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Can female adult obesity be stopped at birth?

e and leptin concentrations. This hyperinsulinemia persisted until 120 days of age in the female progeny, with continuing euglycemia. The leptin levels in the NPY-treated group were not statistically different from the vehicle group. However, given the decline in female adult body weight of the NPY treatment group, plasma leptin concentrations at this age in females, if expressed per unit body weight (g), are significantly increased in the NPY vs. the vehicle group. Similar changes were absent in the male progeny. LH synthesized and released into the circulation by the pituitary in response to hypothalamic LH-releasing hormone (LHRH) and measured as plasma LH concentrations was altered in response to exogenous NPY. Neonatal exogenous intracerebroventricular NPY administration increased plasma LH concentrations at 21, 60, and 120 days, particularly in the females. The 120-day-old and not the 21-day-old males expressed a similar increase in plasma LH concentrations. LH in 35- and 60-day-old male adults was not assessed.

Conclusions

The researchers conclude that the concentrations of fetal/postnatal endogenous NPY content, either as an associated change or an end result of disturbances in circulating insulin and/or leptin concentrations, contribute toward the predetermination of adult appearance and behavior. These observations collectively make fetal/neonatal nutrition/metabolism extremely important, thereby presenting avenues for intervention before the adult onset of altered eating behavior and phenotype.

The researchers also conclude that postnatal exogenous administration of NPY causes central and peripheral changes. The central effect consists of a direct suppression of endogenous hypothalamic NPY concentrations and the indirect effect consists of neonatal hyperinsulinemia and/or hyperleptinemia that in turn chronically suppress hypothalamic NPY concentrations.

This effect is permanent, causing a decline in food intake and body weig
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Contact: Donna Krupa
djkrupa1@aol.com
703-527-7357
American Physiological Society
29-Jul-2003


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