Diabetogenic action of purified anterior pituitary hormones.
Explore the source record for details and available documents.
Pituitary Diseases↗
SEARCH · PubMed Health
Results for “PITUITARY HORMONES”
Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
Bombesin-like immunoreactivity in the forebrain and pituitary and regulation of anterior pituitary hormone release by bombesin in goldfish.
The presence and distribution of bombesin (BBS)/gastrin-releasing peptide (GRP)-like immunoreactivity (IR) was examined in the goldfish pituitary and forebrain. BBS/GRP-like IR nerve fibres were consistently observed throughout the pituitary neurointermediate lobe (NIL); occasionally, BBS/GRP-like material was localized in cells and few fibres within the pars distalis. Within the goldfish forebrain, sparse, fine-beaded BBS/GRP-like IR fibres and few perikarya were detected in the preoptic hypothalamus. BBS/GRP-like IR material was also present in the ventro-posterior hypothalamus and the hypothalamic inferior lobes, and, in particular, within the nucleus lateral tuberis pars anterioris (NLTa) and nucleus lateral tuberis pars posterioris (NLTp), nucleus anterior tuberis (NAT), nucleus recessus lateralis (NRL), nucleus recessus posterioris (NRP), and the nucleus diffusus lobi inferioris (NDLI). Several BBS/GRP-like IR perikarya were observed in periventricular regions of the NLT, NRL, and NRP. Finally, BBS/GRP-like IR material was detected in the nucleus habenularis, the nucleus rotundus, several thalamic nuclei, and the optic tectum of the dorso-posterior diencephalon. The presence of BBS/GRP-like IR material within the preoptic hypothalamus, hypophysial stalk, and in the pituitary suggests that BBS-like peptides may regulate pituitary hormone release in fish. Perifusion of goldfish pituitary fragments with initial pulses of 0.1, 10, 100 or 1,000 nM BBS stimulated both growth hormone (GH) and gonadotropin (GtH-II) release. Repeated pulses of the same dose of BBS generally stimulated GH and GtH-II release to a similar magnitude. These studies provide initial evidence that BBS/GRP-like peptides are present within the central nervous system of teleost fish. The anatomical distribution of BBS/GRP-like IR in goldfish hypothalamic feeding center supports our previous report indicating a role for BBS in the central regulation of food intake in fish. Additionally, the presence of BBS/GRP-like IR material in the pituitary and brain areas associated with the regulation of anterior pituitary hormone secretion, as well as evidence demonstrating a direct action of BBS at the level of the goldfish pituitary to modify GH and GtH-II secretion, indicates that BBS/GRP-like peptides likely act to regulate pituitary hormone release in teleosts.
Animals↗
Neuropeptide Y: a novel neuroendocrine peptide in the control of pituitary hormone secretion, and its relation to luteinizing hormone.
Evidence that establishes neuropeptide Y (NPY) as an important neuromessenger in the regulation of anterior pituitary hormone secretion is reviewed. In particular, NPY plays a critical role in stimulating the episodic, basal pattern of luteinizing hormone (LH) release, as well as the preovulatory surge of LH release in several species. The stimulatory effect of NPY on LH secretion is dependent upon the presence of gonadal hormones and involves amplification of the response of other interacting stimulatory signals. NPY acts at the level of the median eminence to excite the release of LH-releasing hormone (LHRH) via a mechanism that leads to the mobilization of intracellular Ca2+. These stimulatory LHRH responses are mediated by Y1NPY receptors. Moreover, NPY activates postsynaptic messenger pathways that complement and reinforce those affected by norepinephrine, which is another major neuroregulator of LHRH secretion and which is released as a cotransmitter with NPY in the median eminence. Additionally, NPY is released into the hypophyseal portal blood for transportation to the anterior pituitary where it enhances the release of LH in response to LHRH. This facilitatory, modulating effect at the pituitary level involves an allosteric increase in LHRH binding to its receptor leading to augmented influx of Ca2+ from the extracellular space. There is evidence that gonadal steroids regulate NPY neurosecretion in a site-specific manner, and that alterations in NPY secretion may occur in part via a direct action of the steroids on NPY neurons in the brainstem and hypothalamus and in part through an indirect effect involving removal of the inhibitory influence of endogenous opioid peptides. These findings are integrated into an overall hypothesis for induction of the preovulatory LH surge on proestrus requiring an interplay between NPY and other neuronal networks. In aged male rats, due to the inability of hypothalamic NPY neurons to respond appropriately to the trophic effects of androgens, NPY neurosecretion is diminished. Further, a review of the literature reveals that NPY may modulate the secretion of other pituitary hormones through a similar combination of hypothalamic and pituitary actions.
Amino Acid Sequence↗
Roles of pituitary hormones in the regulation of hepatic cytochrome P450IIE1 in rats and mice.
Cytochrome P450IIE1 (P450IIE1) is responsible for the metabolic activation of N-nitrosodimethylamine (NDMA), a potent environmental carcinogen. This P450 enzyme displays a high-affinity NDMA demethylase (NDMAd) activity and is known to be induced by fasting and acetone administration. In the present work, the effects of pituitary hormones on the regulation of P450IIE1 in the liver were investigated and compared in rats and mice. There was no difference in liver microsomal NDMAd activity (nmol/min/mg protein) in rats in the intact (0.38 +/- 0.12), sham-operated (0.44 +/- 0.06), and hypophysectomized (0.52 +/- 0.04) groups. However, hypophysectomy caused a 2-fold increase in hepatic P450IIE1 protein levels as determined by immunoblot analysis. The P450IIE1 mRNA level in hypophysectomized rat was also significantly increased. The levels of blood ketone bodies (acetone, acetoacetate, and beta-hydroxybutyrate) were not different in the intact, sham-operated, and hypophysectomized groups, suggesting that ketone bodies are not involved in the induction of P450IIE1 protein and its mRNA by hypophysectomy. The discrepancy between the NDMAd activity and the increased P450IIE1 protein in rat liver by hypophysectomy can be partially explained by the lower hepatic NADPH-P450 reductase activity (50% that of the control) in the hypophysectomized rats. Upon the induction of liver NDMAd activity by fasting and acetone, hypophysectomy attenuated the effect of acetone but abolished the effect of fasting completely. Nevertheless, fasting still caused a 3-fold increase in the liver P450IIE1 mRNA level. An involvement of pituitary hormones in the regulation of liver microsomal P450IIE1 in mouse, however, was not observed. There was no difference in constitutive NDMAd activity between genetically growth hormone-deficient (lit/lit) mice and their phenotypically normal heterozygotes (lit/+). Fasting for 48 h caused 1.5- to 2-fold induction and acetone caused 2- to 3-fold induction, in both groups. The above changes in enzyme activity were due to the changes of P450IIE1 levels as verified by the immunoblot analysis. In male BALB/c mice, neither the hepatic NDMAd activity nor the P450IIE1 protein level was altered by hypophysectomy. The effects of acetone on the liver NDMAd activity were also similar in hypophysectomized and sham-operated mice. The results suggest that pituitary hormones are important in the regulation of the expression and activity of hepatic P450IIE1 in rats but not in the mouse strains investigated.
Acetone↗
Differential effects of insulin- and proinsulin-induced hypoglycemia on pituitary hormone and catecholamine secretion.
The effects of insulin- and proinsulin-induced hypoglycemia on pituitary hormone and catecholamine secretion were compared in normal men to search for possible hypothalamic or pituitary inhibitory effects of proinsulin on glucocounterregulatory responses. When subjects received 0.1 U/kg i.v. human insulin and 25-38 micrograms/kg i.v. human proinsulin on separate occasions, plasma glucose decreased more rapidly after insulin, and the nadir was slightly lower, but integrated hypoglycemic responses were similar. Cortisol, growth hormone (GH), prolactin, epinephrine, and norepinephrine responses occurred more rapidly after insulin than after proinsulin. Peak and integrated cortisol, GH, and catecholamine responses to insulin and proinsulin were similar, but those of prolactin were reduced after proinsulin when compared with insulin by 42% (P less than .01) and 34% (P less than .05), respectively. When euglycemia was maintained by a variable glucose infusion rate after the injection of insulin and proinsulin, no differences were observed in plasma levels of any of the hormones. The intravenous injection of a dose of proinsulin (6 micrograms/kg), which did not produce hypoglycemia but was the molar equivalent of insulin used in the first protocol, failed to modify the GH or prolactin responses to a combined injection of GH-releasing hormone (1 microgram/kg) and thyrotropin-releasing hormone (500 micrograms). Our results indicate that the onset of pituitary hormone and catecholamine responses to hypoglycemia are related to the rate of plasma glucose decline, with the slower responses to proinsulin reflecting a more gradual onset of hypoglycemia. The magnitude of the cortisol, GH, and catecholamine responses, however, was comparable with proinsulin- and insulin-induced hypoglycemia.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
Congenital combined pituitary hormone deficiency attributable to a novel PROP1 mutation (467insT).
BACKGROUND: Combined pituitary hormone deficiency (CPHD) is an anterior pituitary disorder, commonly resulting in growth retardation. PROP1 gene mutations appear to be frequently responsible for CPHD, particularly in Middle and Eastern Europe and the Americas, but few cases have been reported in Japan. PATIENTS AND DESIGN: Two sisters (aged 8.4 and 4.3 years at presentation) exhibited proportional short stature from about 2 years of age. Genetic analysis determined the nature and location of mutations. RESULTS: Pituitary size by magnetic resonance imaging (MRI) indicated only slight hypoplasia, while hormone analysis revealed deficiencies in secretion of growth hormone (GH), thyroid stimulating hormone, prolactin and gonadotropins; adrenocortinotropin secretion appeared adequate. Genetic analysis revealed a novel familial inherited PROP1 mutation. A unique insertion mutation was found in codon 156 (467insT) located in the transcription-activating region of the PROP1 gene. The resulting PROP1 protein (191 amino acids) would lack the transcription activation domain and consequently be non-functional. CONCLUSION: Gene analysis suggested that the siblings had inherited a unique autosomal recessive PROP1 gene mutation resulting in severe GH deficiency and subsequent growth retardation.
Base Sequence↗
The effects of chronic naloxone on pituitary hormone secretion in female rats.
The effects of a sustained-release implant for naloxone (NAL) on serum concentrations of prolactin (PRL), immunoreactive beta-endorphin (IR-beta-ENDO), growth hormone (GH) and thyroid stimulating hormone (TSH) were evaluated in ovariectomized female rats. After 9 days of exposure to NAL, serum levels of none of these 4 pituitary hormones were altered. However, the NAL implant antagonized the stimulatory effects of morphine (15 and 30 mg/kg body weight) on PRL and IR-beta-ENDO secretion, enhanced the stimulatory effects of morphine on GH secretion, and had no effect on morphine-induced suppression of TSH secretion. These results indicate that while chronic NAL exposure does not, by itself, persistently alter pituitary hormone secretion, it differentially effects the response of these hormones to morphine exposure. These data suggest that chronic treatment with narcotic antagonists may invoke differential compensatory mechanisms to maintain normal hormone secretion.
Animals↗
Melatonin administration and pituitary hormone secretion.
OBJECTIVE: The relationship between the pineal gland and pituitary function remains controversial, while the role of melatonin in the adaptation of the organism to the light-dark cycle of the environment is becoming increasingly recognized. The aim of this study was to investigate the effect of a manipulation of the melatonin rhythm on pituitary hormone secretion in man. DESIGN: Double-blind controlled clinical study. SUBJECTS: Ten adult healthy male volunteers, aged 21-33 years, were studied on two occasions: once after the administration of melatonin 5 mg orally for 4 days at 1700 hours and once after the administration of placebo, at similar times. On the day of each study the subjects undertook their normal duties but refrained from taking heavy exercise, from smoking and drinking alcohol. MEASUREMENTS: Serum cortisol, growth hormone, prolactin and plasma vasopressin, oxytocin, melatonin, sodium, potassium, osmolality and packed cell volume were measured over the following 24 hours. RESULTS: The cortisol peak was advanced and prolactin release increased after melatonin administration, while growth hormone was not affected. Vasopressin and oxytocin levels were found to increase during the night in the control study, but the period of the nocturnal increase in vasopressin concentrations was reduced after the administration of melatonin and the nocturnal increase of oxytocin was absent. CONCLUSION: Altering the melatonin rhythm may affect neuroendocrine function, influencing the nocturnal pattern of neurohypophysial hormone secretion, augmenting prolactin release and advancing the peak of cortisol release.
Administration, Oral↗
Long-term follow-up of combined pituitary hormone deficiency in two siblings with a Prophet of Pit-1 gene mutation.
Combined pituitary hormone deficiency (CPHD) is a rare disorder resulting from an impaired pituitary function due to different causes, characterized by impaired secretion of growth hormone (GH) and one or more of the other anterior pituitary hormones. To date, 16 distinct human Prophet of Pit-1 (Prop1) gene mutations have been identified in patients with CPHD, inducing a phenotype involving GH, follicle-stimulating hormone (FSH), luteinizing hormone (LH), prolactin and thyroid-stimulating hormone (TSH), and rarely adrenocorticotropic hormone, deficiency. Herein we present two siblings of different sexes from a family with parental consanguinity presenting the 301-302delAG mutation in the Prop1 gene. The female presented failure of growth from the age of 6 years and was treated for 10 years with GH, ending in a final height (standard deviation score) of -0.28. TSH deficiency was manifested after the initiation of GH and was treated with thyroxine while puberty was initiated with conjugated estrogens. The male presented TSH deficiency since childhood, treated with thyroxine, and growth failure at the age of 14 years, treated for a period of 2 years with GH. Puberty was initiated with increasing doses of testosterone, while human chorionic gonadotropin was added in order to achieve increased testicular volume. In conclusion, these two siblings of different sexes with CPHD carrying the 301-302delAG mutation in the Prop1 gene presented a variable phenotype characterized by GH, TSH, LH and FSH deficiency.
Adolescent↗
A mutation in the POU-homeodomain of Pit-1 responsible for combined pituitary hormone deficiency.
Pit-1 is a pituitary-specific transcription factor responsible for pituitary development and hormone expression in mammals. Mutations in the gene encoding Pit-1 have been found in two dwarf mouse strains displaying hypoplasia of growth hormone, prolactin, and thyroid-stimulating, hormone-secreting cell types in the anterior pituitary. A point mutation in this gene was identified on one allele in a patient with combined pituitary hormone deficiency. Mutant Pit-1 binds DNA normally but acts as a dominant inhibitor of Pit-1 action in the pituitary.
Alleles↗
Effect of leptin replacement on pituitary hormone regulation in patients with severe lipodystrophy.
Leptin is important in regulating energy homeostasis. Severe lipodystrophy is associated with leptin deficiency and insulin resistance, hypertriglyceridemia, and hepatic steatosis. Leptin deficiency is also associated with abnormalities of the pituitary hormones in rodent models and patients with congenital absence of leptin. We inquired whether similar abnormalities are seen in patients with lipodystrophy and whether replacement of leptin will make an impact on the regulation of pituitary hormones. Seven female patients (aged 15-42 yr, all diabetic) with lipodystrophy and serum leptin levels less than 4 mg/liter were treated with recombinant methionyl-human leptin (recombinant leptin) in physiological doses in an open-labeled study. The following parameters were evaluated before and at 4 months of leptin treatment: menstrual history, pelvic ultrasonogram, LHRH, TRH, and CRH tests. While on recombinant leptin, mean serum leptin concentration increased from 1.3 +/- 0.3 mg/liter to 11.1 +/- 2.5 mg/liter. Only one of five patients who had intact reproductive systems was cycling normally before leptin therapy, and all five had normal menses by the fourth month of leptin therapy. Serum E2 concentrations increased (110 +/- 44 pmol/liter vs. 546 +/- 247 pmol/liter, P = 0.002), serum T concentrations decreased (3.5 +/- 3.0 nmol/liter vs. 1.3 +/- 0.7 nmol/liter, P = 0.055), and the attenuated LH response to LHRH was corrected with therapy. Serum T(3) and free T(4) were in the normal range before leptin therapy and did not change. However, serum TSH concentrations fell from 2.2 +/- 1.1 microU/ml to 1.2 +/- 0.7 microU/ml (P < 0.001). The percent increase in TSH following TRH administration was similar before (560%) and at 4 months (580%) of leptin therapy. The mean nonstimulated ACTH and cortisol concentrations were, respectively, 6.0 +/- 3.4 pmol/liter and 680 +/- 280 nmol/liter before leptin and did not change after 4 months of therapy (4.2 +/- 1.2 pmol/liter, P = 0.11 and 453 +/- 142 nmol/liter, P = 0.13, respectively). The ACTH and cortisol responses to CRH stimulation were normal both before and after therapy. Leptin replacement improved menstrual abnormalities and low E2 levels and corrected the attenuated LH response to LHRH in a group of young women with lipodystrophy and leptin deficiency. These results add to the growing body of evidence that metabolic signals such as leptin play a role in neuroendocrine regulation.
Adolescent↗
Effects of metal cations on pituitary hormone secretion in vitro.
Increased body burdens of metal cations are known to affect adversely reproductive function in several species. The effects of these metals on gonadal function are well documented. In contrast, little is known about their possible direct effects on pituitary hormone release. The purpose of this study was to determine, in vitro, the effects of nickel, cadmium, and zinc (50 microM) on both baseline and potassium chloride (KCl)-stimulated pituitary luteinizing hormone (LH), prolactin (Prl), and thyroid-stimulating hormone (TSH) release. Anterior pituitary fragments from adult male Long-Evans rats were evaluated using a continuous-flow perifusion system. Baseline and stimulated LH releases were unaffected by nickel and zinc; however, cadmium caused an increase in baseline LH secretion. Baseline Prl release was decreased by zinc, while cadmium resulted in increased release of this hormone. Stimulated Prl release was lower during exposure to zinc but unaltered by nickel and cadmium. Following exposure to zinc, a rebound in stimulated release was noted for all three hormones measured. These results showed that the metal cations tested did have a direct effect on pituitary hormone release at a dose lower than those reported to alter testicular function in vitro. Furthermore, the changes in pituitary hormone secretion varied depending upon the metal and hormone being evaluated.
Animals↗
Human Prop-1: cloning, mapping, genomic structure. Mutations in familial combined pituitary hormone deficiency.
Prop-1 is a newly isolated pituitary-specific paired-like homeodomain transcription factor whose cDNA sequence is well known in mouse. To study its involvement in human combined pituitary hormone deficiency (CPHD), we have isolated the human cDNA ortholog and determined the exon/intron organization and chromosomal localization of the human gene. A Prop-1 defect was characterized in three CPHD families. One missense mutation (R73C) involves a residue conserved in 95% of the more than 400 homeodomain proteins so far identified; in vitro splicing assays demonstrated the functional importance of the second defect, whereas the remaining mutation is a frameshift. Given the disease phenotype documented in the patients, these data, which will facilitate molecular investigations in other patients, demonstrate the crucial role of Prop-1 in the proper development of somatotrophs, lactotrophs, thyreotrophs and gonadotrophs.
Amino Acid Sequence↗
[Endocrinological evaluation of sellar and suprasellar tumor cases (the sixth report)-on pituitary hormone secretion of acromegalic patients before treatment (author's transl)].
1) Pituitary hormone secretion of 14 acromegalic patients was studied before treatment. Incidence of hyporeactive response was 0%, 43%, 29%, 71% and 9% in ACTH, LH, FSH, TSH and PRL respectively. 2) Relatively higher incidence of hyporeactive TSH response in TRH test seems to be characteristic in acromegalic patients. 3) Six of 13 acromegalic patients examined on blood PRL level revealed relatively high blood PRL level over 50ng/ml.
Acromegaly↗
Analysis of pituitary hormones and chromogranin A mRNAs in null cell adenomas, oncocytomas, and gonadotroph adenomas by in situ hybridization.
To study the relationship between null cell adenomas, oncocytomas and gonadotroph adenomas, we analyzed 32 surgically removed formalin-fixed paraffin-embedded pituitary tumors for the expression of pituitary hormone messenger RNAs (mRNAs) by in situ hybridization (ISH). Most tumors were also analyzed for chromogranin A mRNA. To identify the cell type constituting the tumors and to assess hormone content, all tumors were investigated by histology, transmission electron microscopy and immunohistochemistry. Most null cell adenomas (6/11) and gonadotroph adenomas (9/10) expressed the mRNAs for alpha-subunit of glycoprotein hormones whereas only 2/11 oncocytomas expressed alpha-subunit mRNA. FSH beta and/or LH beta mRNA were present in most null cell and gonadotroph adenomas but only in a few oncocytomas. Prolactin (PRL) mRNA was detected in two null cell tumors and in one gonadotroph adenoma, whereas GH and POMC mRNA were present in one null cell adenoma. Chromogranin A mRNA, which codes for the major secretory granule protein, was present in 25/26 tumors including all tumors that were negative for pituitary hormone mRNAs, indicating adequate preservation of specific mRNA transcripts in the paraffin-embedded sections of tumor cells. These results indicate that null cell adenomas and gonadotroph adenomas are closely related neoplasms and that oncocytomas may represent a functionally defective form of null cell adenoma characterized by mitochondrial abundance, which has retained the capacity to synthesize the major secretory granule protein chromogranin A. Although the cytogenesis of null cell adenomas and oncocytomas is not clear, it can be suggested that these two tumor types are derived from a pluripotential precursor cell that is capable of undergoing multidirectional differentiation and synthesizing various hormones, mainly glycoproteins.
Adenoma↗
[Connections between neurosecretion and the so-called posterior pituitary hormones. I. Studies on dried and powdered posterior pituitary tissue (snuff powder)].
Explore the source record for details and available documents.
Humans↗
Effects of naloxone and coffee on anterior pituitary hormones.
Both naloxone, a specific opiate antagonist, and caffeine and other components of coffee powders show influences on opiate receptors and on the secretion of some pituitary hormones. In order to study the possible effect of naloxone and coffee on the secretion pattern of hypophyseal hormones in man, experiments were performed in normal volunteers using either naloxone or coffee alone or both substances. Five healthy normal males, aged 25-30 years, received on three separate occasions and in random order: (i) coffee (4 cups of Italian style "espresso" coffee); or (ii) naloxone 12 micrograms/kg i.v.; or (iii) coffee plus naloxone simultaneously. The results show that naloxone given alone did not modify basal plasma PRL, GH, TSH, FSH or cortisol levels but significantly increased basal LH concentrations. On the other hand, the absorption of four cups of coffee did not modify the values of any of the hormones studied. The combination of the two drugs (coffee + naloxone) did not alter the response of the hormones studied to naloxone alone. It was concluded that coffee drinking, at least in these experimental conditions, does not appear to have any influence on anterior pituitary hormone secretion. Naloxone, on the other hand, is able to stimulate LH secretion even at very low doses.
Adult↗
Optic nerve size evaluated by magnetic resonance imaging in children with optic nerve hypoplasia, multiple pituitary hormone deficiency, isolated growth hormone deficiency, and idiopathic short stature.
OBJECTIVE: To objectively define criteria for intracranial optic nerve (ON) size in ON hypoplasia (ONH) on magnetic resonance imaging (MRI) scans. STUDY DESIGN: Intracranial ON sizes from MRI were compared between 46 children with ONH diagnosed by ophthalmoscopy (group 1, isolated ONH, 8 children; and group 2, ONH associated with abnormalities of the hypothalamic-pituitary axis and septum pellucidum, 38 children) and children with multiple pituitary hormone deficiency (group 3, multiple pituitary hormone deficiency, 14 children), isolated growth hormone deficiency (group 4, isolated growth hormone deficiency, 15 children), and idiopathic short stature (group 5, idiopathic short stature, 10 children). Intracranial ON size was determined by the cross-sectional area, calculated as [pi x (1/2) height x (1/2) width]. RESULTS: Groups 1 and 2 had lower intracranial ON size than did groups 3, 4, and 5 (P < .001). No patients in groups 3 through 5 who had MRI after 12 months of age (when 95% adult size of ONs is attained) had ONs <2.9 mm 2 . Visual acuity correlated significantly with ON size (P < .01). CONCLUSIONS: Magnetic resonance imaging of the ONs with cross-sectional area <2.9 mm 2 in a short child more than 12 months of age, with or without hypothalamic-pituitary axis abnormalities, confirms the clinical diagnosis of ONH.
Adolescent↗