Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P01275 (glucagon)
26,492 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Serine dehydratase (L-serine hydro-lyase, EC 4.2.1.13) WAS DEMONSTRATED IN LIVER TISSUE OF RATS BY AN INdirect immunofluorescent method. In the adult rat liver, serine dehydratase was localized to periportal hepatocytes, diffusely in their cytoplasm. The enzyme-specific fluorescence was absent or extremely low in the centrolobular hepatocytes. It was not demonstrated in nonparenchymal cells. Feeding a 90% protein diet for 5 days caused marked induction of this enzyme in the periportal and midzonal hepatocytes but no induction in the centrolobular hepatocytes. In the newborn rat liver, there was no apparent intralobular heterogeneity seen in the distribution of serine dehydratase, either before or after dietary induction. After 1 week of age, there was a gradual development of the intralobular hetero-geneity of the enzyme, which was emphasized by dietary stimulation. A comparative study of the induction pattern between the livers of intact and adrenalectomized rats suggested that there is no heterogeneity among serine-dehydratase-positive cells with respect to hormonal regulation of this enzyme by either glucagon or cortisone.
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PMID:Immunohistochemical demonstration of serine dehydratase in rat liver. 16 93

Solubilization of myocardial adenylate cyclase abolished responsiveness to glucagon and catecholamines, two of the hormones which activate the membrane-bound enzyme. Adenylate cyclase freed of detergent by DEAE-cellulose chromatography continues to remain unresponsive to hormone stimulation. However, adding purified bovine brain phospholipids--phosphotidylserine and monophosphatidylinositol--restored responsiveness to glucagon and catecholamines, respectively. 125-i-glucagon binding appeared to be independent of phospholipid, since equal binding was observed in the presence or absence of detergent and in the presence or absence of phospholipids. Chromatography of the solubilized preparation on Sephadex G-100 WAS CHARACTERIZED BY 125-I-glucagon binding and fluoride-stimulatable adenylate cyclase activity appearing in the fractions consistent with the void volume, suggesting a molecular weight greater than 100,000 for the receptor-adenylate cyclase complex. Prior incubation of the binding peak with 125-I-glucagon and rechromatography of the bound glucagon on Sephadex G-100 shifted its elution to a later fraction consistent with a smaller-molecular-weight peak. The molecular weight of this material was 24,000 to 28,000, as determined by SDS polyacrylamide gel electrophoresis. The latter findings are consistent with a dissociable receptor site for glucagon on myocardial adenylate cyclase.
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PMID:Glucagon and adenylate cyclase: binding studies and requirements for activation. 16 84

Stress-induced intestinal barrier dysfunction may be involved in chronic intestinal disorders. Glucagon-like peptide-2 (GLP-2) is an intestinotrophic growth hormone that can rapidly improve intestinal epithelial barrier function. Here, we investigated whether mouse intestine is responsive to chronic psychological stress and whether pretreatment with GLP-2 can ameliorate stress-induced changes. Mice were subjected to water avoidance stress (WAS; 1 h/day for 10 days) with GLP-2 or saline administered 4 h before each WAS session. After the final stress period, the intestine was removed for assessment of physiological/morphological changes. Compared with controls (sham-stressed mice), stressed mice demonstrated enhanced ion secretion and permeability in the jejunum, ileum, and colon. In addition, increased numbers of bacteria were observed adhering to and/or penetrating the epithelium, associated with infiltration of mononuclear cells into the mucosa. GLP-2 treatment improved intestinal barrier function in stressed mice and ameliorated other aspects of impaired host defense. Our study extends previous findings in rats of stress-induced intestinal dysfunction and provides insights into potential novel therapeutics.
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PMID:Stress impairs murine intestinal barrier function: improvement by glucagon-like peptide-2. 1579 4