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Biomedical subjects

N Passariello

Publications and source records attributed to N Passariello.

At least 37 records · Page 2Linked to original sources
PubMed1986

Insulin induces opposite changes in plasma and erythrocyte magnesium concentrations in normal man.

Plasma and erythrocyte magnesium levels were measured by atomic absorption spectrophotometry in 10 healthy volunteers during an oral glucose tolerance test and during an euglycaemic hyperinsulinaemic glucose clamp. At min 180 and 210 of the oral glucose tolerance test, a significant decline in plasma magnesium levels (p less than 0.01 and p less than 0.05 respectively) and a significant increase in erythrocyte magnesium levels (p less than 0.01 and p less than 0.05 respectively) were observed. Similar changes were seen during the second hour of the glucose clamp, during which euglycaemia (4.1 +/- 0.4 mmol/l) was maintained despite hyperinsulinaemia (110-130 mU/l). During in vitro incubations, glucose (5 mmol/l) did not modify erythrocyte magnesium levels. In contrast, erythrocyte magnesium levels were significantly increased (p less than 0.01) by insulin (100 mU/l), an effect entirely abolished by ouabain (5 X 10(-4) mol/l). These results suggest that insulin induces a shift of magnesium from the plasma to the erythrocytes both in vivo and in vitro. These data may help to interprete the abnormalities in magnesium circulating levels frequently reported in diabetic patients.

Adult↗
PubMed1986

Impaired insulin response to glucose but not to arginine in heroin addicts.

Plasma glucose, insulin, glucagon and growth hormone responses to both oral glucose and iv arginine were evaluated in 15 heroin addicts and 15 control subjects matched for age, sex and weight. The heroin users had an exaggerated rise in plasma glucose concentrations following oral sugar, which persisted until the end of the study (102 +/- 5 mg/dl in addicts vs 72 +/- 3 mg/dl in controls at 240 min, p less than 0.01) and significantly lower insulin responses (insulin peak 28 +/- 4 microU/ml in addicts vs 67 +/- 8 microU/ml in controls, p less than 0.01). The inhibitory effect of glucose on glucagon concentrations was less evident in addicts than in controls. The responses of plasma glucose, insulin and glucagon to arginine were not significantly different between addicts and controls, while the growth hormone rise was significantly greater in addicts. These results demonstrate that heroin users have impaired insulin secretion to oral glucose but not to arginine and suggest that: the impaired insulin secretion in heroin addicts is not dependent on beta-cell exhaustion, and a selective inhibition of glucose-induced insulin secretion is operative in these subjects, as it happens in patients with noninsulin-dependent diabetes mellitus.

Adult↗
PubMed1986

Effect of sparteine sulfate on insulin secretion in normal men.

This study aimed at evaluating the influence of sparteine sulfate either upon basal plasma glucose and insulin or glucose-induced insulin secretion in normal man. Thirteen overnight fasted volunteers took part in this study; five of them were submitted to sparteine sulfate bolus (15 mg in 10 ml of saline solution) followed by a slow infusion (90 mg/100 ml X 60 min) and eight subjects underwent two different glucose pulses (20 gr. i.v.) in absence or in presence of sparteine, infused as described above. In basal conditions, along with sparteine infusion, plasma glucose showed a progressive and significant decrease (P less than 0.0001) and plasma insulin was significantly higher from min 10 to 120' (P less than 0.0005-0.001). Even during the glucose-induced insulin secretion, in the presence of sparteine infusion, plasma glucose levels were significantly lower while plasma insulin levels were significantly higher when compared to those observed after glucose alone. The acute insulin response (AIR) was 42 +/- 10 microU/ml after glucose alone vs 67 +/- 9 microU/ml after glucose plus sparteine (P less than 0.05). Total insulinemic areas were significantly different being 1410 +/- 190 vs 2250 +/- 310 microU/ml/min (P less than 0.001) during glucose and glucose plus sparteine infusion, respectively. This study thereby, demonstrates that in normal man sparteine sulfate, administrated by intravenous infusion, is able to increase either basal or glucose-induced insulin secretion.

Adult↗
PubMed1986

Plasma calcitonin variations in normal women and in women with family history of diabetes during pregnancy.

In eight normal pregnant women and in eighteen women with a family history of diabetes, plasma calcitonin (CT), parathyroid hormone (PTH), insulin and glucagon variations and total plasma calcium levels were investigated. Calcitonin, parathyroid hormone and glucagon were all increased during the 2nd and 3rd trimester of pregnancy in normal women (N.W.) and in women with a family history of diabetes (W.F.H.D.). Plasma calcitonin levels were statistically significantly different between the two groups only in the 3rd trimester (118 +/- 4.9 vs 139 +/- 3.6 pg/ml p less than 0.01 in N.W. and W.F.H.D. respectively). Total plasma calcium levels were decreased significantly in the 3rd trimester in both groups: 3rd vs 1st trimester p less than 0.005 and p less than 0.001 in N.W. and W.F.H.D. respectively. Statistically significant difference between the two groups in total insulinemic area (p less than 0.001), in the rapid phase area (p less than 0.01) and insulinogenic index (p less than 0.05) were observed in the 3rd trimester.

Calcitonin↗
PubMed1985

Impaired insulin secretion in human diabetes mellitus. Interactions between naloxone, phentolamine and lysine acetylsalicylate upon glucose induced insulin release.

Non insulin-dependent diabetes mellitus (Type II) is characterized by the loss of the acute insulin response to glucose. Met-enkephalin, catecholamines and prostaglandin E (PGE) have all been reported to inhibit the acute insulin response to glucose in normal humans. To evaluate the hypothesis that an increased sensitivity to these endogenous substances may play a role in defective insulin secretion in diabetes, we evaluated the effects of three blocking drugs upon the impaired insulin response to glucose in Type II diabetic subjects, as well as glucose-induced insulin secretion in normal humans. In diabetics, acute insulin responses to glucose were significantly increased by all the agents tested (naloxone, phentolamine and lysine acetylsalicylate), but only the cyclooxygenase inhibitor significantly augmented second phase insulin secretion and glucose disappearance rates. The combined infusion of the three agents caused a striking increase of the acute insulin response to glucose (response before: 3 +/- 2 uU/ml; after: 22 +/- 6 uU/ml, p less than 0.01). This was accompanied by a ninefold augmentation of the second phase of insulin secretion which was the result of a synergistic interaction between the three drugs (response significantly higher than the sum of single effects). In normals, insulin responses to glucose were also significantly increased by the combined infusions of the drugs, but to a significantly lesser extent than that of diabetics. This different degree of insulin potentiation between normals and diabetics under the infusion of the three agents persisted even when the prestimulus glucose level of normals was matched to that of diabetics by a glucose infusion.(ABSTRACT TRUNCATED AT 250 WORDS)

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

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

Glycosaminoglycans in human diabetes.

The serum concentrations of different glycosaminoglycan fractions have been studied in diabetic subjects without evidence of vascular complications and compared with those of age-and sex-matched normal subjects. Electrophoretic analysis of the various glycosaminoglycan fractions showed an increase in hyalunoric acid and heparin, and a decrease in heparan sulfate, chondroitin-4-sulfate and chondroitin-6-sulfate. Furthermore, the levels of glycosylated haemoglobin A1 were positively correlated with those of hyaluronic acid (r = 0.96, p. less than 0.001) and heparin (r = 0.45, p less than 0.01) in the diabetic group. The present data suggest thah a) in diabetics there is a shift in the metabolism of glycosaminoglycans towards a decreased sulfated glycosaminoglycans/hyaluronic acid ratio; and b) long-lasting hyperglycemia is correlated with the disturbances in the metabolism of glycosaminoglycans.

Adult↗
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↗