[Relation between glycoprotein synthesis and carbohydrate metabolism in the small intestine mucosa. Effect of cholera enterotoxin].
The regulatory properties of adenylate cyclase in small intestinal mucosa were investigated. Glucagon, epinephrine and isoproterenol failed to activate the cAMP synthesis; prostaglandin E1 caused a 2.8-fold, while cholera toxin-a 4.5-fold stimulation. The latter was not able to increase the rate of glucose synthesis from alanine in vitro, but increased markedly the in vivo incorporation of 14C-labeled alanine into the mucus glucosamine. Unlabeled glucosamine excretion was also enhanced 3-fold. This provides evidence for the involvement of glycolysis and gluconeogenesis enzyme systems in the mucosal glycoprotein synthesis. It was assumed that both metabolic pathways may play a common physiological role, namely, to convert carbohydrates and gluconeogenic precursors into the substrate for glucosamine synthesis which is thought to be a rate-limiting step in small intestinal mucus secretion.
Vengrov
P R
PR
Cherkasova
T D
TD
Iurkiv
V A
VA
D000067956:Adenylyl Cyclase Inhibitors; D000262:Adenylyl Cyclases / Q000378:metabolism; D000818:Animals; D050260:Carbohydrate Metabolism; D002772:Cholera Toxin / Q000494:pharmacology*; D000242:Cyclic AMP / Q000378:metabolism; D004789:Enzyme Activation; D005943:Gluconeogenesis; D006023:Glycoproteins / Q000096:biosynthesis*; D007413:Intestinal Mucosa / Q000201:enzymology / Q000378:metabolism*; D007583:Jejunum / Q000201:enzymology / Q000378:metabolism*; D011817:Rabbits
D000067956:Adenylyl Cyclase Inhibitors; D006023:Glycoproteins; D002772:Cholera Toxin; D000242:Cyclic AMP; D000262:Adenylyl Cyclases
Sviaz' sinteza glikoproteidov s obmenom uglevodov v slizistoĭ obolochke tonkoĭ kishki. Vliianie kholernogo énterotoksina.