, and glucagon concentrations was studied in patients with noninsulin-dependent diabetes mellitus and in normal subjects. The subjects were divided according to their body weight into lean (body mass index, less than 25) and obese (body mass index, greater than 29.5) groups. In lean subjects, infusion of 0.5 mg/h beta-endorphin caused significant increases in peripheral plasma glucose and glucagon levels, but no change in plasma insulin. In obese subjects, there was an immediate marked increase in both plasma insulin and glucagon concentrations during the beta-endorphin infusion, but the plasma glucose response was lower than that of lean subjects. In lean diabetic patients, beta-endorphin produced significant simultaneous increments in both insulin and glucagon concentrations and significantly decreased plasma glucose levels. These hormonal responses to beta-endorphin were amplified in the obese diabetic patients. There was a significant correlation (r = 0.61; P less than 0.01) between fasting plasma glucose levels and the integrated insulin area in response to beta-endorphin. The infusion of a lower dose of beta-endorphin (0.05 mg/h) in diabetic patients produced similar increments in both insulin and glucagon levels and also decreased plasma glucose concentration. These results indicate that beta-endorphin may have important glucoregulatory effects in man depending on the dose administered, the presence of obesity, and the prevailing plasma glucose concentration.

Adult↗
PubMed1984

Rapid decrease of platelet aggregation (ADP--and collagen--induced) and of platelet circulating aggregates by the artificial pancreas in insulin-dependent diabetics.

The aim of the present study was to evaluate the role of the strict metabolic control achieved with the aid of an artificial pancreas (Biostator, Miles) on platelet functions in insulin-dependent diabetics (n = 20). Platelet aggregation responses to both ADP and collagen, as well as circulating platelet aggregates according to Wu and Hoak, were determined before and after 24 hours of complete metabolic control; as control group, 18 insulin-dependent diabetics were only monitored without attempts to normalize their blood glucose behaviour. A significant decrease in ADP induced aggregation (p less than 0.01) and circulating platelet aggregates (p less than 0.001) was observed in diabetics during the period of strict metabolic control. No changes were observed in the control group. The present data suggest that the increased platelet activity in diabetes is a consequence of the metabolic derangement of the disease.

Adenosine Diphosphate↗
PubMed1983

[Changes in mean erythrocyte volume and 2,3-diphosphoglycerate in two groups of diabetic subjects].

Mean corpuscular volume and Red Blood Cell 2-3, diphosphoglycerate in insulin dependent diabetics and in non insulin dependent diabetics were evaluated. Only in insulin dependent diabetics an increased mean corpuscular volume was found while in non insulin dependent diabetics red blood cell 2-3, DPG level appears to be reduced. These findings were not correlated with the metabolic parameters neither they seemed to be dependent upon sex, age or vascular disease. The Authors suggest that the increase of mean corpuscular volume might be indicative of a tendency to macromegaloblastosis in insulin dependent diabetics; with regard to RBC 2-3, DPG level it seems to be extremely variable in dependence on oxygen request at the tissue level.

2,3-Diphosphoglycerate↗
PubMed1983

Glucose tolerance and hormonal responses in heroin addicts. A possible role for endogenous opiates in the pathogenesis of non-insulin-dependent diabetes.

Plasma glucose, insulin, glucagon, and growth hormone responses to intravenous glucose stimulation were investigated in 15 heroin-dependent men and in 15 control subjects matched for age, sex, and weight. Although the fasting concentrations of insulin, glucagon, and GH were significantly higher in the heroin addicts, they had markedly reduced plasma insulin responses to intravenous glucose (acute insulin response, calculated as the mean change in insulin levels over 3 to 10 minutes: 10 +/- 5 microU/mL in the addicts v 44 +/- 9 microU/mL in the controls, P less than 0.001) and glucose utilization rates in the diabetic range (KG: 0.96 +/- 0.09%/min in the addicts v 1.65 +/- 0.10%/min in the controls, P less than 0.01). These results show that chronic heroin administration produces a state of fasting hyperinsulinemia even in the absence of obesity, glucose intolerance, and a marked reduction of the first phase of insulin secretion. A possible role for endogenous opiates in the pathogenesis of non-insulin-dependent diabetes is hypothesized.

Adolescent↗
PubMed1983

A role for endogenous prostaglandin E in biphasic pattern of insulin release in humans.

These studies were undertaken to evaluate in humans the possible physiological role of prostaglandins of the E series (PGE) in modulating insulin release and to assess whether endogenous PGE synthesis may account for the biphasic pattern of insulin secretion. We used a square-wave glucose stimulation previously determined to give maximal biphasic insulin release. Infusion of lysine acetylsalicylate to block the synthesis of endogenous PGE increased by twofold total insulin response to glucose and also converted insulin release to a multiphasic pattern. The infusion of exogenous PGE1 (0.2 microgram X kg-1 X min-1) or PGE2 (10 micrograms/min) in addition to lysine acetylsalicylate restored the typical biphasic pattern of insulin release and also decreased total insulin release to values similar to those of control studies. Infusion of either PGE1 or PGE2 in the absence of lysine acetylsalicylate reset insulin secretion to a lower level without altering the kinetics of release. On the basis of these results, it is hypothesized that endogenous PGE released in response to glucose stimulation exert an inhibiting effect on insulin release that becomes biphasic in appearance.

Analgesics↗
PubMed1983

[Effect of pentoxifylline on the dissociation curve of oxyhemoglobin].

In 9 subjects with peripheral vascular insufficiencies the AA. have studied the behaviour of the oxyhaemoglobin dissociation curve before and after pentoxyphilline infusion. After this drug no variations were observed as it regards MCHC, 2-3-DPG and so on; however a positive correlation was found between 2-3-DPG and the Hill number. These results suggest that 2-3-DPG may influence the Hill number (which is the expression of the gradient of the oxyhaemoglobin dissociation curve) and therefore may interfere with O2 transport.

Aged↗
PubMed1982

Calcitonin modulation of insulin and glucagon secretion in man.

These studies were undertaken to evaluate the effect of different doses of calcitonin on insulin and glucagon responses to intravenous glucase loads and to assess the mechanism/s by which calcitonin inhibits insulin secretion in man. In our studies, even the infusion of the 1-U dose of calcitonin was found to inhibit by 45% the acute insulin response to a glucose (20 g) pulse. This effect was associated with a significant decrease in glucose disappearance rates. These negative effects of calcitonin on both insulin secretion and glucose tolerance were dose-related. The inhibition of the acute insulin response to glucose was 65% and up to 90% with the infusion of the 4- and 8-U doses, respectively. The suppressive effect of glucose on glucagon secretion was significantly reduced by calcitonin. The inhibitory effect of calcitonin on insulin responses to glucose (5 g) and glucose tolerance was reversed by both theophylline and calcium. By contrast, infusion of lysine acetylsalicylate to block the synthesis of endogenous prostaglandins did not diminish the inhibitory effect of calcitonin on insulin secretion. These results demonstrate that a) calcitonin inhibits glucose-induced insulin responses and deteriorates glucose tolerance in normal humans in a dose-dependent manner; b) calcitonin reduces the suppressive effect of glucose on glucagon secretion in a dose-related fashion; and c) both theophylline and calcium reverse the inhibitory effect of calcitonin on insulin secretion. It is hypothesized that calcitonin effects on insulin and glucagon release are mediated via a change in calcium redistribution in the islet cells.

Blood Glucose↗
PubMed1982

Glucagon secretion in patients with hypoparathyroidism: effect of serum calcium on glucagon release.

The aim of the present study was to evaluate the influence of changes in the serum calcium concentration upon glucagon secretion in man. For this purpose, a group of subjects with either idiopathic (four cases) or secondary (two cases) hypoparathyroidism was submitted to an arginine test (0.5 g/kg) before and after the correction of hypocalcemia. In the presence of hypocalcemia, the glucagon response to the amino acid was modest and delayed (glucagon peak, 150 +/- 28 pg/ml). The acute correction of hypocalcemia produced a striking increase in basal glucagon levels (125 +/- 24 vs. 75 +/- 15 pg/ml; P less than 0.01) and restored the glucagon peak in response to arginine (270 +/- 50 pg/ml; P less than 0.01). The increase in plasma glucose triggered by arginine was augmented under normocalcemic conditions, while the pattern of plasma insulin response was quite similar. These results indicate that glucagon secretion in man is critically dependent on the serum calcium concentration.

Adult↗
PubMed1982

A possible role of gamma-aminobutyric acid in the control of the endocrine pancreas.

This study examines the effect of baclofen, a specific gamma-aminobutyric acid analog which crosses the blood-brain barrier freely, upon insulin, glucagon, and GH responses to iv glucose in normal man. Normal subjects received two consecutive iv glucose tolerance tests (0.33 g/kg) before and after the acute oral administration of 5, or 10 or 20 mg baclofen, respectively, (10 subjects for each group). The dose of baclofen was divided and given 8 and 1 h before the performance of the posttreatment test. A fourth group of normal subjects served as placebo group (8 subjects). The highest dose of baclofen significantly increased insulin responses to glucose and raised basal glucagon levels (P less than 0.01). No significant change occurred with the other doses. Baclofen produced a dose-related increase in basal GH levels; a 10-fold increase was observed with the 20-mg dose. However, glucose-induced glucagon and GH suppression were not affected by baclofen. Despite the increased hormonal secretions, glucose tolerance did not change after baclofen. These results seem to indicate that gamma-aminobutyric acid may play a role in the neuroendocrine control of the pancreatic islets.

Administration, Oral↗
PubMed1982

Glucose metabolism in patients receiving chronic calcitonin treatment.

The effect of long term (two months) administration of synthetic salmon calcitonin (100 MRC Units per day) on plasma glucose, insulin, C-peptide, glucagon and growth hormone responses to iv glucose and arginine were investigated in patients with either Paget's disease of bone (n = 6) or significant osteoporosis (n = 9). Glucose tolerance did not deteriorate after treatment, despite a reduction in the early insulin response to glucose, resetting of the C-peptide response at a lower level and a reduction in glucose-mediated glucagon suppression. The rise in plasma glucose triggered by arginine was reduced after treatment despite similar hormonal environment. This seems to suggest a positive influence of calcitonin on glucose disposal. The diabetogenic action of acute calcitonin administration is not observed after prolonged administration of the hormone. However, the possibility that calcitonin may produce a diabetic state in subjects with decreased insulin reserve cannot be totally exclused.

Aged↗
PubMed1982

Influence of acetylsalicylic acid on glucose turnover in normal man.

This study was designed to evaluate the influence of intravenous infusion (72 mg min-1) of lysine acetylsalicylate (LAS), an inhibitor of endogenous prostaglandin synthesis, on glucose homeostasis in normal man. LAS infusion produced a transient decrease of both hepatic glucose production (Ra, p less than 0.01) and peripheral glucose uptake (Rd, p less than 0.01). Since Ra fell more than Rd, a slight but significant decrease of plasma glucose concentration occurred. Glucose metabolic clearance rate also showed a rapid, although transient, decrease after the start of LAS infusion. Plasma insulin rose twofold in response to LAS, while plasma glucagon remained unchanged. The failure of the glucose clearance to increase as a consequence of the augmented insulin levels suggests that salicylate compounds may cause a state of insulin resistance.

Adult↗