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- W2516390136 abstract "Neonatal overfeeding leads to developmental programming of adult obesity. We and others have previously shown that neonatally overfed rats maintain an overweight phenotype and increased levels of proinflammatory adipokine leptin. Leptin’s role in a mature and healthy brain is to mediate the hypothalamic regulation of energy balance. In early life however, leptin has a distinct neurotrophic function, stimulating the establishment of hypothalamic feeding circuitry. In this study, we examined the acute and long-term effects of neonatal overfeeding on leptin-mediated development of hypothalamic connectivity. We also assessed the potential for short-term suppression of neonatal leptin’s activity with a leptin antagonist to mitigate the outcomes of neonatal overfeeding. We saw that neonatal overfeeding induces an acute resistance of the arcuate nucleus (ARC) and ventromedial hypothalamus (VMH) pStat3-positive neurons to exogenous leptin. While this leptin resistance is not maintained into adulthood, neonatal overfeeding induces long-term changes in the ARC neuropeptide Y (NPY) density, suggesting there is a long-term disruption of hypothalamic connectivity. Interestingly, short-term neonatal leptin antagonism does not reduce body weight or leptin levels in the neonatally overfed, but suppresses NPY density in control rats to levels similar to those of the overfed. Our findings demonstrate that changes in the availability of neonatal leptin are critical to the development of hypothalamic connectivity. These data also indicate a potential for developmental plasticity to ameliorate the metabolic malprogramming." @default.
- W2516390136 created "2016-09-16" @default.
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- W2516390136 date "2016-10-01" @default.
- W2516390136 modified "2023-09-27" @default.
- W2516390136 title "Abstract # 1759 Age-related effects of neonatal overfeeding on leptin-mediated hypothalamic connectivity" @default.
- W2516390136 doi "https://doi.org/10.1016/j.bbi.2016.07.052" @default.
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