Submitted on December 1, 2005
Accepted on March 2, 2006
Substrate-energy metabolism and metabolic risk factors for cardiovascular disease in relation to fetal growth and adult body composition
Osama A Kensara1, Steve A Wootton1, David I. W. Phillips2, Mayank Patel2, Daniel J Hoffman3, Alan A. Jackson1, and Marinos Elia1*
1 Institute of Human Nutrition, University of Southampton, Southampton, United Kingdom
2 MRC Epidemiology Resource Centre, University of Southampton, Southampton, United Kingdom
3 Department of Nutritional Sciences, Rutgers, the State University of New Jersey, New York, New York, United States
* To whom correspondence should be addressed. E-mail: m.elia{at}soton.ac.uk.
The effect of fetal programming on intermediary metabolism is uncertain. Therefore, we examined whether fetal programming affects oxidative and non-oxidative macronutrient metabolism, and the prevalence of the metabolic syndrome in adult life. Healthy older men aged 64-72 years with either a lower birth weight (LBW;BW, <25th centile; n = 16) or higher birth weight (HBW: BW, >75th centile; n = 13) had measurements of (i) net oxidative metabolism using indirect calorimetry, before and for 6 hours after a mixed meal (3720 kJ) (ii) Post-prandial oxidation of exogenous 13C-palmitic acid. Body composition was measured using dual energy X-ray absorptiometry. After adjustment for current weight and height, the LBW group had a lower resting energy expenditure (REE) in the pre-prandial (4.01 v 4.54 kJ/min; p = 0.015) and post-prandial state (4.60 v 5.20 kJ/min; p = 0.004), and less fat-free mass than the HBW group. BW category was a significant independent and better predictor of REE than weight + height. There were no significant differences between groups in net oxidative and non-oxidative macronutrient (protein, fat, carbohydrate) metabolism (or of exogenous 13C-palmitate), or in the prevalence of the metabolic syndrome, which was present almost twice as commonly in the lower than higher BW group. The study suggests that fetal programming affects both pre- and post-prandial EE in older life by mechanisms that are at least partly related to the mass of the fat-free body. Birth weight was found to be a significant predictor of REE that was independent of adult weight + height.
