1,721,012 research outputs found
α2-Adrenergic stimulation enhances growth hormone secretion in the dog: a presynaptic mechanism?
No full textntravenous administration of clonidine (CLO), (2,4 and 8 ug/kg), a predominantly α2-adrenergic receptor agonist, induced in unanesthetized dogs clear-cut and dose -related rises in plasma GH (cGH) levels. Pretreatment with the selective antagonist of α1-adrenergic receptors prazosin (0.1 mg/Kg iv) left unaltered the cGH rise inducedby 4 ug/Kg of CLO whilst blockade of α2-adrenergic receptors by yohimbine (2.5 mg/Kg iv) completely prevented it. In dogs treated 24 h previously with reserpine (0.5 mg/Kg iv), a depletor of brain catecholamine stores, CLO was ineffective to stimulate cGH release. These data indicate that in the dog the GH-releasing effect of CLO occurs via stimulation of α2-adrenergic receptors and suggest that the latter are located presynaptically in relation to norepinephrine neurons
Effect of agonists and antagonists of cholinergic neurotransmission on growth hormone release in the dog
No full textIn unanesthetized dogs iv administration of the cholinesterase inhibitor eserine (0.5 mg) or the cholinergic muscarinic receptor agonist oxotremorine (0.25 mg) induced a clear-cut rise in plasma canine growth hormone (cGH) levels. Complete suppression of the GH-releasing effect of eserine and oxotremorine was induced by blockade of cholinergic muscarinic receptors by atropine (80 or 20 μg/kg, 30 min before) but not by scopolamine-N-butyl bromide (0.8 mg/dog, 30 min before), an anticholinergic drug which does not cross the blood brain barrier (BBB). In contrast, activation of cholinergic nicotinic receptors by nicotine (6 mg) failed to alter resting cGH concentrations, and pre-treatment with the nicotinic receptor blocker mecamylamine (5 mg, 30 min before) did not counteract the GH-releasing effect of eserine. Other cholinomimetic drugs, e.g. pilocarpine, 4-aminopyridine, carbachol and bethanechol failed to induce a rise in plasma cGH concentrations. These data indicate that: cholinergic muscarinic but not nicotinic receptors located in the central nervous system (CNS) inside the BBB play a facilitatory role in tonic cGH release; pharmacologically distinct muscarinic receptors may exist in the CNS
Muscolar expression of MGF, IGF-1Ea and myostatin in intact and hypofysectomized rats : effects of rhGH and testosterone alone or combined
No full textA follow-up of GH-dependent biomarkers during a 6-month period of the sporting season of male and female athletes
No full textIn order to verify the effects of the sporting season (entailing periods of training, competition, recovery, resting) on GH-dependent parameters in male and female athletes from different sporting disciplines, 47 male and female athletes (3 rowers, 5 swimmers, 7 alpine skiers, 3 soccer players, 7 middle distance runners, 14 sprinters, 4 triathletes, 1 road walker, 3 cyclists) were followed-up for a period of 6 months. Blood samples were taken every two months for the evaluation of IGF-I, N-terminal propeptide of type III procoliagen (PIIINP) and C-terminal cross-linked telopeptide of type I collagen (ICTP). Abnormal IGF-I, PIIINP and ICTP levels were observed during the follow-up period in 7/100 (7%), 9/100 (9.0%) and 8/100 (8%) samples of the male group, respectively, and in 9/88 (10.2%), 1/88 (1.1%) and 0/88 (0%) samples of the female group, respectively. Abnormal levels appeared to be randomly distributed over the different periods of the sporting season and within male and female subjects, with the large majority of abnormal values being found in the younger athletes. Taking into account all the tests done during the 6-month period (no. 564), individual markers failing outside the normal range (for age) were observed in a small number of instances (34/564 tests done, 24/300 for males and 10/264 for females). When our method for the detection of exogenous recombinant GH (rhGH) administration, based on the concomitant determination of these three peripheral GH-dependent markers and on the attribution of specific scores, was applied in the same athlete at a given time point of the 6-month period, the prevalence of a positive score was extremely low (ie, 3/188 samples or 1.6%). Total positive scores were actually recorded in only three male athletes (2 swimmers and 1 skier, aged <21 yr) at one occasion during the 6-month period considered. In contrast, no total positive scores were found in female athletes (ie, 0/88 samples). In conclusion, the concentrations of IGF-1, PIIINP and ICTP were stable and not significantly modified during 6 months of a sporting season (entailing periods of training, competition, recovery, resting) in athletes from different sporting disciplines. Therefore our method, based on the concomitant determination of three peripheral GH-dependent biomarkers appears safe, acceptable, relatively inexpensive and repeatable (in case of positive or suspected values) immediately or at different intervals of the sporting season. Further additional studies are requested to precise the cut-off values for narrower age-class subdivisions in both genders in order to improve the proposed method
Growth hormone response induced by a respiratory muscle endurance training in healthy subjects
No full textTo date, the large majority of studies evaluating growth hormone (GH) response to acute physical exercise has been performed involving gross muscle groups. To the best of our knowledge, none has evaluated the effects of a respiratory muscle endurance training (RMET) on hormonal secretions, particularly on GH release, though some respiratory devices have been widely used in athletes to train respiratory muscles and to improve cardiopulmonary function and physical performance. 8 healthy men underwent an incremental progressive RMET protocol of 11 daily sessions, obtained through the use of a specifically designed respiratory device (Spiro Tiger). The 12th session of RMET (15 min duration: 1 min at a respiration rate of 28 acts/min, 5 min at 32 acts/min, 5 min at 34 acts/min, 4 min at 36 acts/min) was associated with blood samplings for determination of GH, cortisol, ghrelin, glucose, and lactate (LA) levels. GH and cortisol responses significantly increased after a 15-minute RMET session, which, in contrast, inhibited ghrelin secretion. There was a minimal, though significant, increase in LA levels with a significant elevation in glycemia. A 15-minute RMET session, administered after a 11-days incremental progressive RMET protocol, was capable of stimulating GH and cortisol release and suppressing ghrelin secretion. Optimization of incremental progressive RMET protocols would be important to maximize the positive chronic effects of this intervention on somatotropic function and muscle performance
The leukocyte expression of CD36 is reduced in patients with Alzheimer disease and in early phase of dementia
No full textLa transizione menopausale : un milieu biologico-endocrino che predispone alla neurodegenerazione
No full textMuscle expressions of MGF, IGF-IEa and myostatin in intact and hypophysectomized rats : effects of rhGH and testosterone alone or combined
No full textMyostatin and mechano-growth factor (MGF), an isoform of insulin-like growth factor-I (IGF-I), are two important regulators of muscle hypertrophy. The aim of the present study was to investigate the effects of recombinant human growth hormone (rhGH) and/or testosterone on muscle MGF/IGF-IEa/myostatin expression in intact and hypophysectomized rats treated for 15 d with 1) saline or rhGH, 2) sesame oil or testosterone, 3) saline+sesame oil, or rhGH+testosterone (first experiment) or for 7 d with saline or rhGH (second experiment). Animals were killed by decapitation 24 h or 4 d after the last injection (first or second experiment, respectively). Muscle expressions of MGF, IGF-IEa, and myostatin were determined by RT-PCR. A significant increase in the weight of gastrocnemius muscle was observed only in hypophysectomized rats treated with rhGH alone or in combination with testosterone. Administration of rhGH to hypophysectomized rats caused a marked increase in both MGF and IGF-IEa muscle mRNA levels (without any change in the muscle expression of myostatin), an effect that was abolished when testosterone was combined with rhGH. Conversely, in intact rats rhGH increased myostatin muscle mRNA levels without affecting those of MGF and IGF-IEa. Testosterone, alone or combined with rhGH, induced an inhibition of myostatin expression in the muscle of intact rats, but did not change muscle paradigms of hypophysectomized rats. In conclusion, rhGH and/or testosterone anabolic effects in the muscle are mediated by a different expression of MGF/IGF-IEa/myostatin, which is related to the pituitary function
Prolactin lowering effect of amphetamine in normoprolactinemic subjects and in physiological and pathological hyperprolactinemia
No full textThe effect on plasma prolactin (PRL) of d-amphetamine (Amph) was studied in normo- and hyperprolactinemic subjects. In normoprolactinemic women Amph failed to lower plasma PRl levels when infused intravenously over 1 h at the dose of 7.5 mg, but induced at the dose of 15.0 mg a modest inhibition of plasma PRL (maximum PRL inhibition 20 ± 4.5% at 45 min). Likewise, in puerperal women Amph at the dose of 7.5 mg did not decrease significantly plasma PRL levels but it was active in this respect (maximum inhibition 37 ± 10% at 120 min) at the dose of 15.0 mg. In subjects with presumptive evidence of a PRL-secreting adenoma, Amph at either the 7.5 mg or the 15.0 mg dose failed to alter baseline PRL levels. These results indicate that Amph is a poor PRl suppressor in either normo- or hyperprolactinemic subjects. It is proposed that this may be due to the drug's ability to effect release of dopamine mainly from a non-granular pool of the amine
- …
