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Cell‐specific Localization of the Cholecystokinin A Receptor in the Porcine Pancreas
Author(s) -
Schweiger M.,
Erhard M. H.,
Amselgruber W. M.
Publication year - 2000
Publication title -
anatomia, histologia, embryologia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.34
H-Index - 35
eISSN - 1439-0264
pISSN - 0340-2096
DOI - 10.1046/j.1439-0264.2000.00286.x
Subject(s) - cholecystokinin , cholecystokinin receptor , pancreas , receptor , glucagon , biology , medicine , gastrin , endocrinology , extracellular , microbiology and biotechnology , secretion , chemistry , insulin , biochemistry
Summary Cholecystokinin (CCK) produced in the mucosa of the upper small intestine exerts several biological functions. Its secretion in physiological amounts is modulated by the interaction of extracellular regulators and by binding to intracellular receptors of the target cells. The relative affinity of CCK to its receptor has been characterized in various biological and pharmacological studies and it is now well established that CCK has a higher affinity to the CCK A than to the CCK B receptor. Furthermore CCK influences the secretion of pancreatic enzymes in several species but very little is known about the relationship between CCK and the islet hormone‐producing cells in the pig pancreas. The localization of this receptor at the cellular level showed conflicting results in animal studies and has not been described in pigs. The aim of the present study was to characterize the precise cellular location of the CCK A receptor in the porcine pancreas. Polyclonal antiserum was raised against the N‐terminal epitope of the CCK A receptor molecule and used for localization studies. Using immunohistochemistry on methanol/acetic acid‐fixed, paraffin‐embedded pancreas, the CCK A receptor could successfully be localized in islet cells. Parallel staining of serial sections with antibodies directed against insulin and glucagon revealed colocalization with glucagon in alpha cells. No immunoreaction was found in the exocrine pancreas. Our results support the concept that in the porcine species the stimulation of the exocrine pancreas is mediated by the CCK B rather than the CCK A receptor, as it is known for the rat species.