-
The Journal of Endocrinology Feb 1975Pituitary content or concentration of follicle-stimulating hormone (FSH), prolactin and growth hormone in the genetically androgen insensitive male rat... (Comparative Study)
Comparative Study
Pituitary content or concentration of follicle-stimulating hormone (FSH), prolactin and growth hormone in the genetically androgen insensitive male rat pseudohermaphrodite is intermediate between normal male and female rats, while pituitary luteinizing hormone (LH) concentration and serum FSH levels are the same as in the normal male. The concentration of serum LH, prolactin and growth hormone indicated no sexual dimorphism. Although the pseudohermaphrodite is genetically male with a female phenotype, our results suggest some degree of masculinization of the hypothalamic-pituitary system.
Topics: Animals; Body Weight; Disorders of Sex Development; Female; Follicle Stimulating Hormone; Growth Hormone; Luteinizing Hormone; Male; Organ Size; Phenotype; Pituitary Gland; Pituitary Hormones; Prolactin; Radioimmunoassay; Rats
PubMed: 1117235
DOI: 10.1677/joe.0.0640249 -
Peptides Nov 2009To date, there is a dearth of evidence to support functions for melanin-concentrating hormone (MCH) and melanin-concentrating hormone receptors (MCH-R) in mammalian skin... (Review)
Review
To date, there is a dearth of evidence to support functions for melanin-concentrating hormone (MCH) and melanin-concentrating hormone receptors (MCH-R) in mammalian skin physiology including pigmentation, inflammation and immune responses and skin cell proliferation. Much research is therefore still needed to define the roles of the hormone and its receptors in mammalian skin. This will be a crucial step to identifying pathogenic mechanisms that may involve the MCH/MCH-R system in the context of inflammatory and autoimmune skin diseases as well as skin cancers. The following review summarizes the studies which have been carried out to examine the expression and function of MCH and MCH-R in mammalian skin. Recent findings with regard to humoral immune responses to the MCH-R1 in patients with the skin depigmenting disease vitiligo are also discussed.
Topics: Animals; Humans; Hypothalamic Hormones; Mammals; Melanins; Pituitary Hormones; Receptors, Pituitary Hormone; Skin; Skin Pigmentation
PubMed: 19442695
DOI: 10.1016/j.peptides.2009.04.025 -
British Journal of Clinical Pharmacology Dec 1980
Clinical Trial Randomized Controlled Trial
Topics: Epoprostenol; Follicle Stimulating Hormone; Humans; Luteinizing Hormone; Male; Pituitary Hormones, Anterior; Prostaglandins
PubMed: 6781512
DOI: 10.1111/j.1365-2125.1980.tb00524.x -
The Journal of Clinical Endocrinology... Feb 1983In vitro evidence suggests that calcium is involved in the release of anterior pituitary hormones. Therefore, we studied the effect of the slow calcium channel blocker... (Clinical Trial)
Clinical Trial Randomized Controlled Trial
Calcium antagonists and hormone release: effect of nifedipine on luteinizing hormone-releasing hormone and thyrotropin-releasing hormone-induced pituitary hormone release.
In vitro evidence suggests that calcium is involved in the release of anterior pituitary hormones. Therefore, we studied the effect of the slow calcium channel blocker or calcium antagonist nifedipine on the FSH and LH responses to LRH and the TSH and PRL responses to TRH in vivo. Nine normal male subjects were studied on two occasions, and nifedipine (20 mg, by mouth, or matching placebo) was administered in a randomized single blind manner. Blood pressure and heart rate were measured at 0 and 30 min. The patients then received TRH (200 micrograms) and LRH (100 micrograms) iv. Blood levels of FSH, LH, TSH, and PRL were measured by RIA at 0, 30, 50, 60, and 120 min. Nifedipine lowered diastolic blood pressure significantly (--12 +/- 8 mm Hg; P less than 0.005) and increased heart rate (+ 17 /*- 10 beats/min; P less than 0.005), but had no effect on either baseline hormone levels or the incremental response of any hormone to its secretagogue. In contrast to the results of previous studies with verapamil, nifedipine does not inhibit the release of pituitary hormones. More information is required on the precise intracellular actions of these drugs before they can be used to study the role of calcium in hormone release. Nifedipine, however, may be less likely to influence pituitary function than verapamil.
Topics: Adult; Calcium Channel Blockers; Follicle Stimulating Hormone; Gonadotropin-Releasing Hormone; Humans; Luteinizing Hormone; Male; Nifedipine; Pituitary Hormones, Anterior; Prolactin; Pyridines; Thyrotropin; Thyrotropin-Releasing Hormone
PubMed: 6401753
DOI: 10.1210/jcem-56-2-401 -
Hormone Research 1996Pit-1 is a transcription factor which is expressed in the somatotrope, lactotrope, and thyrotrope cell population of the anterior pituitary gland from early fetal... (Review)
Review
Pit-1 is a transcription factor which is expressed in the somatotrope, lactotrope, and thyrotrope cell population of the anterior pituitary gland from early fetal development throughout life. Mutations in the Pit-1 gene result in insufficient expression of this factor, accounting for a form of combined pituitary hormone deficiency for growth hormone (GH), prolactin, and thyroid-stimulating hormone. Clinical presentation at diagnosis can be variable, although all forms finally result in severe growth retardation due to GH deficiency and hypothyroidism. The clinical variability is due to other factors than the exact location of the mutation; however, the type of inheritance seems to correlate well with the genotype. Early detection of Pit-1 abnormalities might prevent the sequelae associated with some early and severe presentations of this disorder.
Topics: Animals; DNA-Binding Proteins; Humans; Pituitary Diseases; Pituitary Gland; Pituitary Hormones; Transcription Factor Pit-1; Transcription Factors
PubMed: 8805025
DOI: 10.1159/000184824 -
Endocrine May 2024Disorders/differences of sex development (DSD) result from variants in many different human genes but, frequently, have no detectable molecular cause.
PURPOSE
Disorders/differences of sex development (DSD) result from variants in many different human genes but, frequently, have no detectable molecular cause.
METHODS
Detailed clinical and genetic phenotyping was conducted on a family with three children. A Sec31a animal model and functional studies were used to investigate the significance of the findings.
RESULTS
By trio whole-exome DNA sequencing we detected a heterozygous de novo nonsense SEC31A variant, in three children of healthy non-consanguineous parents. The children had different combinations of disorders that included complete gonadal dysgenesis and multiple pituitary hormone deficiency. SEC31A encodes a component of the COPII coat protein complex, necessary for intracellular anterograde vesicle-mediated transport between the endoplasmic reticulum (ER) and Golgi. CRISPR-Cas9 targeted knockout of the orthologous Sec31a gene region resulted in early embryonic lethality in homozygous mice. mRNA expression of ER-stress genes ATF4 and CHOP was increased in the children, suggesting defective protein transport. The pLI score of the gene, from gnomAD data, is 0.02.
CONCLUSIONS
SEC31A might underlie a previously unrecognised clinical syndrome comprising gonadal dysgenesis, multiple pituitary hormone deficiencies, dysmorphic features and developmental delay. However, a variant that remains undetected, in a different gene, may alternatively be causal in this family.
Topics: Animals; Child; Child, Preschool; Female; Humans; Male; Mice; Gonadal Dysgenesis; Hypopituitarism; Mice, Knockout; Pedigree; Pituitary Hormones; Vesicular Transport Proteins
PubMed: 38400880
DOI: 10.1007/s12020-024-03701-x -
Annals of Clinical Research 1978
Review
Topics: Animals; Cells, Cultured; Cyclic AMP; Dopamine; Estradiol; Female; Follicle Stimulating Hormone; Gonadotropin-Releasing Hormone; Humans; Luteinizing Hormone; Male; Pituitary Hormones, Anterior; Progesterone; Prolactin; Rats; Receptors, Cell Surface; Somatostatin; Thyroid Hormones; Thyrotropin; Thyrotropin-Releasing Hormone
PubMed: 214010
DOI: No ID Found -
Clinical Endocrinology Jan 1998Exposure to bright light inhibits melatonin secretion in man. As the relationship between melatonin and pituitary function remains controversial, we investigated the... (Clinical Trial)
Clinical Trial Randomized Controlled Trial
OBJECTIVE
Exposure to bright light inhibits melatonin secretion in man. As the relationship between melatonin and pituitary function remains controversial, we investigated the effect of altering the melatonin rhythm by bright light during the early hours of darkness on pituitary hormone secretion in man.
DESIGN
The investigation took the form of a randomized controlled clinical trial.
SUBJECTS
Ten adult healthy male volunteers, who were non-smokers and aged 21-33 years, were studied on two occasions: once during exposure to bright light from 2000 h to 0200 h and once during exposure to normal room lighting over the same period. On each day of the study, the subjects were allowed to sleep after lights were switched off at 0200 h. Observations were also performed when subjects were exposed to normal room lighting from 2000 h to 2400 h, thereafter being allowed to sleep. On each study day the subjects undertook their normal duties but refrained from taking heavy exercise and drinking alcohol.
MEASUREMENTS
Serum cortisol, GH and PRL, plasma vasopressin, oxytocin, melatonin, sodium, potassium and osmolality and packed cell volume were measured over 24 hours.
RESULTS
Bright light delayed the nocturnal melatonin peak by 2 hours and resulted in a decrease in cortisol concentrations. Growth hormone levels decreased but subsequently there was a significantly greater nocturnal increase. The PRL peak was delayed and nocturnal vasopressin concentrations were lower in both the studies where subjects were exposed to a modified sleep schedule.
CONCLUSION
Exposure to bright light during the early hours of darkness delays the nocturnal melatonin peak and alters cortisol, GH, PRL and nocturnal vasopressin secretion, while modification of the sleep pattern decreases vasopressin concentrations and alters its nocturnal peak.
Topics: Adult; Cross-Over Studies; Growth Hormone; Humans; Hydrocortisone; Light; Male; Melatonin; Photic Stimulation; Pituitary Gland; Pituitary Hormones; Prolactin; Sleep; Vasopressins
PubMed: 9509071
DOI: 10.1046/j.1365-2265.1998.00355.x -
Clinical Biochemistry Oct 1981Major advances in our understanding of the synthesis and release of anterior pituitary hormones have been made over the past several years. Neurons of the hypothalamus... (Review)
Review
Major advances in our understanding of the synthesis and release of anterior pituitary hormones have been made over the past several years. Neurons of the hypothalamus have been found to serve as "neuroendocrine transducers" in that they have both electrical and secretory functions. Peptidergic neurons respond to appropriate stimuli with a release of hypothalamic factors into the hypophyseal-portal system. These factors or hormones ultimately control the endocrine function of anterior pituitary cells. Three hormones, Thyrotropin Releasing Hormone (TRH), Gonadotropin Releasing Hormone (GnRH or LHRH) and somatostatin have been identified, synthesized and tested for clinical applications. The clinical assessment of pituitary function has been greatly improved by new and improved radioimmunoassays. One of the recent clinical advances in the area of pituitary disease has been the determination of the relatively high frequency of prolactinomas. Prolactin secreting microadenomas are an important and treatable cause of amenorrhea and infertility in young women. In addition, many pituitary tumors previously believed to be non-functional or "chromophobe adenomas" appear to be prolactinomas. Many new diagnostic and therapeutic techniques are continuing to be developed to improve our management of patients with hypothalamic-pituitary disease.
Topics: Adrenocorticotropic Hormone; Diabetes Mellitus, Type 1; Female; Follicle Stimulating Hormone; Growth Hormone; Humans; Luteinizing Hormone; Male; Pituitary Gland, Anterior; Pituitary Hormone-Releasing Hormones; Pituitary Hormones, Anterior; Prolactin; Radioimmunoassay; Thyrotropin; Thyrotropin-Releasing Hormone
PubMed: 6277529
DOI: 10.1016/s0009-9120(81)90952-8 -
Journal of Clinical Research in... Nov 2020Pycnodysostosis is a rare autosomal recessive osteosclerotic bone disorder associated with short stature and multiple bony abnormalities. Growth hormone (GH) deficiency...
Pycnodysostosis is a rare autosomal recessive osteosclerotic bone disorder associated with short stature and multiple bony abnormalities. Growth hormone (GH) deficiency may contribute to short stature in about 50% of patients. Available literature has rarely reported other pituitary hormone deficiencies in pyknodysostosis. Though the management remains conservative, recombinant human GH (rhGH) has been tried in selected patients. Here we present a case of pycnodysostosis which was evaluated for associated co-morbidities and found to have multiple pituitary hormone deficiencies. A 7-year-old girl was referred to our centre for evaluation of short stature. On examination, she had frontal and occipital bossing, limited mouth opening, hyperdontia with multiple carries, short and stubby digits and short stature. Investigation revealed dense sclerotic bones with frontal and occipital bossing, non-fusion of sutures with obtuse mandibular angle, non-pneumatised sinuses, small ‘J’ shaped sella turcica, acro-osteolysis of digits and absent medullary cavities. gene mutation analysis confirmed the diagnosis of pycnodysostosis. She was screened for associated co-morbidities and was found to have concomitant GH deficiency. Treatment with rhGH brought about an increase of 1 standard deviation score in height over 2 years and also unmasked central hypothyroidism at three months necessitating thyroxine replacement.
Topics: Abnormalities, Multiple; Child; Facies; Female; Human Growth Hormone; Humans; Hypothyroidism; Pituitary Hormones; Pituitary Hormones, Anterior; Prognosis; Pycnodysostosis; Thyroxine; Transcription Factor Pit-1
PubMed: 32248673
DOI: 10.4274/jcrpe.galenos.2020.2019.0194