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At least 271 records · Page 15Linked to original sources
PubMed1999

Defective retinoic acid regulation of the Pit-1 gene enhancer: a novel mechanism of combined pituitary hormone deficiency.

Pit-1 is a pituitary-specific transcription factor responsible for pituitary development and hormone expression in mammals. Pit-1 contains two protein domains, termed POU-specific and POU-homeo, which are both necessary for DNA binding and activation of the GH and PRL genes and regulation of the PRL, TSH-beta subunit (TSH-beta), and Pit-1 genes. Pit-1 is also necessary for retinoic acid induction of its own gene during development through a Pit-1-dependent enhancer. Combined pituitary hormone deficiency is caused by defective transactivation of target genes in the anterior pituitary. In the present report, we provide in vivo evidence that retinoic acid induction of the Pit-1 gene can be impaired by a Pit-1 gene mutation, suggesting a new molecular mechanism for combined pituitary hormone deficiency in man.

Animals↗
PubMed1987

Chronobiological analysis of changes in circadian rhythm of anterior pituitary hormones level during glycemia normalization by means of biostator.

We compared the circadian rhythms of anterior pituitary hormones in 15 patients with noncompensated insulin-dependent diabetes on first and second day treatment with Biostator. The rhythm was evaluated by means of a least squares analysis and presented as the circle of cosinors. In noncompensated diabetes the TSH and prolactin rhythm was maintained, whereas other hormones of the anterior pituitary showed no significant rhythm. In the course of one-day normalization of glycemia by means of Biostator the TSH and prolactin rhythm was maintained, whereas the circadian rhythm of growth hormone and ACTH levels appeared with acrophase at 18.47 and 19.59 hour, respectively. The LH rhythm did not exist, whereas the FSH rhythm was dubious. One may assume that noncompensated diabetes results in the impairment of certain pituitary hormonal rhythms and these disturbances are reversible after restoring of normoglycemia.

Adolescent↗
PubMed1999

The effect of melatonin administration on pituitary hormone secretion in man.

OBJECTIVE: Evidence is accumulating that the nocturnal increase in melatonin may influence pituitary hormone secretion. The aim of this study was to determine the effect of exogenous melatonin, in concencetrations spanning the physiological range, on the release of pituitary hormones in man during daylight hours. DESIGN: A double blind, randomized, crossover study. SUBJECTS: Eight healthy male volunteers with a mean age of 21 +/- 0.5 years were studied on four occasions, observations being made after the adminstration of melatonin in doses of 0.05, 0.5 or 5.0 mg or placebo. They refrained from taking heavy exercise, alcohol and from smoking for 24 h prior to the study. MEASUREMENTS: Serum cortisol, growth hormone, prolactin and plasma oxytocin, vasopressin, sodium, osmolality and packed cell volume were measured in samples taken at 30 minutes intervals for 150 minutes after the administration of melatonin. RESULTS: Melatonin produced dose-dependent changes in circulating concentrations of oxytocin and vasopressin, the 0.5 mg dose being stimulatory, while 5.0 mg was inhibitory. These two doses stimulated growth hormone release, while there was no significant effect on prolactin or cortisol release. CONCLUSIONS: These results confirm that the nocturnal increase in melatonin could contribute to the patterns of oxytocin, vasopressin and growth hormone release seen over 24 h.

Adult↗
PubMed1992

Effects of atrial natriuretic factor on anterior pituitary hormone secretion in normal man.

The effects of intravenous human atrial natriuretic factor ANF(99-126) administration on anterior pituitary hormone secretion have not been extensively investigated in humans. We repeatedly studied 10 healthy volunteers (5 female, 5 male, aged 28 +/- 2 years) on 2 occasions, 3 days apart. In randomized, single blind order, subjects received pretreatment with either placebo or intravenous ANF(99-126) (bolus 100 micrograms/kg, 30-min infusion of 0.1 micrograms/kg.min). Subsequently on both occasions subjects received a combined intravenous bolus injection of pituitary releasing hormones (200 micrograms thyrotropin releasing hormone, 100 micrograms gonadotropin releasing hormone and 100 micrograms human adrenocorticotropin releasing hormone; Bissendorf, Hannover, FRG). Plasma concentrations of adrenocorticotropic hormone (ACTH), cortisol, luteinizing hormone (LH), follicle-stimulating hormone (FSH), growth hormone (GH), thyrotropin (TSH), prolactin, ANF and cyclic guanosine monophosphate (GMP) were determined by radioimmunoassay. ANF(99-126) treatment induced a significant reduction in basal ACTH plasma concentrations and tended to decrease basal plasma cortisol. The TSH response to combined releasing hormone administration was significantly diminished after ANF(99-126) pretreatment. In women, the releasing hormone induced prolactin increase was reduced after ANF(99-126) pretreatment. With the present study design, ANF(99-126) did not alter the basal or releasing hormone stimulated plasma concentrations of cortisol, LH, FSH and GH. Releasing hormone administration did not affect ANF and cyclic GMP plasma levels. In humans, effects of natriuretic peptides on anterior pituitary hormone secretion may have to be considered with investigational or therapeutic administration of ANF analogues or agents interfering with the ANF metabolism.

Adult↗
PubMed1988

Multiple pituitary hormone gradients from inferior petrosal sinus sampling in Cushing's disease.

Pre-operative bilateral simultaneous inferior petrosal sinus sampling with assessment of ACTH levels in the left and right sinuses and the periphery was performed in 9 patients with pituitary dependent Cushing's disease who were subsequently found at surgery to have basophil microadenomata. The novel observation of this study was the pattern of secretion of other pituitary hormones so that significant inter-sinus gradients greater than or equal to 1.4:1 were seen for beta-endorphin (2.8 +/- 1.3, mean +/- SEM), PRL (4.2 +/- 1.3) and GH (6.9 +/- 2.4) as well as for ACTH (5.1 +/- 1.1). There was no inter-sinus gradient for LH, FSH and TSH. In these 9 patients with adenomata, the correlations between the inter-sinus gradients for ACTH and beta-endorphin were r = 0.95 (P less than 0.01), ACTH and PRL r = 0.90 (P less than 0.01) and for ACTH and GH r = 0.89 (P less than 0.05). This close association between the gradients for ACTH and other anterior pituitary hormones could be due either to co-secretion of beta-endorphin, PRL and GH by the ACTH-producing pituitary adenomata or to a paracrine effect of beta-endorphin from the tumours on adjacent pituitary tissue. By reflecting the central pituitary hormone milieu, petrosal sinus sampling can give information about pituitary function unobtainable from peripheral hormone levels.

Adolescent↗
PubMed2006

Cell proliferation and vascularization in mouse models of pituitary hormone deficiency.

Mutations in the transcription factors PIT1 (pituitary transcription factor 1) and PROP1 (prophet of Pit1) lead to pituitary hormone deficiency and hypopituitarism in mice and humans. To determine the basis for this, we performed histological analysis of Pit1- and Prop1-deficient dwarf mouse pituitaries throughout fetal and postnatal development. Pit1-deficient mice first exhibit pituitary hypoplasia after birth, primarily caused by reduced cell proliferation, although there is some apoptosis. To determine whether altered development of the vascular system contributes to hypopituitarism, we examined vascularization from embryonic d 14.5 and throughout development. No obvious differences in vascularization are evident in developing Pit1-deficient pituitaries. In contrast, the Prop1-deficient mouse pituitaries are poorly vascularized and dysmorphic, with a striking elevation in apoptosis. At postnatal d 11, apoptosis-independent caspase-3 activation occurs in thyrotropes and somatotropes of normal but not mutant pituitaries. This suggests that Prop1 and/or Pit1 may be necessary for caspase-3 expression. These studies provide further insight as to the mechanisms of Prop1 and Pit1 action in mice.

Animals↗
PubMed1979

Effects of cimetidine on the secretion of some pituitary hormones.

Cimetidine infused intravenously into 6 healthy volunteers did not induce significant changes in plasma levels of prolactin (hPRL), thyreotropin (hTSH), gonadotropin (hLH and hFSH) and growth hormone (hGH). Conversely it caused a significant increase in prolactin response to TRH without modifying the hTSH response to thyreotropin-releasing hormone (TRH) and gonadotropin response to gonadotropin-releasing hormone (GnRH). Data obtained in these experiments, together with data reported in the literature, suggest that the amplified prolactin response to TRH observed during cimetidine infusion, is likely to be connected with a blockade of H2-receptors rather than to unspecific actions of cimetidine.

Adult↗
PubMed1981

Human pituitary hormones extraction.

In order to know the efficiency of the human pituitary hormone extraction method utilized in the laboratory, six batches of 100 pituitaries each, were collected in acetone. Its delipidization and the initial acid extraction (0.3 M KCl, pH 5.5) of the powder were performed in the presence of 0.1 per cent thioethanol and the extraction was completed with an alkaline solution (0.1 N NaOH + H2O, v/v, pH 10.5). Hields in weight of powder and protein concentration for each fraction were similar to those previously reported by Elrick. Characterization of fractions with disc-gel-electrophoresis demonstrated a reproducible pattern for GH, and some differences among the samples containing the glycoproteins. The hormonal activities determined by radioimmunoassay showed a low contamination of GH in the fractions rich in glycoproteins, but these latter were similarly distributed between the acid and the alkaline extracts. The glycoprotein fraction had an important activity of TSH. The hormonal content per pituitary was calculated from the addition of activities in both extracts and the last residue; GH = 3 mg (4.494 IU); FSH = 761 micrograms (13.410 IU); LH = 782 micrograms (46.920 IU); TSH = 2.939 mg (9.350 IU). It is concluded that the technique is useful since there was a low GH contamination in the glycoprotein fraction and the TSH yield was important.

Electrophoresis, Disc↗
PubMed2006

Genetic screening of combined pituitary hormone deficiency: experience in 195 patients.

CONTEXT: Mutations in transcription factors result in combined pituitary hormone deficiency (CPHD). OBJECTIVE: A genetic screening strategy, based on endocrine and neuroradiological phenotype according to published knowledge, was applied to establish the prevalence of gene defects in each category of patients and provide a useful framework for clinicians to determine the genetic etiology and recurrence risks for individuals and families. DESIGN: One hundred ninety-five CPHD patients from the international GENHYPOPIT network were studied, according to their phenotype, for POU1F1, PROP1, LHX3, LHX4, and HESX1. PATIENTS: Patients selected had two pituitary hormone deficiencies or at least one deficiency with intracerebral malformations. RESULTS: Total prevalence of mutations was 13.3 and 52.4% in 20 patients with familial CPHD history. No mutation of HESX1 was observed in 16 patients harboring septooptic dysplasia. A mutation of LHX4 gene, previously reported, was found in one familial case from 39 patients bearing pituitary stalk interruption syndrome. In 109 patients without extrapituitary abnormalities, 20 had PROP1 mutations, including eight patients with a family history of CPHD. Among 20 patients without pituitary stalk interruption syndrome, no LHX3 gene defect was found, even with a neck rotation deficit. One POU1F1 gene defect was found in one patient presenting the rare postpubertal association of thyrotroph (TSH deficiency) and somatotroph (GH deficiency) deficits. CONCLUSIONS: Mutation of PROP1 gene remains the first to be looked for, and POU1F1 mutations should be sought in GH deficiency and TSH deficiency postpubertal population without extrapituitary malformations. Identification of gene defects allows early treatment of any deficit and prevention of their potentially fatal consequences. Genotyping appears highly beneficial at an individual and familial level.

Adrenocorticotropic Hormone↗