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)

Extracts of the anterior lobe and intermediate lobe of postnatal (P) (Day P1, P7, P14, P21, P28, P35, P42) and adult male Sprague-Dawley rats were analyzed by both a Beta-endorphin (B-END) radioimmunoassay and a radioimmunoassay for N-acetyl-B-END. In the anterior lobe, on P1, less than 2% of the adult level of B-END was present. By P42 this level had increased to 21% of adult levels. In the intermediate lobe, on P1, the B-END levels were less than 0.1% of the adult level, and by P42 this level approached approximately 45% of the adult levels. N-acetylated B-END was identified in both anterior lobe and intermediate lobe from P1 through adulthood. In the anterior lobe at P1, N-acetyl-B-END immunoreactivity contributes approximately 25% of the total B-END immunoreactivity. This level drops to less than 10% by P21, and to adult-like levels by P42 (less than 5%). On the other hand, in the intermediate lobe, the N-acetyl-B-END levels start at 70% of the total B-END immunoreactivity at P1 and by P14 reaches adult-like proportions of 90% or more of the total B-END immunoreactive material.
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PMID:Postnatal ontogeny of acetylated and non-acetylated B-endorphin in rat pituitary. 631 11

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

Because rearing rats in large litters (LLs) protects them from becoming obese, we postulated that LL rearing would protect rats selectively bred to develop diet-induced obesity (DIO) from becoming obese by overcoming their inborn central leptin resistance. Male and female DIO rats were raised in normal litters (NLs; 10 pups/dam) or LLs (16 pups/dam) and assessed for anatomical, biochemical, and functional aspects of leptin sensitivity at various ages when fed low-fat chow or a 31% fat high-energy (HE) diet. LL rearing reduced plasma leptin levels by postnatal day 2 (P2) and body weight gain by P8. At P16, LL DIO neonates had increased arcuate nucleus (ARC) binding of leptin to its extracellular receptors and at P28 an associated increase of their agouti-related peptide and alpha-MSH axonal projections to the paraventricular nucleus. Reduced body weight persisted and was associated with increased ARC leptin receptor binding and sensitivity to the anorectic effects of leptin, reduced adiposity, and enhanced insulin sensitivity in LL DIO rats fed chow until 10 wk of age. The enhanced ARC leptin receptor binding and reduced adiposity of LL DIO rats persisted after an additional 5 wk on the HE diet. Female LL DIO rats had similar reductions in weight gain on both chow and HE diet vs. normal litter DIO rats. We postulate that LL rearing enhances DIO leptin sensitivity by lowering plasma leptin levels and thereby increasing leptin receptor availability and that this both enhances the ARC-paraventricular nucleus pathway development and protects them from becoming obese.
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PMID:Large litter rearing enhances leptin sensitivity and protects selectively bred diet-induced obese rats from becoming obese. 2066 22

Early-life adversity is associated with dysregulation of the hypothalamic-pituitary-adrenal (HPA) axis and increased susceptibility to later-life psychopathology. Specifically, there is mounting evidence suggesting that the immune system plays an important role in central nervous system (CNS) development and in the programing of behavior. The current study investigated how early-life immune challenge affects the development of CNS stress neurocircuitry by examining the gene expression profile of corticotropin-releasing hormone (CRH), CRH receptors, and the major corticosteroid receptors within the limbic-hypothalamic circuit of the developing rodent brain. Mice were administered a 0.05 mg/kg lipopolysaccharide (LPS) injection on postnatal day (P) 3 and 5 and gene expression was assessed using in situ hybridization from P14 to P28. Target genes investigated were CRH, CRH receptor-1 (CRHR1), CRH receptor-2, the mineralocorticoid receptor, and the glucocorticoid receptor (GR). Early LPS challenge resulted in a transient decrease in CRHR1 mRNA expression in the cornuammonis 1 (CA1) and CA3 regions of the hippocampus that were accompanied by increased hippocampal GR mRNA expression in the CA1 region between P14 and P21. This was followed by increased hypothalamic CRH expression in LPS-mice on P28. Our current findings suggest that early-life LPS challenge impacts the developmental trajectory of CNS stress neurocircuitry. These results lend insight into the molecular basis for the later development of stress-related behaviors as previously described in early immune challenge rodents.
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PMID:Developmental alterations in CNS stress-related gene expression following postnatal immune activation. 2273 4