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)

Previous work with chickens (Gallus gallus domesticus) suggests a relationship between depressed thyroid hormone status and enhanced adrenal steroidogenic function. In addition, in hypophysectomized chickens, replacement of the thyroid hormone, 3,5,3'-triiodothyronine (T3), maintains chicken adrenal steroidogenic cell sensitivity to adrenocorticotropin (ACTH) but decreases steroidogenic capacity further than that due to hypophysectomy alone. The present in vivo and in vitro studies were conducted to determine the influence of thyroid status and T3 per se on avian adrenal steroidogenic function. Chicks (1 day old) were thyroidectomized using combined surgical and chemical (6-propyl-2-thiouracil) treatments and were administered a replacement dose of T3 (0, 1.5, 4.5, 15, and 45 microg/kg body wt/day) for 5 weeks. Whereas thyroidectomy (TX) decreased adrenal weight (-20%), it increased relative adrenal weight (mg/100 g body weight) (+171%), trunk plasma corticosterone (+880%), and aldosterone (+124%). In addition, TX increased basal, maximal ACTH-induced, maximal 8-bromo-cyclic AMP-induced, and maximal 25-hydroxycholesterol-supported corticosterone production (+520, +93, +124, and +195%, respectively) and aldosterone production (+578, +288, +280, and +275%, respectively) by isolated adrenal steroidogenic cells. T3, in a dose-dependent manner, reversed the effects of TX on these in vivo and in vitro parameters of adrenal steroidogenic function. Restoration of most of these parameters to those in the sham-treated control was attained with 4.5-15 microg/kg body wt/day. Although some of the effects of TX and T3 replacement on adrenal steroidogenic function may have been mediated through changes in circulating levels of ACTH, other data suggest a direct effect on adrenal steroidogenic cell function. Adrenal steroidogenic cells from sham-treated and TX birds were preincubated (0, 4, and 12 hr) with various concentrations of T3 (0, 0.3, 3, and 30 nM), washed, and then incubated for an additional 2 hr in medium containing the same respective concentrations of T3, with or without a maximal steroidogenic concentration of ACTH (100 nM). T3 had no acute effects on TX-dependent enhancement of adrenal steroidogenic cell function (2-hr incubation). However, with preincubation (4 and 12 hr), T3 inhibited basal and maximal ACTH-induced corticosterone production in a dose-dependent manner. This concentration-dependent, direct effect of T3 was not observed with cells from sham-treated birds. In addition, the ostensibly inactive thyroid hormone metabolite, 3,3',5'-triiodothyronine [reverse T3; 30 nM], was without effect. Taken collectively, these studies indicate that T3 is a direct negative modulator of avian adrenal steroidogenic function.
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PMID:The thyroid hormone, 3,5,3'-triiodothyronine, is a negative modulator of domestic fowl (Gallus gallus domesticus) adrenal steroidogenic function. 924 33

Previous work with growing chickens (Gallus gallus domesticus) indicates that transient dietary protein restriction induces long-term enhancement of adrenal steroidogenic function in response to adrenocorticotropin (ACTH). The present study investigated two possible cellular functions mediating this enhanced response: (a) ACTH signal transduction and dissemination and (b) short-loop feedback inhibition of ACTH-induced corticosterone production by exogenous corticosterone. Cockerels (2 weeks old) were fed isocaloric synthetic diets containing either 20% (control) or 8% (restriction) soy protein for 4 weeks. Adrenal glands were processed for the isolation of adrenal steroidogenic cells nearly devoid of chromaffin cells ( approximately 90% adrenal steroidogenic cells). Results of experiments to assess signal transduction and dissemination indicated that protein restriction selectively enhanced ACTH-induced corticosterone production mediated by the cyclic AMP (cAMP)-dependent pathway. In addition, protein restriction substantially counteracted exogenous corticosterone-dependent inhibition of acute ACTH-induced corticosterone production (by 40.7% vs control). The proximal portion of the cAMP pathway seemed most affected by this stressor. Protein-restricted cells exhibited enhanced homologous sensitization to ACTH (136% greater than that of control cells) which appeared to be localized at a step(s) prior to or at the formation to cAMP. Also, maximal ACTH-induced cAMP production and sensitivity to ACTH in terms of cAMP production by protein-restricted cells were, respectively, 2.2 and 15.8 times those of control cells. However, variable results were obtained from other experiments designed to pinpoint the altered early steps in ACTH-transmembranous signaling. For example, with intact cells, cAMP responses to cholera toxin (CT) and forskolin (FSK) did not corroborate the results suggesting an augmentation of ACTH-signal transduction induced by protein restriction. Furthermore, basal and stimulatable (by ACTH, CT, FSK, and NaF) adenylyl cyclase activities from membranes from protein-restricted cells were, respectively, 47.2 and 40.2% less than those from control cells (normalized to 10(7) cell equivalents of crude membranes). Collectively, these findings suggest that protein restriction stress potentiates ACTH-induced corticosterone secretion by chicken adrenal steroidogenic cells in at least two ways: (1) on the proximal end, by modulating unknown factors which enhance cellular sensitivity to ACTH, ACTH receptor-adenylyl cyclase coupling, and adenylyl cyclase activity, and (2) on the distal end, by suppressing end-product corticosterone negative feedback, thus facilitating an increase in net corticosterone secretion.
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PMID:Dietary protein restriction stress in the domestic fowl (Gallus gallus domesticus) alters adrenocorticotropin-transmembranous signaling and corticosterone negative feedback in adrenal steroidogenic cells. 1008 28

CRH is known as the main stimulator of ACTH release. In representatives of all nonmammalian vertebrates, CRH has also been shown to induce TSH secretion, acting directly at the level of the pituitary. We have investigated which cell types and receptors are involved in CRH-induced TSH release in the chicken (Gallus gallus). Because a lack of CRH type 1 receptors (CRH-R1) on the chicken thyrotropes has been previously reported, two hypotheses were tested using in situ hybridization and perifusion studies: 1) TSH secretion might be induced in a paracrine way involving melanocortins from the corticotropes; and 2) thyrotropes might express another type of CRH-R. For the latter, we have cloned a partial cDNA encoding the chicken CRH-R2. Neither alpha-melanotropin (alpha-MSH) nor its powerful analog Nle4,d-Phe7-MSH could mimic the in vitro TSH-releasing effect of ovine CRH. The nonselective melanocortin receptor blocker SHU91199 did not influence CRH- or TRH-induced TSH secretion. On the other hand, we have found that thyrotropes express CRH-R2 mRNA. The involvement of this CRH receptor in the response of thyrotropes to CRH was further confirmed by the fact that TSH release was stimulated by human urocortin III, a CRH-R2-specific agonist, whereas the TSH response to CRH was completely blocked by the CRH-R blocker astressin and the CRH-R2-specific antagonist antisauvagine-30. We conclude that CRH-induced TSH secretion is mediated by CRH-R2 expressed on thyrotropes.
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PMID:Corticotropin-releasing hormone (CRH)-induced thyrotropin release is directly mediated through CRH receptor type 2 on thyrotropes. 1297 Jan 66

Alpha-melanocyte-stimulating hormone (MSH) is well known as an anorexigenic peptide in the brain of mammals. In addition to this, brain alpha-MSH enhances heat production (HP), indicating that the peptide acts as a catabolic factor in the regulation of energy metabolism. The anorexigenic effect of alpha-MSH is also observed in chicks (Gallus gallus), but no information has been available for its effect on HP. The present study was performed to examine whether intracerebroventricular (ICV) injection of alpha-MSH increases HP in chicks. The injection of alpha-MSH (10 and 100 pmol) did not affect oxygen consumption, carbon dioxide production and HP during the 1 h post-injection period. This result was supported by another result that ICV injection of alpha-MSH did not affect locomotion activity in chicks. In contrast, the respiratory quotient was significantly lowered by the ICV injection of MSH. We also found that alpha-MSH significantly increased plasma non-esterified fatty acid concentrations. In summary, brain alpha-MSH appears to exert generally catabolic effects on lipid metabolism in the chick, but does not appear to be involved in the regulation of HP.
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PMID:Central administration of alpha-melanocyte-stimulating hormone changes lipid metabolism in chicks. 1760 Jul 45

Regulation of arginine vasotocin (AVT), avian neurohypophyseal hormone, is an important component of the hypothalamo-pituitary-adrenal axis. Changes in plasma osmolality levels and sex steroids are known to affect AVT gene expression. The present study reports the effect of water deprivation and testosterone treatment independently, as well as simultaneously, on the pituitary vasotocin receptor VT2R expression and adrenal steroidogenic activity in sexually immature male chicken (Gallus gallus). Birds were divided into four groups- control, water deprived (WD), testosterone injected (TE) and TE treated water deprived (TE+WD). WD decreased and TE treatment alone or in combination with WD (TE+WD) increased VT2R expression compared to the control. Expression of pro-opiomelanocortin (POMC) was also studied since this gene is a polypeptide precursor of ACTH and is under the negative feedback of adrenal corticoids. TE treatment as well as WD separately or when coupled together decreased the POMC mRNA expression in the pituitary but stimulated adrenal steroidogenic activity. Further, VT2R expression decreased in TE+WD compared to TE group, but it was not different from the vehicle treated control group suggesting that the suppressive effect of WD on VT2R expression was inhibited by the stimulatory effect of testosterone. Similarly, although both TE and WD decreased POMC expression and increased steroidogenic activity, no further decrease or increase in these parameters was observed when these two (WD and TE) treatments were combined together. Although, the exact mechanism is not clear, data indicate a stimulatory action of testosterone on VT2R expression and adrenal function despite a decreased expression of POMC mRNA. Results also suggest that testosterone treatment to sexually immature birds, in addition to its effect on hypothalamic AVT neurons (earlier study) and pituitary VT2R expression (present study), masks or inhibits osmotic stress-induced alterations in pituitary-adrenal activity.
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PMID:Testosterone modulates pituitary vasotocin receptor expression and adrenal activity in osmotically stressed chicken. 2085 May 59

Growth hormone-releasing hormone (GHRH) is well known as a stimulator of growth hormone (GH) secretion. GHRH not only stimulates GH release but also modifies feeding behavior and energy homeostasis in rodents. In chickens (Gallus gallus domesticus), on the other hand, two types of GHRH, namely, chicken GHRH (cGHRH) and cGHRH-like peptide (cGHRH-LP), have been identified. The purpose of the present study was to investigate the effect of central injection of cGHRH and cGHRH-LP on feeding behavior in chicks. Intracerebroventricular (ICV) injection of both cGHRH and cGHRH-LP (0.04 to 1 nmol) significantly decreased food intake without any abnormal behavior in chicks. Furthermore, the feeding-inhibitory effect was not abolished by co-injection of the antagonist for pituitary adenylate cyclase-activating polypeptide (PACAP) or corticotropin-releasing hormone (CRH) receptors, suggesting that the anorexigenic effect of cGHRH and cGHRH-LP might not be related to the PACAP and CRH systems in the brain of chicks. Finally, 24-h food deprivation increased mRNA expression of cGHRH but not cGHRH-LP in the diencephalon. These results suggest that central cGHRH is related to inhibiting feeding behavior and energy homeostasis in chicks.
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PMID:Central administration of chicken growth hormone-releasing hormone decreases food intake in chicks. 2544 98

The purpose of the present study was to clarify whether acute injection of stress-related hormones, corticosterone (CORT), norepinephrine (NE) and epinephrine (E) affect food passage in the crop of chicks (Gallus gallus). Subcutaneous (SQ) injection of CORT significantly retarded the food passage in the crop of chicks. Intraperitoneal (IP) injection of NE and E also significantly decreased the crop emptying rate. Additional experiments by using agonists of adrenergic receptors found that IP injection of phenylephrine and clonidine but not isoproterenol retarded the food passage in the crop of chicks. These results demonstrated that the effect of NE and E would be mediated by alpha-1-, alpha-2- rather than beta-adrenergic receptor. Finally, we found that injection of CORT, NE and E had no effect on the number of defecations while intracerebroventricular injection of corticotropin-releasing hormone and urocortin-3 significantly increased it. These results suggest that CORT, NE and E might affect the food passage in the upper digestive tract in chicks.
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PMID:Acute injections of corticosterone, norepinephrine and epinephrine retards food passage in the crop of chicks. 2651 62

Urocortin 3 (UCN3) is a neuropeptide believed to regulate stress-coping responses by binding to type 2 corticotropin-releasing hormone receptors. Here, we report the cloning and brain distribution of UCN3 mRNA in a sauropsid-the chicken, Gallus gallus. Mature chicken UCN3 is predicted to be a 40-amino acid peptide showing high sequence similarity to human (93%), mouse (93%), and Xenopus (88%) UCN3. During the last third of embryonic development, UCN3 mRNA levels changed differentially in the various brain parts. In all brain parts, UCN3 mRNA levels tended to increase toward hatching, except for caudal brainstem, where a gradual decrease was observed during the last week of embryonic development. In cerebellum, a rapid increase in gene expression occurred between embryonic days 17 and 19. Using in situ hybridization, UCN3 mRNA was found to be expressed predominantly in the hypothalamus, pons, and medulla of posthatch chick brains, but not in some areas that are among the main expression sites in rodents, such as the brain areas where in mammals the median preoptic nucleus and the medial amygdala are located. This suggests that the roles of UCN3 in chicken, and perhaps sauropsids in general, are not all identical to those in rodents.
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PMID:Spatial and temporal expression profiles of urocortin 3 mRNA in the brain of the chicken (Gallus gallus). 2839 19