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International Journal of Endocrinology
Volume 2013 (2013), Article ID 870487, 7 pages
Research Article

Intrahepatic Lipid Content and Insulin Resistance Are More Strongly Associated with Impaired NEFA Suppression after Oral Glucose Loading Than with Fasting NEFA Levels in Healthy Older Individuals

1MRC Epidemiology Unit, Institute of Metabolic Science, Addenbrooke's Hospital, P.O. Box 285 Hills Road, Cambridge CB20QQ, UK
2Galway Diabetes Research Centre, School of Medicine, Clinical Science Institute, NUI Galway, Galway, Ireland
3Metabolic Research Laboratories, Institute of Metabolic Science, Cambridge CB20QQ, UK
4Wolfson Brain Imaging Centre, University of Cambridge, Cambridge CB20QQ, UK
5MRC Lifecourse Epidemiology Unit, University of Southampton, Southampton SO166YD, UK

Received 8 January 2013; Revised 17 March 2013; Accepted 11 April 2013

Academic Editor: Carine Beysen

Copyright © 2013 Francis M. Finucane et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Introduction. The mechanisms underlying the association between insulin resistance and intrahepatic lipid (IHL) accumulation are not completely understood. We sought to determine whether this association was explained by differences in fasting non-esterified fatty acid (NEFA) levels and/or NEFA suppression after oral glucose loading. Materials and Methods. We performed a cross-sectional analysis of 70 healthy participants in the Hertfordshire Physical Activity Trial (39 males, age 71.3 ± 2.4 years) who underwent oral glucose tolerance testing with glucose, insulin, and NEFA levels measured over two hours. IHL was quantified with magnetic resonance spectroscopy. Insulin sensitivity was measured with the oral glucose insulin sensitivity (OGIS) model, the leptin: adiponectin ratio (LAR), and the homeostasis model assessment (HOMA). Results. Measures of insulin sensitivity were not associated with fasting NEFA levels, but OGIS was strongly associated with NEFA suppression at 30 minutes and strongly inversely associated with IHL. Moreover, LAR was strongly inversely associated with NEFA suppression and strongly associated with IHL. This latter association (beta = 1.11 [1.01, 1.21], ) was explained by reduced NEFA suppression ( after adjustment). Conclusions. Impaired postprandial NEFA suppression, but not fasting NEFA, contributes to the strong and well-established association between whole body insulin resistance and liver fat accumulation.