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1 Department of Pharmacology, The University of Melbourne, Melbourne, Victoria, Australia
2 Department of Biochemistry and Molecular Biology, Monash University, Melbourne, Victoria, Australia
* To whom correspondence should be addressed. E-mail: mjmorris{at}unimelb.edu.au.
Early life nutrition impacts upon subsequent risk of obesity and hypertension. Several brain chemicals responsible for both feeding and cardiovascular regulation are altered in obesity. We examined effects of early postnatal overnutrition on blood pressure, brain neuropeptide Y (NPY) and adiposity markers. Rat pup litters were adjusted to either 3 or 12 male
animals (overnutrition and control, respectively) on day 1 of life. After weaning, rats were given either a palatable high-fat diet or standard chow. Smaller litter pups were
significantly heavier by 17 days of age. By 16 weeks, the effect of litter size was masked by that of diet, post-weaning. Small and normal litter animals fed a high-fat diet had similar increases in body weight, plasma insulin, leptin and adiponectin concentrations, leptin
mRNA and fat masses relative to chow fed animals. An increase in 11
-hydroxysteroid dehydrogenase-1 mRNA in white adipose tissue, and a decrease in uncoupling protein-1mRNA in brown adipose tissue in both small litter groups at 16 weeks of age, may represent a programming effect of the altered litter size. NPY concentration in the
paraventricular nucleus of the hypothalamus was reduced in high-fat fed groups. Blood pressure was significantly elevated at 13 weeks in high fat fed animals. This study
demonstrates that overnourishment during early postnatal development leads to profound changes in body weight at weaning, which tended to abate with maturation. Thus, the
effects of long-term dietary intervention post-weaning can override those of litter sizeinduced obesity.
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