Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01189 (beta-endorphin)
 21,003 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Availability of recombinant growth hormone (GH) and development of long-acting formulations of this material will undoubtedly lead to widespread use of GH in animal industry and in medicine. GH can act, directly or indirectly, on multiple targets, but its influence on the reproductive system and on the hormonal control of reproduction is poorly understood. Overexpression of GH genes in transgenic animals provides a unique opportunity to study the effects of long-term GH excess. Transgenic mice overexpressing bovine, ovine, or rat GH (hormones with actions closely resembling, if not identical to, those of endogenous [mouse] GH), exhibit enhancement of growth, increased adult body size, and reduced life-span as well as a number of endocrine and reproductive abnormalities. Ectopic overexpression of bovine GH (bGH) driven by metallothionein or phosphoenolpyruvate carboxykinase promoters is associated with altered activity of hypothalamic neurons which produce somatostatin, loss of adenohypophyseal GH releasing hormone (GHRH) receptors, and suppression of endogenous (mouse) GH release. Elevation of plasma levels of GH (primarily bGH) and insulin-like growth factor (IGF-I) in these transgenic mice leads to increases in the number of hepatic GH and prolactin (PRL) receptors, in the serum levels of GH-binding protein (GHBP), in the percent of GHBP complexed with GH, and in the circulating insulin levels. In addition, plasma adrenocorticotropic hormone (ACTH) and corticosterone levels are elevated. Plasma levels of luteinizing hormone (LH), as well as its synthesis and release, are not consistently affected, but follicle-stimulating hormone (FSH) levels are suppressed, apparently due to pre- and post-translational effects. Pituitary lactotrophs exhibit characteristics of chronic enhancement of secretory activity, and plasma PRL levels are elevated. Prolactin responses to mating or to pharmacological blockade of dopamine synthesis are abnormal. Reproductive life span and efficiency are reduced in both sexes, with the severity and frequency of reproductive deficits being related to plasma bGH levels. Most transgenic females expressing high levels of bGH are sterile due to luteal failure. Overexpression of human GH which, in the mouse, interacts with both GH and PRL receptors leads to additional endocrine and reproductive abnormalities including stimulation of LH beta mRNA levels and LH secretion, loss of responsiveness to testosterone feedback, overstimulation of mammary glands, enhanced mammary tumorigenesis, and hypertrophy of accessory reproductive glands in males.
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PMID:Neuroendocrine and reproductive consequences of overexpression of growth hormone in transgenic mice. 807 44

IGF-I is expressed in somatotrophs, and IGF-I receptors are expressed in most somatotrophs and some corticotrophs in the mouse pituitary gland. Our recent study demonstrated that IGF-I stimulates the proliferation of corticotrophs in the mouse pituitary. These results suggested that somatotrophs regulate corticotrophic functions as well as somatotrophic functions by the mediation of IGF-I molecules. The present study aimed to clarify factors regulating pituitary IGF-I expression and also the roles exerted by IGF-I within the mouse anterior pituitary gland. Mouse anterior pituitary cells were isolated and cultured under serum-free conditions. GH (0.5 or 1 microg/ml), ACTH (10(-8) or 10(-7) M), GH-releasing hormone (GHRH; 10(-8) or 10(-7) M), dexamethasone (DEX; 10(-8) or 10(-7) M) and estradiol-17beta (e2; 10(-11) or 10(-9) M) were given for 24 h. IGF-I mRNA levels were measured using competitive RT-PCR, and GH and pro-opiomelanocortin (POMC) mRNA levels were measured using Northern blotting analysis. GH treatment significantly increased IGF-I mRNA levels (1.5- or 2.1-fold). ACTH treatment did not alter GH and IGF-I mRNA levels. IGF-I treatment decreased GH mRNA levels (0.7- or 0.5-fold), but increased POMC mRNA levels (1.8-fold). GH treatment (4 or 8 microg/ml) for 4 days increased POMC mRNA levels. GHRH treatment increased GH mRNA levels (1.3-fold), but not IGF-I mRNA levels. DEX treatment significantly decreased IGF-I mRNA levels (0.8-fold). e2 treatment did not affect IGF-I mRNA levels. GH receptor mRNA, probably with GH-binding protein mRNA, was detected in somatotrophs, and some mammotrophs and gonadotrophs by in situ hybridization using GH receptor cDNA as a probe. These results suggested that IGF-I expression in somatotrophs is regulated by pituitary GH, and that IGF-I suppresses GH expression and stimulates POMC expression at the transcription level. Pituitary IGF-I produced in somatotrophs is probably involved in the regulation of somatotroph and corticotroph functions.
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PMID:IGF-I regulates pro-opiomelanocortin and GH gene expression in the mouse pituitary gland. 1284 38

We investigated changes in mRNA expression of the somatotropic, thyrotropic, and corticotropic axes of Langshan (LS) and Arbor Acres (AA) broiler chickens during embryonic and postnatal development. We found an inverse expression profile between pituitary growth hormone (GH) and hepatic GH receptor mRNA [postnatal d (P)28 to P42], insulin-like growth factor (IGF)-I, and IGF-IR (P0 to P42), respectively. Hepatic IGF-I was a major point of control in the GH-IGF axis from P0 to P28. Pituitary GH-releasing hormone receptor may serve an autocrine-paracrine function from P0 to P28, and hypothalamic ghrelin may affect growth by stimulating the release of hepatic IGF-I from embryonic d (E)8 to P28. Hypothalamic ghrelin might interact with corticotropin-releasing hormone (CRH) from P0 to P28. Hepatic IGF-binding protein-2 regulated growth by regulating hepatic IGF-II bioavailability from P0 to P42. Hepatic IGF-binding protein-5 was an important IGF mediator. A coexpression profile was found between hypothalamic GH-releasing hormone (E10 to E16 and P0 to P42), somatostatin (SS; P0 to P28), thyrotropin-releasing hormone (E10 to E16 and P0 to P28), ghrelin (P0 to P42), and pituitary GH mRNA, hypothalamic SS (P0 to P28), corticotropin-releasing hormone (P0 to P42), thyrotropin-releasing hormone (E10 to E18 and P0-P42), and thyroid-stimulating hormone-beta mRNA, respectively. Moreover, AA chickens were fed a nutrient-rich AA diet (as a control group) and LS chickens were fed either a less nutritious LS diet or the AA diet. Langshan and AA chickens fed the same AA diet showed no differences in pituitary GH, hypothalamic SS, ghrelin, hepatic IGF-I, or GH receptor mRNA. Our data indicate that select genes may show parallel expression during certain periods of development, and that differences in BW and gene expression respond differently to nutrient intake in LS and AA chickens. Our findings may help improve the molecular breeding of chickens.
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PMID:Expression of genes involved in the somatotropic, thyrotropic, and corticotropic axes during development of Langshan and Arbor Acres chickens. 1880 71