Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:1.1.1.1 (alcohol dehydrogenase)
 9,284 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Some pituitary hormones secrete hormones while others do not. Nonsecreting tumors can interfere with normal pituitary hormone secretion and produce tumor symptoms and signs like headaches and visual field defects. The most frequent hormone-secreting tumors are prolactinomas. Growth hormone or ACTH or gonadotropin or gonadotropin-alpha and beta chain-producing tumors are less frequent, TSH producing tumors are extremely rare. The most important elements of the diagnostic work-up are clinical signs and symptoms, assessment of pituitary function (measurement of TSH, free T4, LH, FSH, oestradiol/free testosteron, growth hormone, IGF-1, prolactin, ACTH, Cortisol, serum and urine osmolality), CT and/or MRI and, in patients with large tumors, a visual field exam. The treatment of choice of pituitary tumors is often surgery. Alternative therapies are radiation treatment (in nonoperable patients or when hormone levels are persistently elevated after pituitary surgery) and drug treatment (dopamine agonists in hyperprolactinemia, somatostatin analogues in acromegaly). Pituitary hormone deficiencies are treated depending on the specific deficiency with thyroxine, cortisone, oestrogen/gestagen/testosterone gonadotropines or ADH analogues.
 ...
PMID:[Hypophyseal dysfunction and tumors]. 158 68

Growth hormone has previously been shown to increase the activity of alcohol dehydrogenase in primary hepatocyte culture from male rats. In this study, continuous exposure of cultured hepatocytes to growth hormone (1 microgram/ml) resulted in parallel increased in the enzyme activity of alcohol dehydrogenase and immunoreactive protein. Growth hormone increased the incorporation of [3H]leucine into alcohol dehydrogenase protein relative to the incorporation into cytosolic protein. The abundance of alcohol dehydrogenase mRNA increased on Days 3 and 4 of continuous exposure of the hepatocytes to growth hormone and returned to control levels on Day 5 of culture. Growth hormone increased the rate of transcription of the alcohol dehydrogenase gene as demonstrated by nuclear runoff experiments. These observations indicate that the effect of growth hormone in enhancing alcohol dehydrogenase activity is due to increased synthesis of the enzyme which is initiated at the level of gene transcription.
 ...
PMID:Influence of growth hormone on the synthesis of rat liver alcohol dehydrogenase in primary hepatocyte culture. 280 27

The effect of experimental diabetes on the activity of liver alcohol dehydrogenase was studied in males and females of two strains of rats. Alloxan diabetes of 8 weeks duration increased the activity of alcohol dehydrogenase in Sprague-Dawley males by about 50%. This effect was also observed in rats rendered diabetic with streptozotocin. However, there was no increase in the enzyme activity in female Sprague-Dawley rats. The magnitude of the increase was much less in diabetic Wistar-Kyoto males than in Sprague-Dawley males. Plasma concentrations of thyroxine were lower in diabetic animals than in controls, but this effect of diabetes did not correlate with changes in alcohol dehydrogenase activity. There was no reduction in plasma testosterone concentration in diabetic Sprague-Dawley rats. Growth hormone levels were not increased in the diabetic rats. The mechanism of the increase in liver alcohol dehydrogenase activity in diabetic male Sprague-Dawley rats is unknown.
 ...
PMID:The effect of experimental diabetes on liver alcohol dehydrogenase activity in rats. 293 14

We investigated the maintenance of alcohol dehydrogenase (ADH) and estrogen receptors in primary cultures of rat hepatocytes. Female hepatocytes partially lose ADH activity and completely lose estrogen receptors during 4 days in culture. Growth hormone, which induces both the enzyme and receptor in vivo, did not induce either in vitro.
 ...
PMID:Loss of sexual differentiation of rat hepatocytes in short-term culture. 342 90

Growth hormone (GH) increases the transcription of the rat class I alcohol dehydrogenase (ADH) gene. Two transcription factors, the CCAAT/enhancer binding protein (C/EBP) and the liver activator protein (LAP), were previously shown to bind to the ADH promoter at nucleotide positions -11 to -22 relative to the start-site of transcription and to activate the ADH promoter in co-transfection experiments. In this study, exposure of cultured rat hepatocytes to GH (1 micrograms/ml) for 4 days increased LAP mRNA, but not C/EBP mRNA, in conjunction with an increase in ADH mRNA. GH, in transient transfection experiments of primary rat hepatocyte cultures, activated an ADH promoter-reporter gene construct containing the C/EBP binding site, but failed to activate a construct containing a 4-bp mutation at this site. These results suggest that the effect of GH in enhancing ADH promoter activity is mediated by LAP binding to the C/EBP site.
 ...
PMID:Regulation of the rat class I alcohol dehydrogenase gene by growth hormone. 846 83

Growth hormone (GH) enhances rat liver alcohol dehydrogenase (ADH) due to an increase in enzyme synthesis, which is mediated at the level of transcription. Previous studies have shown that the effect of GH in enhancing activation of the ADH promoter is mediated by C/EBP beta binding to region -22 to -11 relative to the start of transcription. In this study, STAT5b and C/EBP beta were found to bind to adjacent nucleotide sequences on a region between -226 and -194. Expression vectors for both STAT5b and C/EBP beta independently activated the promoter. Furthermore, the expression vector for the GH receptor also activated the ADH promoter, and this effect was abrogated by mutations of the adjacent STAT5b and C/EBP beta binding sites. These observations indicate that the enhancing effect of GH is mediated by both STAT5b and C/EBP beta.
 ...
PMID:Effect of STAT5b on rat liver alcohol dehydrogenase. 1141 83

Growth hormone (GH) recently has been shown to be expressed in the neonatal rat lung during alveolarization. The possible functional importance of lung GH in lung function, therefore, has been assessed by determining changes in GH-responsive proteins in the developing rat lung after the overexpression of the GH gene in this tissue. GH overexpression was achieved using an adenovirus that expressed the mouse GH gene. This adenovirus was effective in inducing mouse GH expression in cultured rat lung L2 epithelial cells. It was also shown to be strongly expressed in the alveoli of 14-day-old rat pup lungs 10 days after it was administered by intratracheal injection, during a period of rapid lung development. Expression of the transgene in these pups was accompanied by changes in lung protein concentrations determined by two-dimensional gel electrophoresis and mass spectrometry. The lung concentrations of specific enzymes (nucleotide diphosphate kinase B, Cu/Zn superoxide dismutase, glutathione-S-transferase, and aldehyde reductase-1) were increased by the adenoviral expression of mouse GH, as were the concentrations of beta subunit G-protein calponin 2, beta-5 tubulin, retinoblastoma binding protein 4, and fetuin A. In contrast, the lung concentrations of haptoglobin and major acute phase alpha-1 protein were reduced by adenoviral expression of mouse GH. Although most of these proteins have not previously been identified as GH-responsive proteins, these results demonstrate actions of GH in the rat lung and support the possibility that GH acts as an autocrine/paracrine during early lung development.
 ...
PMID:Growth hormone (GH) action in the developing lung: changes in lung proteins after adenoviral GH overexpression. 1612 21

Growth hormone (GH) transgenic amago salmon (Oncorhynchus masou) were generated with a construct containing the sockeye salmon GH1 gene fused to the metallothionein-B (MT-B) promoter from the same species. This transgene directed significant growth enhancement with transgenic fish reaching approximately four to five times greater weight than control salmon in F(2) and F(3) generations. This drastic growth enhancement by GH transgene is well known in fish species compared with mammals, however, such fish can show morphological abnormalities and physiological disorders like other GH transgenic animals. GH is known to have many acute effects, but currently there are no data describing the chronic effects of over-expression of GH on various hepatic genes in GH transgenic fish. Hepatic gene expression is anticipated to play very important roles in many physiological functions and growth performance of transgenic and control salmon. To examine these effects, we performed subtractive hybridization (using cDNA generated from liver RNA) in both directions to identify genes both increased and decreased in transgenic salmon relative to controls (576 clones were isolated and sequenced in total). Heme oxygenase, vitelline envelope protein, Acyl-coA binding protein, NADH dehydrogenase, mannose binding lectin-associated serine protease, hemopexin-like protein, leucyte-derived chemotaxin2 (LECT2), and many other genes were obtained in higher clone frequencies suggesting enhanced expression. In contrast, complement C3-1, lectin, rabin, alcohol dehydrogenase, Tc1-like transposase, Delta6-desaturase, and pentraxin genes were obtained in lower frequencies. Microarray analysis was also performed to obtain quantitative expression data for these subtracted cDNA clones. Analysis of fish across seasons was also conducted using both F(2) and F(3) salmon. Results of the microarray data essentially corresponded with those of the subtraction data when both F(2) and F(3) fish were completely immature, but the expression pattern was changed when fish approached maturation. Genes showing enhanced expression in GH transgenic fish in F(2) and F(3) by array analysis were vitelline envelope protein, hemopexin-like protein, heme-oxygenase, inter alpha-trypsin inhibitor, LECT2, GTP cyclohydrolase I feedback regulatory protein (GFRP), and bikunin. Reduced expression genes were lectin, Delta6-desaturase, apolipoprotein, and pentraxin. In particular, lectin was found to be highly suppressed in all F(2) and immature F(3) salmon. Further, serum lysozyme activity, one of innate immunity, was significantly (p<0.05) decreased in both F(2) and F(3) GH transgenic fish. These results indicate that the GH transgene fish had altered hepatic gene expression relating to iron-metabolism, innate immunity, reproduction, and growth.
 ...
PMID:Changes in hepatic gene expression related to innate immunity, growth and iron metabolism in GH-transgenic amago salmon (Oncorhynchus masou) by cDNA subtraction and microarray analysis, and serum lysozyme activity. 1722 41