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https://hdl.handle.net/2440/65024
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Type: | Journal article |
Title: | Impaired fat oxidation after a single high-fat meal in insulin-sensitive nondiabetic individuals with a family history of type 2 diabetes |
Author: | Heilbronn, L. Gregersen, S. Shirkhedkar, D. Hu, D. Campbell, L. |
Citation: | Diabetes, 2007; 56(8):2046-2053 |
Publisher: | Amer Diabetes Assoc |
Issue Date: | 2007 |
ISSN: | 0012-1797 0012-1797 |
Statement of Responsibility: | Leonie K. Heilbronn, Søren Gregersen, Deepali Shirkhedkar, Dachun Hu and Lesley V. Campbell |
Abstract: | Individuals with insulin resistance and type 2 diabetes have an impaired ability to switch appropriately between carbohydrate and fatty acid oxidation. However, whether this is a cause or consequence of insulin resistance is unclear, and the mechanism(s) involved in this response is not completely elucidated. Whole-body fat oxidation and transcriptional regulation of genes involved in lipid metabolism in skeletal muscle were measured after a prolonged fast and after consumption of either high-fat (76%) or high-carbohydrate (76%) meals in individuals with no family history of type 2 diabetes (control, n = 8) and in age- and fatness-matched individuals with a strong family history of type 2 diabetes (n = 9). Vastus lateralis muscle biopsies were performed before and 3 h after each meal. Insulin sensitivity and fasting measures of fat oxidation were not different between groups. However, subjects with a family history of type 2 diabetes had an impaired ability to increase fatty acid oxidation in response to the high-fat meal (P < 0.05). This was related to impaired activation of genes involved in lipid metabolism, including those for peroxisome proliferator–activated receptor coactivator-1α (PGC1α) and fatty acid translocase (FAT)/CD36 (P < 0.05). Of interest, adiponectin receptor-1 expression decreased 23% after the high-fat meal in both groups, but it was not changed after the high-carbohydrate meal. In conclusion, an impaired ability to increase fatty acid oxidation precedes the development of insulin resistance in genetically susceptible individuals. PGC1α and FAT/CD36 are likely candidates in mediating this response. |
Keywords: | Muscle, Skeletal Humans Diabetes Mellitus, Type 2 Insulin Fats Dietary Fats Heat-Shock Proteins Transcription Factors Biopsy Pedigree Gene Expression Regulation Oxidation-Reduction Thermogenesis Adult Health Female Male Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha CD36 Antigens |
Rights: | © 2007 by the American Diabetes Association. |
DOI: | 10.2337/db06-1687 |
Published version: | http://dx.doi.org/10.2337/db06-1687 |
Appears in Collections: | Aurora harvest 5 Molecular and Biomedical Science publications |
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