Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038358 (gastric ulcer)
 5,179 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The output and concentration of gastric glycoproteins in gastric juice from patients with chronic duodenal and gastric ulcer and from controls, have been determined in the basal state and following pentagastrin stimulation. Patients with gastric ulcer had a significantly higher basal glycoprotein output, basal glycoprotein concentration and stimulated glycoprotein concentration than patients with duodenal ulcer or controls. The basal and stimulated glycoprotein output in gastric juice from patients with duodenal ulcer and controls was independent of ABO blood group and secretor status. The carbohydrate composition of the gastric glycoproteins has also been determined in the basal state, and following stimulation of gastric juice by pentagastrin, which did not influence the carbohydrate composition of the molecules. The principal carbohydrate components were galactose, N-acetylglucosamine, fucose, N-acetylgalactosamine, and sialic acid. Small amounts of mannose and glucose were detected in some gastric glycoprotein samples. The carbohydrate composition of the glycoproteins varied according to the ABO blood group and secretor status of the individual. Glycoproteins form stimulated gastric juice from non-secretors of groups A and O had a higher sialic acid content than glycoproteins from secretors of the same blood groups. There were no significant differences in the carbohydrate composition of glycoproteins from patients with chronic gastric and duodenal ulcer compared with gastric glycoproteins from control subjects of the same blood group and secretor status.
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PMID:Gastric glycoproteins in chronic peptic ulcer. 106 83

Helicobacter pylori infects over half of the world's population and is thought to be a leading cause of gastric ulcer, gastric carcinoma, and gastric malignant lymphoma of mucosa-associated lymphoid tissue type. Previously, we reported that a gland mucin (MUC6) present in the lower portion of the gastric mucosa containing alpha1,4-N-acetylglucosamine (alpha1,4GlcNAc)-capped core 2-branched O-glycans suppresses H. pylori growth by inhibiting the synthesis of alpha-glucosyl cholesterol, a major constituent of the H. pylori cell wall (Kawakubo et al. 2004. Science. 305:1003-1006). Therefore, we cloned the genomic DNA encoding cholesterol alpha-glucosyltransferase (HP0421) and expressed its soluble form in Escherichia coli. Using this soluble HP0421, we show herein that HP0421 sequentially acts on uridine diphosphoglucose and cholesterol in an ordered Bi-Bi manner. We found that competitive inhibition of HP0421 by alpha1,4GlcNAc-capped core 2-branched O-glycan is much more efficient than noncompetitive inhibition by newly synthesized alpha-glucosyl cholesterol. Utilizing synthetic oligosaccharides, alpha-glucosyl cholesterol, and monosaccharides, we found that alpha1,4GlcNAc-capped core 2-branched O-glycan most efficiently inhibits H. pylori growth. These findings together indicate that alpha1,4GlcNAc-capped O-glycans suppress H. pylori growth by inhibiting HP0421, and that alpha1,4GlcNAc-capped core 2 O-glycans may be useful to treat patients infected with H. pylori.
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PMID:Alpha1,4GlcNAc-capped mucin-type O-glycan inhibits cholesterol alpha-glucosyltransferase from Helicobacter pylori and suppresses H. pylori growth. 1845 30