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Diabetes Publish Ahead of Print published online ahead of print April 24, 2007
DOI: 10.2337/db06-1687
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Original Research

Impaired fat oxidation after a single high fat meal in insulin sensitive non-diabetic individuals with a family history of type 2 diabetes.

Leonie K. Heilbronn1, Søren Gregersen2, Deepali Shirkhedkar1, Dachun Hu1, and Lesley V. Campbell1

1 Diabetes and Obesity Program, Garvan Institute of Medical Research, NSW, Australia
2 Department of Endocrinology and Metabolism, Aarhus University Hospital, Denmark

Correspondence: l.heilbronn{at}garvan.org.au

Background/Objective:Individuals with insulin resistance and type 2 diabetes (DM2) have an impaired ability to switch appropriately between carbohydrate (CHO) 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 are not completely elucidated.

Research Design and Methods: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 CHO (76%) meals in individuals with no family history of DM2 (CON, n=8) and age and fatness matched individuals with a strong family history of DM2 (REL, n=9). Vastus lateralis muscle biopsies were performed prior to and 3-h after each meal.

Results:Insulin sensitivity and fasting measures of fat oxidation were not different between groups. However, RELS 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 PGC1{alpha} and FAT/CD36 (p<0.05). Of interest, adiponectin receptor-1 expression decreased 225% following the high fat meal in both groups, but was not changed following the high CHO meal.

Conclusion:An impaired ability to increase fatty acid oxidation precedes the development of insulin resistance in genetically susceptible individuals. PGC1{alpha} and FAT/CD36 are likely candidates in mediating this response.


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[Abstract] [Full Text] [PDF]


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