| Cholesterol gallstones in alloxan-diabetic mice. | |
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MedLine Citation:
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PMID: 3783046 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Normal and alloxan-diabetic male mice (Crj-ICR) were fed a diet containing 0.5% cholesterol for 5 and 10 weeks, and gallbladder bile was analyzed for cholesterol, phospholipids and bile acids, feces for sterols and bile acids, and plasma and liver for cholesterol, phospholipids, and triglycerides. Normal mice developed no gallstones but the diabetic mice developed cholesterol gallstones with an incidence of 70% by 5 weeks and 80% by 10 weeks after feeding of the cholesterol diet. Diabetic mice fed the ordinary diet also developed stones (23%) by 10 weeks. In the diabetic mice, the gallbladder was enlarged about threefold, and biliary lipid concentration, diet intake, and fecal excretion of sterols and bile acids increased but body weight decreased. Cholic acid and beta-muricholic acid comprised over 40% each of the total biliary bile acids in normal mice, but cholic acid increased to about 80% and beta-muricholic acid decreased to a few percent in the diabetic mice. Fecal excretion of bile acids increased after cholesterol feeding in both normal and diabetic mice, but the increased bile acid in the normal animals was beta-muricholic acid and that in the diabetic mice was deoxycholic acid. The mice that developed gallstones showed a marked increase in biliary cholesterol value and decreases in gallbladder bile and bile acid concentration, but no difference in biliary and fecal bile acid composition, bile acid synthesis, fecal sterols, or plasma and liver lipid levels. Cholesterol absorption was increased in the diabetic mice when examined by plasma 14C/3H ratio and fecal 14C-labeled sterol excretion after a single oral administration of [14C]cholesterol and a simultaneous intravenous injection of [3H]cholesterol. These data led to the conclusion that cholesterol gallstones developed in alloxan-diabetic mice fed excess cholesterol, due to the hyperphagia and the enhancement of cholesterol absorption caused by increases in the synthesis and secretion of cholic acid. |
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Authors:
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T Akiyoshi; K Uchida; H Takase; Y Nomura; N Takeuchi |
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Publication Detail:
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Type: Journal Article |
Journal Detail:
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Title: Journal of lipid research Volume: 27 ISSN: 0022-2275 ISO Abbreviation: J. Lipid Res. Publication Date: 1986 Sep |
Date Detail:
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Created Date: 1987-01-07 Completed Date: 1987-01-07 Revised Date: 2004-11-17 |
Medline Journal Info:
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Nlm Unique ID: 0376606 Medline TA: J Lipid Res Country: UNITED STATES |
Other Details:
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Languages: eng Pagination: 915-24 Citation Subset: IM |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Administration, Oral Animals Bile / analysis Bile Acids and Salts / analysis Body Weight Cholelithiasis / analysis*, complications Cholesterol / administration & dosage, analysis* Cholic Acid Cholic Acids / analysis Diabetes Mellitus, Experimental / complications, metabolism* Feces / analysis Lipids / blood Liver / analysis, anatomy & histology Male Mice Mice, Inbred ICR Organ Size |
| Chemical | |
Reg. No./Substance:
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0/Bile Acids and Salts; 0/Cholic Acids; 0/Lipids; 39016-49-4/muricholic acid; 57-88-5/Cholesterol; 81-25-4/Cholic Acid |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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