Document Detail


Short-term adaptation of postprandial lipoprotein secretion and intestinal gene expression to a high-fat diet.
MedLine Citation:
PMID:  19196952     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Western diet is characterized by a hypercaloric and hyperlipidic intake, enriched in saturated fats, that is associated with the increased occurrence of metabolic diseases. To cope with this overload of dietary lipids, the intestine, which delivers dietary lipids to the body, has to adapt its capacity in lipid absorption and lipoprotein synthesis. We have studied the early effects of a high-fat diet (HFD) on intestinal lipid metabolism in mice. After 7 days of HFD, mice displayed normal fasting triglyceridemia but postprandial hypertriglyceridemia. HFD induced a decreased number of secreted chylomicrons with increased associated triglycerides. Secretion of larger chylomicrons was correlated with increased intestinal microsomal triglyceride transfer protein (MTP) content and activity. Seven days of HFD induced a repression of genes involved in fatty acid synthesis (FAS, ACC) and an increased expression of genes involved in lipoprotein assembly (apoB, MTP, and apoA-IV), suggesting a coordinated control of intestinal lipid metabolism to manage a high-fat loading. Of note, the mature form of the transcription factor SREBP-1c was increased and translocated to the nucleus, suggesting that it could be involved in the coordinated control of gene transcription. Activation of SREBP-1c was partly independent of LXR. Moreover, HFD induced hepatic insulin resistance whereas intestine remained insulin sensitive. Altogether, these results demonstrate that a short-term HFD is sufficient to impact intestinal lipid metabolism, which might participate in the development of dyslipidemia and metabolic diseases.
Authors:
Sandra Jimena Hernández Vallejo; Malik Alqub; Serge Luquet; Céline Cruciani-Guglielmacci; Philippe Delerive; Jean-Marc Lobaccaro; Athina-Despina Kalopissis; Jean Chambaz; Monique Rousset; Jean-Marc Lacorte
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2009-02-05
Journal Detail:
Title:  American journal of physiology. Gastrointestinal and liver physiology     Volume:  296     ISSN:  0193-1857     ISO Abbreviation:  Am. J. Physiol. Gastrointest. Liver Physiol.     Publication Date:  2009 Apr 
Date Detail:
Created Date:  2009-03-31     Completed Date:  2009-06-17     Revised Date:  2009-11-19    
Medline Journal Info:
Nlm Unique ID:  100901227     Medline TA:  Am J Physiol Gastrointest Liver Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  G782-92     Citation Subset:  IM    
Affiliation:
Université Pierre et Marie Curie-Paris 6, UMR S 872, INSERM, U 872, Paris, France.
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MeSH Terms
Descriptor/Qualifier:
Adaptation, Physiological
Animals
DNA-Binding Proteins / genetics,  metabolism
Dietary Fats / administration & dosage*,  pharmacology*
Gene Expression Regulation / drug effects*
Intestines / metabolism*
Lipoproteins / secretion*
Male
Mice
Mice, Knockout
Orphan Nuclear Receptors
Postprandial Period / physiology*
Receptors, Cytoplasmic and Nuclear / genetics,  metabolism
Sterol Regulatory Element Binding Protein 1 / genetics,  metabolism
Time Factors
Weight Gain
Grant Support
ID/Acronym/Agency:
//Howard Hughes Medical Institute
Chemical
Reg. No./Substance:
0/DNA-Binding Proteins; 0/Dietary Fats; 0/Lipoproteins; 0/Orphan Nuclear Receptors; 0/Receptors, Cytoplasmic and Nuclear; 0/Srebf1 protein, mouse; 0/Sterol Regulatory Element Binding Protein 1; 0/liver X receptor

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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