Abnormal gastric histology and decreased acid production in cholecystokinin-B/gastrin receptor-deficient mice
The cholecystokinin (CCK)-B/gastrin receptor is one of several regulators of gastric acid secretion and mucosal growth. To elucidate the contribution of this receptor relative to other trophic and secretory factors, mice that lack the CCK-B/gastrin receptor have been generated and studied. Both alle...
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| Veröffentlicht in: | Gastroenterology (New York, N.Y. 1943) N.Y. 1943), 1997, Vol.112 (1), p.280-286 |
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| container_title | Gastroenterology (New York, N.Y. 1943) |
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| creator | Langhans, Nancy Rindi, Guido Chiu, Mary Rehfeld, Jens F. Ardman, Blair Beinborn, Martin Kopin, Alan S. |
| description | The cholecystokinin (CCK)-B/gastrin receptor is one of several regulators of gastric acid secretion and mucosal growth. To elucidate the contribution of this receptor relative to other trophic and secretory factors, mice that lack the CCK-B/gastrin receptor have been generated and studied.
Both alleles of the CCK-B/gastrin receptor were inactivated by targeted gene disruption. Analysis of the mice included measurement of basal gastric pH and plasma gastrin levels. In addition, multiple gastric mucosal cell types were identified by immunostaining and quantified.
Homozygous mutant mice were viable, fertile, and appeared grossly normal into adulthood. The receptor-deficient mice exhibited a marked increase in basal gastric pH (from 3.2 to 5.2) and an approximately 10-fold elevation in plasma gastrin concentration compared with wild-type controls. In the stomach of mutant animals, parietal and enterochromaffin-like cells were decreased, providing a likely explanation for the reduction in acid output. In the antrum, a decrease in somatostatin cell density and an increase in the gastrin cell number were observed, consistent with the concomitant elevation in circulating gastrin.
Together, these findings demonstrate the importance of the CCK-B/gastrin receptor in maintaining the normal cellular composition and function of the gastric mucosa. |
| doi_str_mv | 10.1016/S0016-5085(97)90000-7 |
| format | Article |
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Both alleles of the CCK-B/gastrin receptor were inactivated by targeted gene disruption. Analysis of the mice included measurement of basal gastric pH and plasma gastrin levels. In addition, multiple gastric mucosal cell types were identified by immunostaining and quantified.
Homozygous mutant mice were viable, fertile, and appeared grossly normal into adulthood. The receptor-deficient mice exhibited a marked increase in basal gastric pH (from 3.2 to 5.2) and an approximately 10-fold elevation in plasma gastrin concentration compared with wild-type controls. In the stomach of mutant animals, parietal and enterochromaffin-like cells were decreased, providing a likely explanation for the reduction in acid output. In the antrum, a decrease in somatostatin cell density and an increase in the gastrin cell number were observed, consistent with the concomitant elevation in circulating gastrin.
Together, these findings demonstrate the importance of the CCK-B/gastrin receptor in maintaining the normal cellular composition and function of the gastric mucosa.</description><identifier>ISSN: 0016-5085</identifier><identifier>EISSN: 1528-0012</identifier><identifier>DOI: 10.1016/S0016-5085(97)90000-7</identifier><identifier>PMID: 8978369</identifier><identifier>CODEN: GASTAB</identifier><language>eng</language><publisher>New York, NY: Elsevier Inc</publisher><subject>Animals ; Biological and medical sciences ; Cell Division ; Gastric Acid - metabolism ; Gastric Mucosa - pathology ; Gastrins - blood ; Gastroenterology. Liver. Pancreas. Abdomen ; Genetic Vectors ; Liver. Biliary tract. Portal circulation. Exocrine pancreas ; Medical sciences ; Mice ; Mice, Inbred C57BL ; Mice, Inbred CBA ; Mice, Knockout ; Other diseases. Semiology ; Parietal Cells, Gastric - pathology ; Receptor, Cholecystokinin B ; Receptors, Cholecystokinin - deficiency ; Receptors, Cholecystokinin - genetics ; Receptors, Cholecystokinin - physiology</subject><ispartof>Gastroenterology (New York, N.Y. 1943), 1997, Vol.112 (1), p.280-286</ispartof><rights>1997 American Gastroenterological Association</rights><rights>1997 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c554t-70e906a6d0f0117346c6a41a3e0bb9e10bcd8ec338a7511383464d1cf85b21523</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/S0016-5085(97)90000-7$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3548,4022,27922,27923,27924,45994</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=2585761$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/8978369$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Langhans, Nancy</creatorcontrib><creatorcontrib>Rindi, Guido</creatorcontrib><creatorcontrib>Chiu, Mary</creatorcontrib><creatorcontrib>Rehfeld, Jens F.</creatorcontrib><creatorcontrib>Ardman, Blair</creatorcontrib><creatorcontrib>Beinborn, Martin</creatorcontrib><creatorcontrib>Kopin, Alan S.</creatorcontrib><title>Abnormal gastric histology and decreased acid production in cholecystokinin-B/gastrin receptor-deficient mice</title><title>Gastroenterology (New York, N.Y. 1943)</title><addtitle>Gastroenterology</addtitle><description>The cholecystokinin (CCK)-B/gastrin receptor is one of several regulators of gastric acid secretion and mucosal growth. To elucidate the contribution of this receptor relative to other trophic and secretory factors, mice that lack the CCK-B/gastrin receptor have been generated and studied.
Both alleles of the CCK-B/gastrin receptor were inactivated by targeted gene disruption. Analysis of the mice included measurement of basal gastric pH and plasma gastrin levels. In addition, multiple gastric mucosal cell types were identified by immunostaining and quantified.
Homozygous mutant mice were viable, fertile, and appeared grossly normal into adulthood. The receptor-deficient mice exhibited a marked increase in basal gastric pH (from 3.2 to 5.2) and an approximately 10-fold elevation in plasma gastrin concentration compared with wild-type controls. In the stomach of mutant animals, parietal and enterochromaffin-like cells were decreased, providing a likely explanation for the reduction in acid output. In the antrum, a decrease in somatostatin cell density and an increase in the gastrin cell number were observed, consistent with the concomitant elevation in circulating gastrin.
Together, these findings demonstrate the importance of the CCK-B/gastrin receptor in maintaining the normal cellular composition and function of the gastric mucosa.</description><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Cell Division</subject><subject>Gastric Acid - metabolism</subject><subject>Gastric Mucosa - pathology</subject><subject>Gastrins - blood</subject><subject>Gastroenterology. Liver. Pancreas. Abdomen</subject><subject>Genetic Vectors</subject><subject>Liver. Biliary tract. Portal circulation. Exocrine pancreas</subject><subject>Medical sciences</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Inbred CBA</subject><subject>Mice, Knockout</subject><subject>Other diseases. Semiology</subject><subject>Parietal Cells, Gastric - pathology</subject><subject>Receptor, Cholecystokinin B</subject><subject>Receptors, Cholecystokinin - deficiency</subject><subject>Receptors, Cholecystokinin - genetics</subject><subject>Receptors, Cholecystokinin - physiology</subject><issn>0016-5085</issn><issn>1528-0012</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1997</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkE9vFCEYh4nR1G3tR2jCwRg9jIVhGOBk2saqSZMeas-EeXmnRWdghVmT_fay3c1e5QCH3_P-4SHkgrPPnPH-8oHVu5FMy49GfTKsnka9IisuW93UrH1NVkfkLTkt5VdFjND8hJxoo7TozYrMV0NMeXYTfXJlyQHocyhLmtLTlrroqUfI6Ap66iB4us7Jb2AJKdIQKTynCWFb-d8hhthcX-6bRJoRcL2k3HgcAwSMC50D4DvyZnRTwfPDe0Yeb7_-vPne3N1_-3FzddeAlN3SKIaG9a73bGScK9H10LuOO4FsGAxyNoDXCEJopyTnQlei8xxGLYe2_l-ckQ_7vnXfPxssi51DAZwmFzFtilVaKdGaroJyD0JOpWQc7TqH2eWt5czuNNsXzXbn0BplXzRbVesuDgM2w4z-WHXwWvP3h9wVcNOYXYRQjlgrtVQ9r9iXPYZVxt-A2ZadLEAfqsHF-hT-s8g_Yl2alw</recordid><startdate>1997</startdate><enddate>1997</enddate><creator>Langhans, Nancy</creator><creator>Rindi, Guido</creator><creator>Chiu, Mary</creator><creator>Rehfeld, Jens F.</creator><creator>Ardman, Blair</creator><creator>Beinborn, Martin</creator><creator>Kopin, Alan S.</creator><general>Elsevier Inc</general><general>Elsevier</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>1997</creationdate><title>Abnormal gastric histology and decreased acid production in cholecystokinin-B/gastrin receptor-deficient mice</title><author>Langhans, Nancy ; Rindi, Guido ; Chiu, Mary ; Rehfeld, Jens F. ; Ardman, Blair ; Beinborn, Martin ; Kopin, Alan S.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c554t-70e906a6d0f0117346c6a41a3e0bb9e10bcd8ec338a7511383464d1cf85b21523</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1997</creationdate><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Cell Division</topic><topic>Gastric Acid - metabolism</topic><topic>Gastric Mucosa - pathology</topic><topic>Gastrins - blood</topic><topic>Gastroenterology. Liver. Pancreas. Abdomen</topic><topic>Genetic Vectors</topic><topic>Liver. Biliary tract. Portal circulation. Exocrine pancreas</topic><topic>Medical sciences</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Mice, Inbred CBA</topic><topic>Mice, Knockout</topic><topic>Other diseases. Semiology</topic><topic>Parietal Cells, Gastric - pathology</topic><topic>Receptor, Cholecystokinin B</topic><topic>Receptors, Cholecystokinin - deficiency</topic><topic>Receptors, Cholecystokinin - genetics</topic><topic>Receptors, Cholecystokinin - physiology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Langhans, Nancy</creatorcontrib><creatorcontrib>Rindi, Guido</creatorcontrib><creatorcontrib>Chiu, Mary</creatorcontrib><creatorcontrib>Rehfeld, Jens F.</creatorcontrib><creatorcontrib>Ardman, Blair</creatorcontrib><creatorcontrib>Beinborn, Martin</creatorcontrib><creatorcontrib>Kopin, Alan S.</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Gastroenterology (New York, N.Y. 1943)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Langhans, Nancy</au><au>Rindi, Guido</au><au>Chiu, Mary</au><au>Rehfeld, Jens F.</au><au>Ardman, Blair</au><au>Beinborn, Martin</au><au>Kopin, Alan S.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Abnormal gastric histology and decreased acid production in cholecystokinin-B/gastrin receptor-deficient mice</atitle><jtitle>Gastroenterology (New York, N.Y. 1943)</jtitle><addtitle>Gastroenterology</addtitle><date>1997</date><risdate>1997</risdate><volume>112</volume><issue>1</issue><spage>280</spage><epage>286</epage><pages>280-286</pages><issn>0016-5085</issn><eissn>1528-0012</eissn><coden>GASTAB</coden><abstract>The cholecystokinin (CCK)-B/gastrin receptor is one of several regulators of gastric acid secretion and mucosal growth. To elucidate the contribution of this receptor relative to other trophic and secretory factors, mice that lack the CCK-B/gastrin receptor have been generated and studied.
Both alleles of the CCK-B/gastrin receptor were inactivated by targeted gene disruption. Analysis of the mice included measurement of basal gastric pH and plasma gastrin levels. In addition, multiple gastric mucosal cell types were identified by immunostaining and quantified.
Homozygous mutant mice were viable, fertile, and appeared grossly normal into adulthood. The receptor-deficient mice exhibited a marked increase in basal gastric pH (from 3.2 to 5.2) and an approximately 10-fold elevation in plasma gastrin concentration compared with wild-type controls. In the stomach of mutant animals, parietal and enterochromaffin-like cells were decreased, providing a likely explanation for the reduction in acid output. In the antrum, a decrease in somatostatin cell density and an increase in the gastrin cell number were observed, consistent with the concomitant elevation in circulating gastrin.
Together, these findings demonstrate the importance of the CCK-B/gastrin receptor in maintaining the normal cellular composition and function of the gastric mucosa.</abstract><cop>New York, NY</cop><pub>Elsevier Inc</pub><pmid>8978369</pmid><doi>10.1016/S0016-5085(97)90000-7</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Biological and medical sciences Cell Division Gastric Acid - metabolism Gastric Mucosa - pathology Gastrins - blood Gastroenterology. Liver. Pancreas. Abdomen Genetic Vectors Liver. Biliary tract. Portal circulation. Exocrine pancreas Medical sciences Mice Mice, Inbred C57BL Mice, Inbred CBA Mice, Knockout Other diseases. Semiology Parietal Cells, Gastric - pathology Receptor, Cholecystokinin B Receptors, Cholecystokinin - deficiency Receptors, Cholecystokinin - genetics Receptors, Cholecystokinin - physiology |
| title | Abnormal gastric histology and decreased acid production in cholecystokinin-B/gastrin receptor-deficient mice |
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