neuromedin-c and Metabolism--Inborn-Errors

neuromedin-c has been researched along with Metabolism--Inborn-Errors* in 1 studies

Other Studies

1 other study(ies) available for neuromedin-c and Metabolism--Inborn-Errors

ArticleYear
An animal model of congenital defect of gene expression of cholecystokinin (CCK)-A receptor.
    Biochemical and biophysical research communications, 1995, May-25, Volume: 210, Issue:3

    Expressions of the CCK-A and B receptor genes in fetal and adult pancreas of OLETF rats were examined by the reverse transcriptase polymerase chain reaction followed by Southern blot hybridization. The pancreatic responses to various stimulants were examined in vitro and results were compared with those of control (LETO) rats. CCK-A receptor mRNA was not expressed in the fetal pancreas of either strain or in the adult pancreas of OLETF rats, but was expressed in the adult pancreas of LETO rats. CCK-B receptor mRNA was expressed in fetal and adult pancreas in both strains. Southern blot hybridization indicated a difference in gene structure in the two strains. The maximal effective concentrations of neuromedin C, carbachol, and secretin for amylase secretion and intracellular Ca2+ movement stimulated by carbachol and neuromedin C were similar in the two strains. CCK-8 and the non-sulfated form stimulated amylase secretion only in LETO rats. These results suggest that OLETF rats are a new model of a congenital defect of the CCK-A receptor gene and should be useful for determining CCK receptor function.

    Topics: Amylases; Animals; Base Sequence; Blotting, Southern; Bombesin; Brain; Calcium; Carbachol; Disease Models, Animal; DNA Primers; Female; Fetus; Gene Expression; Male; Metabolism, Inborn Errors; Molecular Sequence Data; Pancreas; Peptide Fragments; Polymerase Chain Reaction; Pregnancy; Rats; Rats, Inbred Strains; Receptor, Cholecystokinin A; Receptor, Cholecystokinin B; Receptors, Cholecystokinin; Reference Values; Secretin; Sincalide; Species Specificity

1995