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Toxicology Letters Nov 1999Cadmium specifically modify amine metabolism at the central nervous system and pituitary hormone secretions. Thus, the physiological functions controlled by these... (Review)
Review
Cadmium specifically modify amine metabolism at the central nervous system and pituitary hormone secretions. Thus, the physiological functions controlled by these hormones can be modulated by cadmium. This xenobiotic is associated with deleterious effects on the gonadal function and with changes in the secretory pattern of other pituitary hormones like prolactin, ACTH, GH or TSH. The observed changes in pituitary hormone secretion do not correlate with the modifications of central nervous system metabolism of the neurotransmitters involved in their regulation. The accumulative data indicates the existence of a disruption in the regulatory mechanisms of the hypothalamic-pituitary axis. The physiological significance of these effects remains to be elucidated.
Topics: Adrenocorticotropic Hormone; Animals; Cadmium; Follicle Stimulating Hormone; Growth Hormone; Humans; Hypothalamus; Luteinizing Hormone; Male; Neurotransmitter Agents; Pituitary Hormones; Prolactin
PubMed: 10597030
DOI: 10.1016/s0378-4274(99)00159-9 -
General and Comparative Endocrinology Aug 2023The secretion of vertebrate pituitary hormones is regulated by multiple hypothalamic factors, which, while generally activating unique receptor systems, ultimately...
The secretion of vertebrate pituitary hormones is regulated by multiple hypothalamic factors, which, while generally activating unique receptor systems, ultimately propagate signals through interacting intracellular regulatory elements to modulate hormone exocytosis. One important family of intracellular regulators is the monomeric small GTPases, a subset of which (Arf1/6, Rac, RhoA, and Ras) is highly conserved across vertebrates and regulates secretory vesicle exocytosis in many cell types. In this study, we investigated the roles of these small GTPases in basal and agonist-dependent hormone release from dispersed goldfish (Carassius auratus) pituitary cells in perifusion experiments. Inhibition of these small GTPases elevated basal LH and GH secretion, except for Ras inhibition which only increased basal LH release. However, variable responses were observed with regard to LH and GH responses to the two goldfish native gonadotropin-releasing hormones (GnRH2 and GnRH3). GnRH-dependent LH release, but not GH secretion, was mediated by Arf1/6 GTPases. In contrast, inhibition of Rac and RhoA GTPases selectively enhanced GnRH3- and GnRH2-dependent GH release, respectively, while Ras inhibition only enhanced GnRH3-evoked LH secretion. Together, our results reveal novel divergent cell-type- and ligand-specific roles for small GTPases in the control of goldfish pituitary hormone exocytosis in unstimulated and GnRH-evoked release.
Topics: Animals; Goldfish; Monomeric GTP-Binding Proteins; Growth Hormone; Pituitary Gland; Gonadotropin-Releasing Hormone; Pituitary Hormones; Cells, Cultured
PubMed: 37060929
DOI: 10.1016/j.ygcen.2023.114287 -
Cytokine & Growth Factor Reviews Jun 1996The protein mediator known as macrophage migration inhibitory factor (MIF) was one of the first cytokine activities to be discovered and was described 30 years ago to be... (Review)
Review
The protein mediator known as macrophage migration inhibitory factor (MIF) was one of the first cytokine activities to be discovered and was described 30 years ago to be a T cell-derived factor that inhibited the random migration of macrophages. Despite the long-standing association of MIF with activated lymphocytes, the precise role of MIF in host responses remained undefined. Recent studies however, have led to the description of a pituitary mediator that appears to act as the natural, counter-regulatory hormone for glucocorticoid action within the immune system. Isolated as a product of an anterior pituitary cell line, this protein was sequenced and found to have the same structure as MIF. The major role of MIF appears to be to act at an inflammatory site or lymph node to counter-balance the inhibitory effects of steroids on the primary immune response, which must necessarily be mounted to eliminate the source of infection or tissue invasion.
Topics: Animals; Antibody Formation; Cytokines; Glucocorticoids; Humans; Inflammation; Macrophage Migration-Inhibitory Factors; Models, Molecular; Pituitary Hormones
PubMed: 8864351
DOI: 10.1016/1359-6101(96)00008-1 -
Pituitary 2007This clinical review summarizes current approaches to diagnosis and treatment of anterior pituitary hormone deficiency. The diagnostic value of endocrine function tests... (Review)
Review
This clinical review summarizes current approaches to diagnosis and treatment of anterior pituitary hormone deficiency. The diagnostic value of endocrine function tests and replacement strategies for hydrocortisone, thyroxine, sex steroids, and growth hormone replacement are reviewed. Female androgen deficiency syndrome and the current role of DHEA and testosterone replacement in women are also discussed.
Topics: Adrenal Insufficiency; Adult; Diagnostic Techniques, Endocrine; Female; Hormone Replacement Therapy; Human Growth Hormone; Humans; Hydrocortisone; Hypogonadism; Hypopituitarism; Male; Pituitary Hormones, Anterior; Testosterone
PubMed: 17265188
DOI: 10.1007/s11102-007-0001-6 -
Peptides Nov 2009
Topics: Animals; Feeding Behavior; Humans; Hypothalamic Hormones; Melanins; Neuropeptides; Pituitary Hormones; Receptors, Pituitary Hormone
PubMed: 19765628
DOI: 10.1016/j.peptides.2009.09.014 -
European Journal of Endocrinology Nov 2009Severe GH deficiency (GHD) in adults has been described as a clinical entity. However, some of the features associated with GHD could be due to unphysiological and... (Review)
Review
Severe GH deficiency (GHD) in adults has been described as a clinical entity. However, some of the features associated with GHD could be due to unphysiological and inadequate replacement of other pituitary hormone deficiencies. This may be true for glucocorticoid replacement that lacks a biomarker making dose titration and monitoring difficult. Moreover, oral estrogen replacement therapy decreases IGF1 levels compared with the transdermal route, which attenuates the responsiveness to GH replacement therapy in women. In addition, in untreated female hypogonadism, oral estrogen may augment the features associated with GHD in adult women. Important interactions between the hormones used for replacing pituitary hormone deficiency occur. Introducing GH replacement may unmask both an incipient adrenal insufficiency and central hypothyroidism. Therefore, awareness and proper monitoring of these hormonal interactions are important in order to reach an optimal replacement therapy. This review will focus on the complex hormonal interactions between GH and other pituitary hormones in GHD and in GH replacement.
Topics: Administration, Cutaneous; Administration, Oral; Adrenal Insufficiency; Adult; Biomarkers; Estrogen Replacement Therapy; Estrogens; Female; Glucocorticoids; Human Growth Hormone; Humans; Hypopituitarism; Hypothyroidism; Male; Middle Aged; Pituitary Hormones; Severity of Illness Index; Sex Factors; Thyroxine
PubMed: 19684055
DOI: 10.1530/EJE-09-0319 -
Experimental and Clinical Endocrinology... 1997Synthesis of pituitary hormones was shown to be efficiently regulated at the transcriptional level. The specialized function of the five cell types in the anterior... (Review)
Review
Synthesis of pituitary hormones was shown to be efficiently regulated at the transcriptional level. The specialized function of the five cell types in the anterior pituitary is controlled by ubiquitous as well as cell-specific transcription factors. Pit-1 is such a cell-specific regulator found only in lacto-, somato- and thyrotropes which could be shown to be essential for basal expression of growth hormone (GH) and prolactin (Prl) genes and the regulated expression of Prl and thyrotropin (TSH) beta-subunit genes. Identification of distinct binding sites for transcription factors and some of the mechanisms of transcriptional control shed light on the complex regulation of pituitary hormone gene expression which is exemplified for the TSH beta gene. The control of basal as well as positively and negatively regulated expression of some pituitary hormone genes becomes fairly well understood by the investigation of the role of Pit-1. Identification of different mutations in the human pit-1 gene supported the role of this protein for combined pituitary hormone deficiency (CPHD) characterized by the deficiency of GH, prolactin and TSH.
Topics: Animals; DNA-Binding Proteins; Gene Expression Regulation; Humans; Mutation; Pituitary Hormones; Pituitary Hormones, Anterior; Thyrotropin; Transcription Factor Pit-1; Transcription Factors
PubMed: 9285205
DOI: 10.1055/s-0029-1211751 -
Life Sciences Aug 1982Anatomical and biochemical studies have identified a hypothalamic tubero-infundibular GABAergic system, which plays a functional role on anterior pituitary hormone... (Review)
Review
Anatomical and biochemical studies have identified a hypothalamic tubero-infundibular GABAergic system, which plays a functional role on anterior pituitary hormone secretion. Experimental and clinical evidence support the presence of a dual component in the action of GABA; one mediated via the central nervous system and the other exerted directly at the anterior pituitary level. The two sites of action may be responsible for the excitatory and inhibitory effects of GABA on pituitary hormone and especially prolactin secretion. The future characterization of this system will provide a better understanding of the involvement of GABA in the physiology of anterior pituitary hormone secretion and will contribute to the development of new pharmacological agents for the therapy of neuroendocrine disorders.
Topics: Adrenocorticotropic Hormone; Animals; Female; Growth Hormone; Humans; In Vitro Techniques; Luteinizing Hormone; Male; Pituitary Gland, Anterior; Pituitary Hormones, Anterior; Prolactin; Rats; Receptors, Cell Surface; Receptors, GABA-A; Thyrotropin; gamma-Aminobutyric Acid
PubMed: 6294431
DOI: 10.1016/0024-3205(82)90537-9 -
Acta Endocrinologica Jun 1991The neurotransmitter histamine participates in the neuroendocrine regulation of pituitary hormone secretion by an indirect action at a hypothalamic level where... (Review)
Review
The neurotransmitter histamine participates in the neuroendocrine regulation of pituitary hormone secretion by an indirect action at a hypothalamic level where histaminergic neurons are abundant. The effect of histamine is caused by activation of postsynaptic H1- or H2-receptors. Histamine stimulates the secretion of ACTH, beta-endorphin (mediated by CRH and AVP), alpha-MSH (mediated by dopamine and peripheral catecholamines), and PRL (mediated by dopamine, serotonin and AVP), and participates in the stress-induced release of these hormones and possibly in the suckling- and estrogen-induced PRL release. The release of GH and TSH is predominantly inhibited by histamine; however, uncertainty exists regarding its role and the hypothalamic factors involved. Histamine increases the secretion of LH in females (mediated by GnRH), and may be involved in the mediation of the estrogen-induced LH surge. AVP and oxytocin are stimulated by histamine, probably by an effect in the supraoptic and paraventricular nuclei of the hypothalamus.
Topics: Animals; Endocrine Glands; Histamine; Humans; Nervous System Physiological Phenomena; Pituitary Hormones
PubMed: 2068891
DOI: 10.1530/acta.0.1240609 -
Annales D'endocrinologie Feb 2008Congenital hypopituitarism is characterized by multiple pituitary hormone deficiency, including somatotroph, thyrotroph, lactotroph, corticotroph or gonadotroph... (Review)
Review
DEFINITION
Congenital hypopituitarism is characterized by multiple pituitary hormone deficiency, including somatotroph, thyrotroph, lactotroph, corticotroph or gonadotroph deficiencies, due to mutations of pituitary transcription factors involved in pituitary ontogenesis.
INCIDENCE
Congenital hypopituitarism is rare compared with the high incidence of hypopituitarism induced by pituitary adenomas, transsphenoidal surgery or radiotherapy. The incidence of congenital hypopituitarism is estimated to be between 1:3000 and 1:4000 births.
CLINICAL SIGNS
Clinical presentation is variable, depending on the type and severity of deficiencies and on the age at diagnosis. If untreated, main symptoms include short stature, cognitive alterations or delayed puberty.
DIAGNOSIS
A diagnosis of combined pituitary hormone deficiency (CPHD) must be suspected when evident causes of hypopituitarism (sellar tumor, postsurgical or radioinduced hypopituitarism...) have been ruled out. Clinical, biological and radiological work-up is very important to better determine which transcription factor should be screened. Confirmation is provided by direct sequencing of the transcription factor genes.
AETIOLOGY
Congenital hypopituitarism is due to mutations of several genes encoding pituitary transcription factors. Phenotype varies with the factor involved: PROP1 (somatolactotroph, thyrotroph, gonadotroph and sometimes corticotroph deficiencies; pituitary hyper and hypoplasia), POU1F1 (somatolactotroph and thyrotroph deficiencies, pituitary hypoplasia), HESX1 (variable pituitary deficiencies, septo-optic dysplasia), and less frequently LHX3 (somatolactotroph, thyrotroph and gonadotroph deficiencies, limited head and neck rotation) and LHX4 (variable pituitary deficiencies, ectopic neurohypophysis, cerebral abnormalities).
MANAGEMENT
An appropriate replacement of hormone deficiencies is required. Strict follow-up is necessary because patients develop new deficiencies (for example late onset corticotroph deficiency in patients with PROP1 mutations). GENETIC COUNSELLING: Type of transmission varies with the factor and the mutation involved (recessive transmission for PROP1 and LHX3, dominant for LHX4, autosomal or recessive for POU1F1 and HESX1).
PROGNOSIS
It is equivalent to patients without pituitary deficiencies if treatment is started immediately when diagnosis is confirmed, and if a specialized follow-up is performed.
Topics: Diagnosis, Differential; Homeodomain Proteins; Hormone Replacement Therapy; Humans; Hypopituitarism; Pituitary Hormones; Transcription Factor Pit-1
PubMed: 18291347
DOI: 10.1016/j.ando.2008.01.001