Developmental programming studies have revealed an association between low birth weight and adult disease. Maternal protein restriction is a well-known method for inducing low birth weight. In our studies we show that the timing of maternal protein restriction produces distinct effects on the phenotype of the adult offspring. We have previously shown that low protein diet given throughout pregnancy and lactation results in lower body weights, hyperphagia, increased involuntary energy expenditure and decreased liver triglyceride content. Decreased liver triglyceride content could be due to an increase in lipid utilization and/or a decrease in lipid synthesis. We have previously evaluated hepatic lipid utilization and found it to be similar between control and low protein offspring. Therefore the first objective was to evaluate the status of lipid synthesis in the liver. The status of fatty acid uptake, de novo fatty acid synthesis and triglyceride biosynthesis in the liver was similar between control and low protein adult offspring. The decrease in liver triglyceride content could be due to an increase in peripheral triglyceride utilization in white and/or brown adipose tissue. Accelerated postnatal growth following intrauterine growth restriction has been associated with increased susceptibility to metabolic diseases. The second objective was to evaluate the effects of low protein diet given selectively during gestation followed by a balanced diet during lactation. Crossfostering intrauterine growth restricted offspring to control dams during lactation resulted in catch-up growth. Despite this accelerated postnatal growth, intrauterine growth restricted offspring had similar body weights, food consumption, energy expenditure, body composition, and plasma lipid and hormone profiles compared to control offspring at 2, 6 and 12 months of age. Exposure of the adult offspring to the metabolic stress of a chronic high fat diet did not produce distinct effects in the intrauterine growth restricted offspring. Lastly, the third objective was to evaluate the status of hepatic lipid metabolism in this model. Ageing and high fat diet feeding resulted in greater lipid accumulation in the livers of male offspring but the magnitudes of increase were similar between intrauterine growth restricted and control offspring. Intrauterine growth restriction with or without accelerated neonatal growth does not seem to imprint detrimental phenotypic or metabolic consequences in the adult offspring.
|School:||University of the Sciences in Philadelphia|
|School Location:||United States -- Pennsylvania|
|Source:||DAI-B 78/08(E), Dissertation Abstracts International|
|Subjects:||Nutrition, Pharmacy sciences|
|Keywords:||Developmental programming, Fatty acids, Liver triglycerides, Protein restriction|
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