48,506 research outputs found
Opioids stimulate growth hormone (GH) release in man independently of GH-releasing hormone.
No full textThe Met-enkephalin analog DAMME [D-Ala2,MePhe4-Met-enkephalin-(o)-o1, FK 33-824] can stimulate GH secretion in man. In this study we investigated the effects of the guanyl derivative of DAMME (G-DAMME) on the serum GH response to an analog of GHRH in normal men. GHRH-(1-29)NH2 and G-DAMME each induced a rise in serum GH, and the increase was greater when both were given together. Since the GHRH-(1-29)NH2 dose (100 micrograms) used was a maximally stimulatory one, these results suggest that the enhancing effect of G-DAMME on GHRH-induced GH release may be mediated through inhibition of somatostatin release. Z9 1
Adrenergic stimulation of the human pituitary-adrenal axis is attenuated by an analog of met-enkephalin.
No full textIt has previously been suggested that endogenous opioid peptides may suppress the pituitary-adrenal axis in man by inhibiting an excitatory alpha 1-adrenoceptor input to neural mechanisms liberating corticotrophin-releasing factor or factors (CRFs). This hypothesis has been tested here by investigating the effect of the met-enkephalin analog, DAMME (FK-33,824), on the elevation in serum cortisol induced by the catecholamine-releasing agent d-amphetamine (10 and 25 mg p.o.) and the direct alpha 1-adrenoceptor agonist methoxamine (6 micrograms/kg/min i.v.) in two groups of 6 normal male subjects. In both studies, the rise in serum cortisol was significantly attenuated by the analog of met-enkephalin. These data suggest that exogenous opioids act as a site downstream to the alpha 1-adrenoceptor input to CRF release; it appears that opioids modulate adrenocorticotrophic hormone release in man at a minimum of two distinct and separate sites. Z9 1
Interleukin 1beta and interleukin-6 specifically increase the release of prostaglandin E2 from rat hypothalamic explants in vitro
No full textThe effect of growth hormone replacement therapy on adrenal androgen secretion in adult onset hypopituitarism
No full textOBJECTIVE: Growth hormone replacement therapy in GH-deficient children is associated with enhanced adrenal androgen production, raising the possibility that GH might stimulate adrenocortical hormone secretion. This has not been extensively investigated in adults to date. GH is a potent modulator of the activity of the 11beta-hydroxysteroid dehydrogenase type 1 (11beta-HSD1) enzyme and by altering cortisol metabolism can affect the function of the hypothalamo-pituitary-adrenal (HPA) axis and therefore potentially of adrenal androgen secretion. This study examined the effects of GH replacement in GH-deficient adults on adrenal androgen secretion. DESIGN: Prospective study of the effect of GH replacement therapy on adrenal androgen production in patients with adult onset hypopituitarism over a 12-month period. PATIENTS AND METHODS: Thirty adult GH-deficient patients were classified into two groups according to their cortisol responses to an insulin-induced hypoglycaemia or a glucagon stimulation test: 13 patients were adrenocorticotropic hormone (ACTH)-sufficient (nine females, age 45.1 +/- 3 years), whereas 17 patients were ACTH-deficient (11 females, age 45.5 +/- 3 years). Serum samples were collected before patients were initiated on GH replacement therapy using a dose titration regimen, and after 6 and 12 months on GH therapy for measurement of serum IGF-I, dehydroepiand-rosterone sulphate (DHEAS), Delta4-Androstenedione (A4), testosterone, cortisol, sex hormone binding globulin (SHBG) and cortisol binding globulin (CBG). RESULTS: Six months after the initiation of GH replacement therapy, serum IGF-I levels were within the normal age-related reference range in both groups of patients and this was maintained at 12 months [in all patients 0 vs. 6 months: median (interquartile range): 92.5 ng/ml (73-116 ng/ml) vs. 191 ng/ml (159-224 ng/ml), P < 0.01]. In both ACTH-sufficient and -deficient groups of GH-deficient patients, pretreatment serum DHEAS levels were lower than the normal age-related reference range (P < 0.01); the ACTH-deficient patients had significantly lower DHEAS levels than the ACTH-sufficient patients [median (interquartile range): 0.5 micro mol/l (0.4-1.2 micro mol/l) vs. 1.5 micro mol/l (0.6-2.7 micro mol/l), P < 0.05]. Following GH replacement therapy, median levels of serum DHEAS levels rose from 1.5 micro mol/l (0.6-2.7 micro mol/l) to 1.9 micro mol/l (1.9-3.9 micro mol/l) in ACTH-sufficient patients, increasing in 11 of the 13 patients (P < 0.02). In this group, the median percentage increase from baseline was 32% at 6 months (P < 0.05). In contrast, baseline serum DHEAS levels [0.5 micro mol/l (0.4-1.2 micro mol/l)] declined in or from the measurable range in 47% of ACTH-deficient patients [median -16%; range -36-0] and only in one patient a + 0.2 micro mol/l increase was observed. GH dose requirements tended to be lower in ACTH-sufficient patients [1.2 U/day (0.8-1.4 U/day) vs. 1.6 U/day (1.0-2.0 U/day); P = 0.062]. There were no significant changes in serum testosterone, A4, SHBG and/or CBG levels, compared to the pretreatment levels, in either group of patients over the 12 months of GH replacement. CONCLUSIONS: This study shows that median serum DHEAS levels are significantly lower in GH-deficient patients, even those with intact ACTH reserve, than in aged-matched controls. GH replacement therapy is associated with a significant increase in mean serum DHEAS only in ACTH-sufficient patients. These findings are consistent with either (i) GH stimulation of adrenal androgen production in the permissive presence of ACTH or (ii) an inhibitory effect of GH on 11beta-HSD type 1 activity leading to enhanced cortisol clearance, subsequent activation of the HPA axis and ACTH-mediated androgen secretion
Melatonin and its analogs inhibit the basal and stimulated release of hypothalamic vasopressin and oxytocin in vitro
No full textStudio dell'effetto della melatonina e suoi analoghi sul rilascio di ossitocina e vasopressina in un modello di espianti di ipotalamo in vitro: i dati indicano un effetto inibitorio sul rilascio dei due ormoni, sia in consizioni basali che sotto stimolazione con KC
G. M. Hopkins
No full text[sound recording] / Brendan O'Grady. G. B. Shaw by Fran Frazer.; 1 sound cassette (60 minutes); Broadcast on CFCY Radio, Charlottetown, March 07 & 11, 1974.; G. B. ShawSource type: Electronic(1
Arginine is unlikely to exert neuroendocrine effects in human via the generation of nitric oxide
No full textDifferential effects of neuroexcitatory aminoacids on CRH-41 and vasopressin release from rat hypothalamic explants
No full textStudio sull'effetto degli aminoacidi eccitatori NMDA, kainato e quisqualato sul rilascio di CRH da espianti di ipotalamo di ratto in vitro, e suo significato nella regolazione neuroendocrin
Erratum to: Effect of moderate red wine intake on cardiac prognosis after recent acute myocardial infarction of subjects with Type 2 diabetes mellitus (Diabetic Medicine, (2006), 23, 9, (974-981), 10.1111/j.1464-5491.2006.01886.x)
No full textIn an article by Marfella et al, the author name C. Saron is incorrect and should be listed as C. Sardu. Therefore the correct author list is: R. Marfella, F. Cacciapuoti, M. Siniscalchi, F. C. Sasso, F. Marchese, F. Cinone, E. Musacchio, M. A. Marfella, L. Ruggiero, G. Chiorazzo, D. Liberti, G. Chiorazzo, G. F. Nicoletti, C. Sardu, F. D'Andrea, C. Ammendola, M. Verza and L. Coppola.In an article by Marfella et al, the author name C. Saron is incorrect and should be listed as C. Sardu. Therefore the correct author list is: R. Marfella, F. Cacciapuoti, M. Siniscalchi, F. C. Sasso, F. Marchese, F. Cinone, E. Musacchio, M. A. Marfella, L. Ruggiero, G. Chiorazzo, D. Liberti, G. Chiorazzo, G. F. Nicoletti, C. Sardu, F. D'Andrea, C. Ammendola, M. Verza and L. Coppola
- …
