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Effects of early postnatal overnutrition on the hypothalamic DNA methylation pattern

ABSTRACT: Investigate the persistent effects of early postnatal overnutrition on the developmental establishment of the DNA methylation in the mouse hypothalamus.

ORGANISM(S): Mus musculus

PROVIDER: GSE32477 | GEO | 2012/05/01

SECONDARY ACCESSION(S): PRJNA147799

REPOSITORIES: GEO

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Effects of early postnatal overnutrition on the hypothalamic DNA methylation pattern

Project description:Investigate the persistent effects of early postnatal overnutrition on the developmental establishment of the DNA methylation in the mouse hypothalamus. Early postnatal overnutrition was induced in mice by reducing the litter size from normally 9 (C) to 4 (SL) pups per litter. Hypothalami were collected from both C and SL mice at the age of postnatal day 180 (P180). Genome-wide DNA methylation difference between SL and C were detected by MSAM. Equal amount of genomic DNA from 5 hypothalami of the same group were pooled as one MSAM sample. Two pooled DNA samples for each group were used for comparison that meant total 10 hypothalami for each group. 500ng pooled DNA was serially digested with SmaI and XmaI followed by adaptor ligation and PCR amplification. Two cohybridizations were performed to compare DNA methylation between SL and C hypothalami, with day swap.

2012-04-30 | E-GEOD-32477 | biostudies-arrayexpress

Maternal dietary fat during lactation shapes single nucleus transcriptomic profile of postnatal offspring hypothalamus in a sexually dimorphic manner in mice

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Hypothalamic gene expression in small litter vs control mouse (postnatal overnutrition)

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Transcriptome of early postnatal brain development of eIF2B-R132H/R132H mutant mice relative to wild-types.

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Single-cell analysis of early chick hypothalamic development reveals that hypothalamic cells are induced from prethalamic-like progenitors.

Project description:Purpose: scRNA-Seq was performed to profile chicken hypothalamus development.

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Early Leptin Intervention Reverses Perturbed Energy Balance Regulating Hypothalamic Neuropeptides in the Pre- and Postnatal Calorie Restricted Offspring

Project description:Pre- and postnatal calorie restriction is associated with postnatal growth restriction, reduced circulating leptin concentrations and perturbed energy balance. Hypothalamic regulation of energy balance demonstrates enhanced orexigenic (NPY, AgRP) and diminished anorexigenic (POMC, CART) neuropeptide expression (PN21) setting the stage for subsequent development of obesity. Leptin replenishment during the early postnatal period (PN2-PN8) led to reversing the hypothalamic orexigenic:anorexigenic neuropeptide ratio at PN21 by only reducing the orexigenic (NPY, AgRP) without affecting the anorexigenic (POMC, CART) neuropeptide expression. This hypothalamic effect was mediated via enhanced leptin receptor (ObRb) signaling that involved increased pSTAT3 but reduced PTP1B. This was further confirmed by an increase in body weight at PN21 in response to intracerebroventricular administration of antisense ObRb oligonucleotides (PN2-PN8). The change in the hypothalamic neuropeptide balance in response to leptin administration caused increased oxygen consumption, carbon dioxide production and physical activity which resulted in increased milk intake (PN14) with no change in body weight. This is in contrast to the reduction in milk intake with no effect on energy expenditure and physical activity observed in controls. We conclude that pre- and postnatal calorie restriction perturbs hypothalamic neuropeptide regulation of energy balance setting the stage for hyperphagia and reduced energy expenditure, hallmarks of obesity. Leptin in turn reverses this phenotype by increasing hypothalamic ObRb signaling (sensitivity) and affecting only the orexigenic arm of the neuropeptide balance.

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