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Biomedical subjects

M Zini

Publications and source records attributed to M Zini.

13 recordsLinked to original sources
PubMed1992

Long-term therapy with high-dose simvastatin does not affect adrenocortical and gonadal hormones in hypercholesterolemic patients.

Simvastatin is an effective hypocholesterolemic drug that inhibits cholesterol synthesis selectively in the liver, but could have potential side effects on the adrenal gland, ovary, and testis, as these three glands use cholesterol for their hormonal biosynthesis. In this report, we examined adrenal and sex steroids in 10 type IIA hypercholesterolemic patients (three with familial [FH] and seven with polygenic hypercholesterolemia) over a period of 1 year on simvastatin therapy in order to confirm in vivo its selective action. Furthermore, we evaluated the adrenal reserve by a corticotropin rapid test, before starting treatment and again at the end of the third month on 20 mg of simvastatin per day, then at the sixth and 12th month on 40 mg/d. There was a significant lowering of total cholesterol (TC) (-31%), low-density lipoprotein cholesterol (LDL-C) (-39%), and apolipoprotein (apo) B (-39%); no statistically significant differences were seen in cortisol response to the corticotropin test between baseline and simvastatin-treated patients. No variation of any sex steroid was observed in patients of either gender. We conclude that long-term therapy with high-dose simvastatin does not interfere with either adrenocortical function or sex hormone production.

Adrenal Cortex Hormones↗
PubMed1992

The late growth hormone rise induced by oral glucose is enhanced by cholinergic stimulation with pyridostigmine in normal subjects.

OBJECTIVE: We have investigated the late GH rise occurring 3-5 hours after oral glucose administration. We have assessed the effect of endogenous cholinergic enhancement with pyridostigmine on the delayed GH rise following oral glucose loading in normal subjects. DESIGN: Placebo or 75 g oral glucose was given to the normal subjects 3 hours before 120 mg oral pyridostigmine or placebo. Four tests were carried out at random. (0 min) + placebo (180 min); test 2: glucose (0 min) + placebo (180 min); test 3: placebo (0 min) + pyridostigmine (180 min); test 4: glucose (0 min) + pyridostigmine (180 min). SUBJECTS: We studied eight normal subjects (four male and four female), ages 19-29 years, body mass indices 18-22 kg/m2. MEASUREMENTS: Plasma glucose and serum GH concentrations were measured for 6 hours after oral glucose or placebo administration. RESULTS: Pyridostigmine treatment significantly enhanced the GH releasing effect of prior (3 h) oral glucose. Late GH peak obtained by oral glucose loading rose from (mean +/- SEM) 17.4 +/- 4.6 to 37.2 +/- 9.0 mU/l (P < 0.05) after pyridostigmine, while GH peak following placebo plus pyridostigmine was 12.4 +/- 2.0 mU/l (P < 0.05 vs glucose plus pyridostigmine). The analysis of GH area under curves (AUCs) in the second phase of the tests (180-360 min) confirmed that glucose plus pyridostigmine released a greater amount of GH (4128 +/- 764 mU/l/3h) than glucose (1694 +/- 494 mU/l/3h, P < 0.001) or pyridostigmine alone (1292 +/- 150 mU/I/3h, P < 0.001). CONCLUSIONS: Pyridostigmine, an indirect cholinergic drug likely to inhibit somatostatin secretion from the hypothalamus, enhanced the late GH releasing activity of oral glucose. There is evidence that glucose suppresses plasma GH initially by increasing hypothalamic somatostatin release. This would result in an increase in the pituitary stores of GH. We propose that the delayed GH rise after oral glucose occurs when there is a fall in hypothalamic somatostatinergic tone; this is further reduced by the administration of pyridostigmine. At this time the pituitary stores of GH are released as a consequence of resumption of hypothalamic GHRH activity. This leads to the late GH rise.

Administration, Oral↗
PubMed1992

Sinus node function in hyperthyroid patients.

We have studied the electrophysiology of the sinus node and the role of the autonomic nervous system on sinus node function in 8 thyrotoxic patients of both sexes, 37.5 +/- 4.3 (mean +/- SE) yr old. The resting heart rate (RHR), the sino-atrial conduction time (SACT), and the sinus node recovery time (SNRT) were measured in the untreated condition (basal), after sympathetic blockade with propranolol 0.2 mg/kg body weight (BW) i.v. infusion, and after complete autonomic blockade with the additional administration of atropine 0.04 mg/kg BW i.v. bolus. 1) In the thyrotoxic patients the RHR was higher [117 +/- 6 beats per min (bpm)] than in 20 normal subjects (73 +/- 1 bpm, P less than 0.001), whereas the SACT and SNRT values were not different. 2) After sympathetic blockade with propranolol, the RHR decrement and SACT increase were greater in the hyperthyroid patients than in normal subjects, whereas there was no difference in SNRT values between the two groups. 3) In the thyrotoxic patients the complete autonomic blockade reestablished the electrophysiological parameters to values similar to those observed in basal condition. In conclusion, in thyrotoxic patients the intrinsic activity of the sinus node is increased. It appears that this is a direct consequence of thyroid hormone excess, rather than an effect of extrinsic influences exerted by the autonomic nervous system on sinus node activity.

Adolescent↗
PubMed1991

Effect of pyridostigmine and pirenzepine on GH responses to GHRH in hyperthyroid patients.

OBJECTIVE: We wished to investigate whether thyrotoxicosis can influence the cholinergic modulation of GH secretion. DESIGN: Pyridostigmine was given orally, then GHRH injected i.v., and levels were measured. In a separate study, pirenzepine was injected i.v., then GHRH, and growth hormone levels were measured. PATIENTS: Thyrotoxic patients were compared with normal subjects. MEASUREMENTS: GH was measured from -30 to +120 minutes at intervals of 15 minutes. RESULTS: Pyridostigmine markedly increased GH responses to GHRH in normal subjects, but not in thyrotoxic patients. Pirenzepine abolished the GH response to GHRH in thyrotoxic patients. CONCLUSIONS: GH responses to GHRH in hyperthyroid patients were suppressed by cholinergic muscarinic receptor blockade with pirenzepine. Activation of cholinergic pathways with pyridostigmine did not increase GH responses to GHRH in these patients. This may be a consequence of increased hypothalamic cholinergic function or reduced hypothalamic GHRH activity in hyperthyroidism. Our findings demonstrate a further mechanism by means of which thyroid status may affect the secretory activity of the somatotroph.

Adolescent↗
PubMed1990

Triiodothyronine administration reduces serum growth hormone levels and growth hormone responses to thyrotropin-releasing hormone in patients with anorexia nervosa.

The aim of this study was to test the hypothesis that low serum T3 concentrations may promote an abnormal growth hormone (GH) response to thyrotropin-releasing hormone (TRH) in patients with anorexia nervosa. Eight anorexic women and two anorexic men, ages 15-25 years, with low free T3 circulating levels (mean +/- SEM = 2.8 +/- 0.3 pmol/l) were studied. A TRH test (200 micrograms IV) was carried out under basal conditions and repeated following treatment with oral T3 (1.5 micrograms/kg BW/day) for eight days. Following T3 administration, GH levels dropped significantly from a baseline of 7.1 +/- 1.3 micrograms/l to 3.1 +/- 0.7 micrograms/l (p less than 0.02), as did GH peak responses to TRH (9.0 +/- 1.0 micrograms/l vs 4.4 +/- 0.8 micrograms/l, p less than 0.01). ANOVA and analysis of area under the curve (AUC) confirmed that after T3 treatment there was a significant reduction in TRH-induced GH release in these patients (GH AUC: 902 +/- 132 micrograms/l vs. 456 +/- 91 micrograms/l, p less than 0.02). TSH responses to TRH, which were normal prior to T3 treatment, completely disappeared following it, and PRL responses to TRH also were diminished. Although our experimental approach does not permit a conclusion that low T3 levels were the primary reason for these changes, the data support the theory that low T3 circulating levels may facilitate abnormal GH secretion and the GH-releasing activity of intravenous TRH.

Adolescent↗
PubMed1990

Effect of oral glucose on the late growth hormone rise and growth hormone responses to GHRH in normal subjects.

A late rise in serum GH occurs 3-5 h following oral glucose in man. In order to investigate the mechanisms through which this occurs we have studied the late GH rise after oral glucose during administration of a supramaximal dose of GHRH. In eight normal subjects, oral glucose (100 g) greatly enhanced the GH responses to a supramaximal dose of GHRH (50 micrograms bolus, followed immediately by 100 micrograms/h infusion for 3 h) given 3.5 h after the glucose. GH peak (mean +/- SEM) elicited by GHRH (bolus + infusion) rose from 55.2 +/- 20.4 to 133.4 +/- 29.6 mU/l (P less than 0.02) after glucose pretreatment. In conclusion, it is likely that the late rise in GH secretion induced by oral glucose occurs via a non-GHRH-dependent mechanism. These data are consistent with the hypothesis that the delayed GH response to glucose is a consequence of reduced release of somatostatin from the hypothalamus.

Administration, Oral↗
PubMed1988

Alpha-2-adrenergic pathways release growth hormone via a non-GRF-dependent mechanism in normal human subjects.

Administration of a supramaximal dose of GRF 1-44 (200 micrograms, i.v.) to normal human volunteers increased GH levels while a further bolus of GRF (200 micrograms i.v.) given 2 hours later failed to increase plasma GH levels. In contrast, alpha-adrenergic receptor agonism with either propranolol-adrenaline infusion or clonidine increased plasma GH levels at a time when GH responses to this supramaximal dose of GRF were absent. This indicates that alpha-adrenergic pathways stimulate GH secretion through a non-GRF-dependent mechanism in normal human subjects.

Adult↗