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Predicate | Object |
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rdf:type | |
lifeskim:mentions |
umls-concept:C0006777,
umls-concept:C0007090,
umls-concept:C0007648,
umls-concept:C0009368,
umls-concept:C0012155,
umls-concept:C0034693,
umls-concept:C0034721,
umls-concept:C0035820,
umls-concept:C0086225,
umls-concept:C0392762,
umls-concept:C0441889,
umls-concept:C0719630,
umls-concept:C1518896,
umls-concept:C1521761,
umls-concept:C1880177,
umls-concept:C1998811,
umls-concept:C2826787
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pubmed:issue |
3
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pubmed:dateCreated |
1990-8-2
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pubmed:abstractText |
To elucidate the role and quantitative contribution of several exogenous factors which may regulate colon crypt mitotic activity, proliferative zone height (PZH) and crypt height, groups of rats were subjected to various feeding regimens both with and without treatment with the colon carcinogen, 1,2-dimethylhydrazine (DMH). The rats were divided into two major groups and one group was given eight weekly injections of DMH base at 9.5 mg kg-1 body weight. Throughout this period and for two additional weeks the rats were isocalorically fed either a defined nutritionally complete diet with different levels of dietary cellulose or they were parenterally (i.v.) fed a nutritionally complete liquid formula with different caloric levels. The rats were then injected with colchicine 3 h prior to sacrifice to arrest and to collect dividing cells at metaphase. The results of multiple regression analysis of all data were interpreted to indicate that parenteral feeding caused dramatic suppression of the colon crypt height (CH) and of the number of metaphase figures per crypt (MC). Increased cellulose intake stimulated CH but suppressed MC. The CH was also stimulated by DMH. CH was positively correlated to PZH and MC. The MC was suppressed by cellulose intake and negatively correlated to PZH but was positively correlated to CH. The PZH was positively correlated to CH. These findings were related to the role of luminal food, functional workload, kcal intake and treatment with DMH on the measured colon crypt parameters. A quantitative assessment of factors that regulate the measured colonic crypt parameters was accomplished.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/1,2-Dimethylhydrazine,
http://linkedlifedata.com/resource/pubmed/chemical/Carcinogens,
http://linkedlifedata.com/resource/pubmed/chemical/Cellulose,
http://linkedlifedata.com/resource/pubmed/chemical/Dietary Carbohydrates,
http://linkedlifedata.com/resource/pubmed/chemical/Dimethylhydrazines,
http://linkedlifedata.com/resource/pubmed/chemical/Methylhydrazines
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pubmed:status |
MEDLINE
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pubmed:month |
May
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pubmed:issn |
0008-8730
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
23
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
227-35
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:2113428-1,2-Dimethylhydrazine,
pubmed-meshheading:2113428-Animals,
pubmed-meshheading:2113428-Carcinogens,
pubmed-meshheading:2113428-Cellulose,
pubmed-meshheading:2113428-Colon,
pubmed-meshheading:2113428-Dietary Carbohydrates,
pubmed-meshheading:2113428-Dimethylhydrazines,
pubmed-meshheading:2113428-Energy Intake,
pubmed-meshheading:2113428-Enteral Nutrition,
pubmed-meshheading:2113428-Epithelial Cells,
pubmed-meshheading:2113428-Male,
pubmed-meshheading:2113428-Methylhydrazines,
pubmed-meshheading:2113428-Mitosis,
pubmed-meshheading:2113428-Parenteral Nutrition,
pubmed-meshheading:2113428-Rats,
pubmed-meshheading:2113428-Rats, Inbred Strains,
pubmed-meshheading:2113428-Regression Analysis
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pubmed:year |
1990
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pubmed:articleTitle |
Quantitative contribution of factors regulating rat colonic crypt epithelium: role of parenteral and enteral feeding, caloric intake, dietary cellulose level and the colon carcinogen DMH.
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pubmed:affiliation |
Department of Cellular and Structural Biology, University of Texas Health Science Center, San Antonio 78284.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
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