Small-bowel resection. Oral intake is the stimulus for hyperplasia
Small-bowel resection leads to hyperplasia of the residual small intestine, However, the factors initiating small-bowel hyperplasia are not clearly understood, although oral intake either by direct contact with the small bowel or via hormonal or neurovascular factors has been suggested as the major...
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| Veröffentlicht in: | American journal of digestive diseases 1976-07, Vol.21 (7), p.542-546 |
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| container_title | American journal of digestive diseases |
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| creator | Levine, G M Deren, J J Yezdimir, E |
| description | Small-bowel resection leads to hyperplasia of the residual small intestine, However, the factors initiating small-bowel hyperplasia are not clearly understood, although oral intake either by direct contact with the small bowel or via hormonal or neurovascular factors has been suggested as the major stimulus. In order to determine whether oral intake is an obligatory prerequisite for small-intestinal hyperplasia, we compared rats one week after undergoing a 70-cm proximal intestinal resection with sham-operated animals. Resected, orally fed rats demonstrated small-intestinal hyperplasia, whereas resected and sham-operated intravenously alimented rats did not. There were no differences in gut weight, mucosal weight, mucosal protein, or DNA between resected or sham-operated intravenously alimented rats. These data provide direct experimental proof that oral intake is a necessary stimulus for small-intestinal hyperplasia after resection. |
| doi_str_mv | 10.1007/bf01464760 |
| format | Article |
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Oral intake is the stimulus for hyperplasia</title><source>MEDLINE</source><source>Springer Nature - Complete Springer Journals</source><creator>Levine, G M ; Deren, J J ; Yezdimir, E</creator><creatorcontrib>Levine, G M ; Deren, J J ; Yezdimir, E</creatorcontrib><description>Small-bowel resection leads to hyperplasia of the residual small intestine, However, the factors initiating small-bowel hyperplasia are not clearly understood, although oral intake either by direct contact with the small bowel or via hormonal or neurovascular factors has been suggested as the major stimulus. In order to determine whether oral intake is an obligatory prerequisite for small-intestinal hyperplasia, we compared rats one week after undergoing a 70-cm proximal intestinal resection with sham-operated animals. Resected, orally fed rats demonstrated small-intestinal hyperplasia, whereas resected and sham-operated intravenously alimented rats did not. There were no differences in gut weight, mucosal weight, mucosal protein, or DNA between resected or sham-operated intravenously alimented rats. 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Oral intake is the stimulus for hyperplasia</title><title>American journal of digestive diseases</title><addtitle>Am J Dig Dis</addtitle><description>Small-bowel resection leads to hyperplasia of the residual small intestine, However, the factors initiating small-bowel hyperplasia are not clearly understood, although oral intake either by direct contact with the small bowel or via hormonal or neurovascular factors has been suggested as the major stimulus. In order to determine whether oral intake is an obligatory prerequisite for small-intestinal hyperplasia, we compared rats one week after undergoing a 70-cm proximal intestinal resection with sham-operated animals. Resected, orally fed rats demonstrated small-intestinal hyperplasia, whereas resected and sham-operated intravenously alimented rats did not. There were no differences in gut weight, mucosal weight, mucosal protein, or DNA between resected or sham-operated intravenously alimented rats. These data provide direct experimental proof that oral intake is a necessary stimulus for small-intestinal hyperplasia after resection.</description><subject>Animals</subject><subject>Body Weight</subject><subject>Eating</subject><subject>Hyperplasia - etiology</subject><subject>Intestine, Small - pathology</subject><subject>Intestine, Small - surgery</subject><subject>Male</subject><subject>Parenteral Nutrition</subject><subject>Postoperative Complications</subject><subject>Rats</subject><subject>Stress, Physiological</subject><issn>0002-9211</issn><issn>1573-2568</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1976</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNo90DtPwzAYhWELcSuFhZnBEwNSyvf5moy0ooBUqQMwR3ZqqwGnCXYi1H9PUQvTWR6d4SXkGmGCAPreekChhFZwREYoNc-YVPkxGQEAywqGeE4uUvoA4Ezn8oyc5gy5wBGZvjYmhMy23y7Q6JKr-rrdTOgymkDrTW8-Ha0T7deOpr5uhjAk6ttI19vOxS6YVJtLcuJNSO7qsGPyPn98mz1ni-XTy-xhkVVc6D5Db43wXJkV96IwzBhdSGNEJTRyLZUFWwFTDFSFBcdce2BeWKkcrqRkOR-T2_1vF9uvwaW-bOpUuRDMxrVDKnMupEahd_BuD6vYphSdL7tYNyZuS4Tyt1c5nf_12uGbw-tgG7f6p_tA_Ac4UWPy</recordid><startdate>197607</startdate><enddate>197607</enddate><creator>Levine, G M</creator><creator>Deren, J J</creator><creator>Yezdimir, E</creator><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>197607</creationdate><title>Small-bowel resection. Oral intake is the stimulus for hyperplasia</title><author>Levine, G M ; Deren, J J ; Yezdimir, E</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c347t-1fba4f36ad3f49a2aa795aa4c4713756b0bc026206c193187f02f4b56e1d55283</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1976</creationdate><topic>Animals</topic><topic>Body Weight</topic><topic>Eating</topic><topic>Hyperplasia - etiology</topic><topic>Intestine, Small - pathology</topic><topic>Intestine, Small - surgery</topic><topic>Male</topic><topic>Parenteral Nutrition</topic><topic>Postoperative Complications</topic><topic>Rats</topic><topic>Stress, Physiological</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Levine, G M</creatorcontrib><creatorcontrib>Deren, J J</creatorcontrib><creatorcontrib>Yezdimir, E</creatorcontrib><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>American journal of digestive diseases</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Levine, G M</au><au>Deren, J J</au><au>Yezdimir, E</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Small-bowel resection. Oral intake is the stimulus for hyperplasia</atitle><jtitle>American journal of digestive diseases</jtitle><addtitle>Am J Dig Dis</addtitle><date>1976-07</date><risdate>1976</risdate><volume>21</volume><issue>7</issue><spage>542</spage><epage>546</epage><pages>542-546</pages><issn>0002-9211</issn><eissn>1573-2568</eissn><abstract>Small-bowel resection leads to hyperplasia of the residual small intestine, However, the factors initiating small-bowel hyperplasia are not clearly understood, although oral intake either by direct contact with the small bowel or via hormonal or neurovascular factors has been suggested as the major stimulus. In order to determine whether oral intake is an obligatory prerequisite for small-intestinal hyperplasia, we compared rats one week after undergoing a 70-cm proximal intestinal resection with sham-operated animals. Resected, orally fed rats demonstrated small-intestinal hyperplasia, whereas resected and sham-operated intravenously alimented rats did not. There were no differences in gut weight, mucosal weight, mucosal protein, or DNA between resected or sham-operated intravenously alimented rats. These data provide direct experimental proof that oral intake is a necessary stimulus for small-intestinal hyperplasia after resection.</abstract><cop>United States</cop><pmid>821341</pmid><doi>10.1007/bf01464760</doi><tpages>5</tpages></addata></record> |
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| ispartof | American journal of digestive diseases, 1976-07, Vol.21 (7), p.542-546 |
| issn | 0002-9211 1573-2568 |
| language | eng |
| recordid | cdi_crossref_primary_10_1007_BF01464760 |
| source | MEDLINE; Springer Nature - Complete Springer Journals |
| subjects | Animals Body Weight Eating Hyperplasia - etiology Intestine, Small - pathology Intestine, Small - surgery Male Parenteral Nutrition Postoperative Complications Rats Stress, Physiological |
| title | Small-bowel resection. Oral intake is the stimulus for hyperplasia |
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