| Targeted intestinal overexpression of the immediate early gene tis7 in transgenic mice increases triglyceride absorption and adiposity. | |
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MedLine Citation:
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PMID: 16085642 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Following loss of functional small bowel surface area due to surgical resection, the remnant gut undergoes an adaptive response characterized by increased crypt cell proliferation and enhanced villus height and crypt depth, resulting in augmented intestinal nutrient absorptive capacity. Previous studies showed that expression of the immediate early gene tis7 is markedly up-regulated in intestinal enterocytes during the adaptive response. To study its role in the enterocyte, transgenic mice were generated that specifically overexpress TIS7 in the gut. Nucleotides -596 to +21 of the rat liver fatty acid-binding protein promoter were used to direct abundant overexpression of TIS7 into small intestinal upper crypt and villus enterocytes. TIS7 transgenic mice had increased total body adiposity and decreased lean muscle mass compared with normal littermates. Oxygen consumption levels, body weight, surface area, and small bowel weight were decreased. On a high fat diet, transgenic mice exhibited a more rapid and proportionately greater gain in body weight with persistently elevated total body adiposity and increased hepatic fat accumulation. Bolus fat feeding resulted in a greater increase in serum triglyceride levels and an accelerated appearance of enterocytic, lamina propria, and hepatic fat. Changes in fat homeostasis were linked to increased expression of genes involved in enterocytic triglyceride metabolism and changes in growth with decreased insulin-like growth factor-1 expression. Thus, TIS7 overexpression in the intestine altered growth, metabolic rate, adiposity, and intestinal triglyceride absorption. These results suggest that TIS7 is a unique mediator of nutrient absorptive and metabolic adaptation following gut resection. |
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Authors:
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Yuan Wang; Hristo Iordanov; Elzbieta A Swietlicki; Lihua Wang; Christine Fritsch; Trey Coleman; Clay F Semenkovich; Marc S Levin; Deborah C Rubin |
Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S. Date: 2005-08-05 |
Journal Detail:
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Title: The Journal of biological chemistry Volume: 280 ISSN: 0021-9258 ISO Abbreviation: J. Biol. Chem. Publication Date: 2005 Oct |
Date Detail:
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Created Date: 2005-10-10 Completed Date: 2005-12-13 Revised Date: 2008-11-21 |
Medline Journal Info:
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Nlm Unique ID: 2985121R Medline TA: J Biol Chem Country: United States |
Other Details:
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Languages: eng Pagination: 34764-75 Citation Subset: IM |
Affiliation:
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Department of Medicine, Washington University School of Medicine, St. Louis, Missouri 63110, USA. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Adipose Tissue
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metabolism* Animals Blotting, Northern Body Composition Body Weight Calorimetry Cell Proliferation Enterocytes / cytology, metabolism Fatty Acid-Binding Proteins / genetics Gene Expression Regulation* Glucose / metabolism Growth Hormone / blood Homeostasis Immediate-Early Proteins / genetics*, physiology* Immunoblotting Immunohistochemistry Insulin / blood Insulin-Like Growth Factor I / metabolism Intestines / metabolism Leptin / blood Lipids / chemistry Liver / metabolism Membrane Proteins / genetics*, physiology* Mice Mice, Transgenic Microscopy, Electron Oxygen Consumption Promoter Regions, Genetic Rats Reverse Transcriptase Polymerase Chain Reaction Time Factors Triglycerides / chemistry, metabolism* Up-Regulation |
| Grant Support | |
ID/Acronym/Agency:
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AG20091/AG/NIA NIH HHS; DK46122/DK/NIDDK NIH HHS; DK50466/DK/NIDDK NIH HHS; DK52574/DK/NIDDK NIH HHS; DK56341/DK/NIDDK NIH HHS; DK61216/DK/NIDDK NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Fatty Acid-Binding Proteins; 0/Ifrd1 protein, mouse; 0/Immediate-Early Proteins; 0/Leptin; 0/Lipids; 0/Membrane Proteins; 0/Triglycerides; 11061-68-0/Insulin; 50-99-7/Glucose; 67763-96-6/Insulin-Like Growth Factor I; 9002-72-6/Growth Hormone |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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