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)

In the present study, we investigated the influence of dietary protein restriction stress on adrenal steroidogenic function of the domestic turkey. Immature male turkeys (2 weeks old) were fed isocaloric synthetic diets containing either 28% (control) or 8% (restriction) soy protein for 4 weeks. Trunk plasma was processed for the determination of adrenocorticotropin (ACTH), corticosterone, aldosterone, and total 3, 5, 3'-triiodothyronine (T3). In addition, adrenal glands were processed for the isolation of defined, density-separable, adrenal steroidogenic cell subpopulations: three low-density adrenal steroidogenic cell subpopulations [LDAC-1 (rho = 1.0350-1.0490 g/ml). LDAC-2 (rho = 1.0490-1.0570 g/ml), and LDAC 3 (rho = 1.0370-1.0585 g/ml)] and a high-density subpopulation [HDAC (rho = 1.0590-1.0720 g/ml)], and the steroidogenic function of these cell subpopulations was evaluated. Protein restriction did not influence plasma ACTH However, it increased relative adrenal weight (mg/100 g body wt) (+37.8%) and plasma corticosterone (+317%). By contrast, it depressed plasma aldosterone (-51.2%). In addition, it caused a modest depression in plasma T3 (-25.9%). At the cellular level, protein restriction induced panhypofunction. Basal corticosteroid (aldosterone and corticosterone) production values of LDAC-1, -2, and -3 and HDAC from protein-restricted birds were, respectively, 42.9, 47.9, 30.8, and 57.5% less than those of corresponding cell subpopulations from control birds. In addition, maximal corticosteroid production values of LDAC-1, -2, and -3 and HDAC from protein-restricted birds, in response to ACTH, angiotensin II (AngII), and 25-hydroxycholesterol support, were depressed by 56.8, 55.1, 22.7, and 42.9%, respectively. Interestingly, LDAC-3 was relatively refractory to the influence of this stressor. By contrast, there was the lack of a concentration-dependent aldosterone response of LDAC-1 and -2 to AngII with protein restriction. This was not due to a failure in cell function since aldosterone responses of these cell subpopulations to ACTH and to 25-hydroxycholesterol support were apparent. In addition, the concentration of AngII receptors of cell subpopulations from protein-restricted turkeys, if anything, was greater than that of cell subpopulations from control turkeys. Protein restriction also altered the cell subpopulation composition of the adrenal gland: compared to control, it decreased the proportion of LDAC-2 by 42.3% and increased the proportion of LDAC-3 and HDAC by 68.7 and 302%, respectively. Thus, dietary protein restriction induces adrenal steroidogenic hypofunction in turkeys. In addition, the present study suggests that this nutritional stressor induces marked remodeling of the steroidogenic tissue in the turkey adrenal gland.
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PMID:Dietary protein restriction stress in the domestic turkey (Meleagris gallopavo) induces hypofunction and remodeling of adrenal steroidogenic tissue. 944 31

The present study focused on the cellular remodeling of steroidogenic tissue in the domestic turkey (Meleagris gallopavo) adrenal gland in response to dietary protein restriction stress. Immature male turkeys (1 week old) were fed isocaloric synthetic diets containing either 28% (control) or 8% (restriction) soy protein for 4 weeks. Adrenal glands were processed for the isolation of density- separable, visibly distinct adrenal steroidogenic cell subpopulations: three low-density subpopulations [LDAC-1 (rho = 1. 0350-1.0490 g/ml), LDAC-2 (rho = 1.0490-1.0570 g/ml), and LDAC-3 (rho = 1.0570-1.0585 g/ml)] and one high-density subpopulation [HDAC (rho = 1.0590-1.0720 g/ml)]. Dietary protein restriction increased the proportion of LDAC-3 and HDAC by 98 and 350%, respectively, and decreased LDAC-2 by 46%. LDAC-1 also showed signs of proportional decrement. To determine the role of cell death in this process, the potential for apoptosis was assessed in adrenal tissue and isolated adrenal steroidogenic cells using short-term culture followed by analysis of oligonucleosome formation. Basal, culture-triggered oligonucleosome formation of tissue and cells derived from protein-restricted birds was 80% greater than that of tissue and cells derived from control birds. This differential in apoptotic potential persisted with a variety of treatments, in vitro. Apoptotic potential was suppressed by human adrenocorticotropin and enhanced by angiotensin II (Ang II). The proapoptotic effect of Ang II (100 nM) with adrenal fragments was inhibited by the Ang II receptor antagonist [Sar(1), Ile(8)]ang II (10 microM) to below basal values (by about 60%), but the inhibition was surmountable by high concentrations (10 and 100 microM) of Ang II. The antagonist also attenuated basal, culture-triggered DNA fragmentation of tissue and cells, suggesting that at least part of the basal DNA fragmentation was due to intrinsically generated Ang II. Differences in apoptotic potential were also apparent with cell subpopulations. Compared to control subpopulations, protein restriction enhanced basal oligonucleosome formation in LDAC-1 and -2 by 38 and 122%, respectively, and reduced it in LDAC-3 and HDAC by 53 and 70%, respectively. These data suggest a role for apoptotic cell death in the remodeling of turkey adrenal steroidogenic tissue induced by dietary protein restriction. In addition, other data suggest that Ang II is an important regulator of adrenal steroidogenic cell turnover in the avian adrenal gland.
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PMID:Remodeling of turkey adrenal steroidogenic tissue induced by dietary protein restriction: the potential role of cell death. 1084 98

The paraventricular nucleus of the hypothalamus (PVH) plays a central role in regulating the hypothalamic-pituitary-adrenal (HPA) axis. Medial parvocellular neurons of the PVH (mpPVH) integrate sensory and humoral inputs to maintain homeostasis. Humoral inputs include glucocorticoids secreted by the adrenals, which down-regulate HPA activation. A primary glucocorticoid target is the population of mpPVH neurons that synthesize and secrete corticotropin-releasing factors, the most potent of which is corticotropin-releasing hormone (CRH). Although CRH gene (crh) expression is known to be down-regulated by glucocorticoids, the mechanisms by which this process occurs are still poorly understood. To begin this study we postulated that glucocorticoid repression of crh involves HDAC recruitment to the region of the crh proximal promoter. To evaluate this hypothesis, we treated hypothalamic cells that express CRH with the HDAC inhibitor trichostatin A (TSA). As predicted, treatment with TSA led to increased CRH mRNA levels and crh promoter activity. Although co-treatment with Dex (10(-7)M) reduced the TSA effect on mRNA levels, it failed to reduce promoter activity; however co-transfection of HDAC1 but not 3 restored Dex inhibition. A distinction between HDAC1 and 3 was also apparent with respect to crh promoter occupancy. Dex led to increased HDAC1 but not HDAC3 occupancy. In vivo studies revealed that CRH-immunoreactive (-ir) neurons contained HDAC1- and HDAC3-ir. Collectively, these data point to a role for HDAC1 in the physiologic regulation of crh.
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PMID:Histone deacetylase 1 (HDAC1) participates in the down-regulation of corticotropin releasing hormone gene (crh) expression. 2146 44