Search PubMed⌕ Search

Biomedical subjects

L Capretti

Publications and source records attributed to L Capretti.

84 records · Page 5Linked to original sources

TSH and PRL responses to domperidone and TRH in men with insulin-dependent diabetes mellitus of different duration.

The effect of domperidone, a specific blocker of dopamine receptors, on serum TSH and PRL levels was evaluated in 16 euthyroid men affected by insulin-dependent diabetes mellitus (IDDM) of different duration and in 7 age-matched normal controls. Diabetics were divided into 2 groups of 8 men according to the duration of their disease (group I: 1-9 years; group II: 11-18 years). Both groups had normal basal levels of TSH and PRL. Responses of these hormones to domperidone were similar in normal controls and in group I diabetics, whereas they were significantly reduced in patients of group II. When all 16 diabetics were studied together, a significant negative correlation was found between mean maximal peaks of TSH and PRL responses to domperidone and duration of diabetes. In order to evaluate whether the reduced effect of domperidone in diabetics was due to alterations of the dopaminergic control of TSH and PRL secretion, the domperidone test was repeated in 6 normal controls and in 6 diabetics of group II after infusion of dopamine (4 micrograms/kg/min for 2 h). Dopamine infusion induced parallel decreases in TSH and PRL concentrations, without modifying hormonal secretory patterns in response to domperidone. These data suggested that the reduced TSH and PRL responses to domperidone in diabetics were not due to alterations of the dopaminergic control of pituitary function but to a defect at the pituitary level. To test this hypothesis, TSH and PRL responses to TRH were evaluated in group I and group II diabetics and in normal controls.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Effect of domperidone on the release of insulin after intravenous glucose load in man.

To determine whether the blockade of the dopaminergic system is capable of modifying glucose-induced insulin release in man, the responses of insulin to an iv glucose load were measured at various domperidone infusion rates. The infusion of 5 micrograms/kg/min of domperidone increased significantly plasma insulin levels during the acute phase of glucose-induced insulin release and lowered plasma glucose values at 50 and 60 min; the k of glucose disappearance improved significantly. At lower domperidone infusion rates the acute increment of insulin after glucose load was indistinguishable from the response observed at 5 micrograms/kg/min until 0.5 microgram/kg/min, while similar responses in control and experimental tests were observed at 0.25 microgram/kg/min. A group of subjects was submitted to an arginine load in order to establish whether the effect observed with domperidone was specific for the glucose-induced insulin release; but, this time, we did not observe any significant effect during the domperidone-induced dopaminergic blockade. Furthermore, we also measured the plasma prolactin levels, to see whether the specific and well known effect of domperidone on prolactin release matches with the effect on beta-cell function. As far as prolactin is concerned, we observed a dose response effect of domperidone infusion, with a detectable elevation of prolactin at infusion rate of 0.25 microgram/kg/min. Since domperidone is a specific antagonist of dopamine D2-receptors, we propose that dopamine might exert a specific inhibiting effect on glucose-induced insulin release through this class of dopamine receptors.

Adult↗

Lack of effect of intravenous metformin on plasma concentrations of glucose, insulin, C-peptide, glucagon and growth hormone in non-diabetic subjects.

A study was carried out to evaluate the acute effect of an intravenous injection of metformin on the fasting plasma concentrations of glucose, insulin, C-peptide, glucagon and growth hormone in 15 non-diabetic subjects. Metformin (1 g) was administered as a bolus in a peripheral vein and blood was sampled 2, 5, 10, 15 and 30 minutes after the drug injection. No significant change in fasting concentration of glucose nor in C-peptide, insulin, glucagon and growth hormone fasting levels was noticed. It is concluded that metformin does not possess an acute direct hypoglycaemic effect in non-diabetic subjects and does not acutely affect the basal activity of endocrine pancreas and pituitary gland in releasing insulin, glucagon and growth hormone.

Adult↗

The growth hormone response to thyrotropin-releasing hormone in insulin-dependent diabetics involves a cholinergic mechanism.

In order to establish whether cholinergic receptors mediate GH secretion induced by TRH in insulin-dependent diabetes, 10 patients were treated with pirenzepine, an anticholinergic agent, and tested with TRH. Basal concentrations of GH were elevated in these patients and 8 of 10 patients responded to TRH with a significant rise in GH levels. Pretreatment with pirenzepine (40 mg given iv 10 min before TRH) suppressed the TRH-induced GH rise. Pirenzepine had no effect on TRH-induced TSH release. This finding suggests that a cholinergic mechanism is involved in the paradoxical response of GH to TRH in diabetic patients.

Adult↗

Evidence that basal beta cell activity may play a role in determining insulin sensitivity in healthy man.

Aim of this investigation was to correlate basal beta cell function and insulin sensitivity in healthy man. A group of 10 healthy subjects with normal body weight and glucose tolerance was studied. Insulin sensitivity was assessed by glucose disappearance rate after insulin injection (0.1 IU/kg body weight). Beta cell secretion rate was estimated by the evaluating of fasting C peptide circulating levels. A positive and significant relationship was observed between fasting C peptide concentrations and coefficients of insulin sensitivity (r = 0.694, p less than 0.05). We conclude that in healthy man basal beta cell secretion rate plays an important role in determining the peripheral sensitivity to insulin. In particular, hormone sensitivity is directly proportional to pancreatic hormone production in basal condition.

Adult↗

Influence of hypothalamus on glucose utilization by adipose tissue of normal rats.

This study was designed to investigate whether Ventro-Medial and Ventro-Lateral Hypothalamus exert a direct effect upon the glucose uptake by rat adipose tissue. VMH, VLH and pieces of cortex as controls were removed from normal rats fasted for either 6 h (Exp. A), or 14 h (Exp. B), or made hyperglycemic by i.p. injection of glucose (Exp. C). The tissue pieces were then incubated for 30 minutes at 37 degrees C in Gey-Gey buffer. Aliquots of these incubates were then added to flasks containing epididimal fat pads of rats fasted 6 h, U-14C-glucose and unlabeled glucose to a final concentration of 1 mg/ml and incubated for additional 3 h at 37 degrees C. In exp. A the glucose utilization by adipose tissue was not affected by the addition of either VMH or VLH incubation media, when compared to controls. In exp. B a significant increase of glucose utilization was elicited by the addition of VLH incubates, while in exp. C the addition of VLH incubation media produced a significant decrease of glucose uptake by adipose tissue. The addition of VMH incubates had no significant effect in any of these experimental conditions. These results support the hypothesis that a hypothalamic factor may have a direct action upon glucose utilization by the adipose tissue, independently of the control exerted by hypothalamus on insulin and glucagon release.

Adipose Tissue↗

Intravenously infused substance P enhances basal and growth hormone (GH) releasing hormone-stimulated GH secretion in normal men.

The effect of synthetic substance P (SP), infused intravenously (IV) in doses of 0.5, 1, or 1.5 pmol/kg-1/min-1 over 60 min, on GH secretion was evaluated in seven healthy men. Substance P tests and a control test with normal saline were randomly performed at weekly intervals. No untoward side effects or changes in blood pressure were observed during SP infusions. Serum GH concentrations did not change when normal saline, the lowest dose, or the middle dose of SP were infused. In contrast, GH levels rose significantly when the highest dose of SP was given, with a mean peak two times higher than baseline. Further studies were performed to test the possible influence of SP on the GH response to GH-RH. For this purpose, seven other healthy men were tested with GH-RH (1 micrograms/kg body weight in an IV bolus) during saline or SP (1.5 pmol/Kg-1/min-1 x 60 min) infusion. The GH-RH induced a significant GH rise, with a mean peak seven times higher than baseline. When subjects were infused with SP, the GH response to GH-RH was greatly enhanced, with a mean peak 12 times higher than baseline. These results demonstrate for the first time in humans that the systemic infusion of SP stimulates GH secretion, and suggest that SP might interact with GH-RH in the stimulation of GH secretion.

Adult↗