| Dietary restriction of mice on a high-fat diet induces substrate efficiency and improves metabolic health. | |
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MedLine Citation:
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PMID: 21830320 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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High energy intake and, specifically, high dietary fat intake challenge the mammalian metabolism and correlate with many metabolic disorders such as obesity and diabetes. However, dietary restriction (DR) is known to prevent the development of metabolic disorders. The current western diets are highly enriched in fat, and it is as yet unclear whether DR on a certain high-fat (HF) diet elicits similar beneficial effects on health. In this research, we report that HF-DR improves metabolic health of mice compared with mice receiving the same diet on an ad libitum basis (HF-AL). Already after five weeks of restriction, the serum levels of cholesterol and leptin were significantly decreased in HF-DR mice, whereas their glucose sensitivity and serum adiponectin levels were increased. The body weight and measured serum parameters remained stable in the following 7 weeks of restriction, implying metabolic adaptation. To understand the molecular events associated with this adaptation, we analyzed gene expression in white adipose tissue (WAT) with whole genome microarrays. HF-DR strongly influenced gene expression in WAT; in total, 8643 genes were differentially expressed between both groups of mice, with a major role for genes involved in lipid metabolism and mitochondrial functioning. This was confirmed by quantitative real-time reverse transcription-PCR and substantiated by increase in mitochondrial density in WAT of HF-DR mice. These results provide new insights in the metabolic flexibility of dietary restricted animals and suggest the development of substrate efficiency. |
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Authors:
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Loes P M Duivenvoorde; Evert M van Schothorst; Annelies Bunschoten; Jaap Keijer |
Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't |
Journal Detail:
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Title: Journal of molecular endocrinology Volume: 47 ISSN: 1479-6813 ISO Abbreviation: J. Mol. Endocrinol. Publication Date: 2011 Aug |
Date Detail:
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Created Date: 2011-08-08 Completed Date: 2011-10-17 Revised Date: 2012-03-02 |
Medline Journal Info:
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Nlm Unique ID: 8902617 Medline TA: J Mol Endocrinol Country: England |
Other Details:
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Languages: eng Pagination: 81-97 Citation Subset: IM |
Affiliation:
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Department of Human and Animal Physiology, Wageningen University, Marijkeweg 40, 6709 GP Wageningen, PO Box 338, 6700 AH Wageningen, The Netherlands. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Adiponectin
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blood Adipose Tissue, White / metabolism, physiopathology Animals Caloric Restriction* Carbohydrate Metabolism / genetics Cholesterol / blood DNA, Mitochondrial / metabolism Dietary Fats / administration & dosage* Epididymis / metabolism, physiopathology Gene Expression Profiling Glucose / metabolism Glucose Tolerance Test Health* Insulin / blood Leptin / blood Lipid Metabolism / genetics* Male Metabolic Networks and Pathways / genetics Mice Mice, Inbred C57BL Mitochondria / genetics Obesity / blood, physiopathology Oligonucleotide Array Sequence Analysis Organ Size Transcription, Genetic Weight Gain Weight Loss |
| Chemical | |
Reg. No./Substance:
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0/Adiponectin; 0/DNA, Mitochondrial; 0/Dietary Fats; 0/Insulin; 0/Leptin; 50-99-7/Glucose; 57-88-5/Cholesterol |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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