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The effect of insulin treatment versus insulin resistance on microRNA expression in the hypothalamic neuronal cell line mHypoE-46.

ABSTRACT: The goal of this study was to determine the microRNAs altered upon the development of insulin resistance in a murine hypothalamic Neuropeptide Y/Agouti-related Peptide expressing cell line mHypoE-46

ORGANISM(S): Mus musculus

PROVIDER: GSE125951 | GEO | 2022/07/31

REPOSITORIES: GEO

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The effect of insulin treatment versus insulin resistance on microRNA expression in the hypothalamic neuronal cell line mHypoE-46.

Project description:The effect of insulin treatment versus insulin resistance on microRNA expression in the hypothalamic neuronal cell line mHypoE-46.

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Cancer anorexia: the role of serotonin in hypothalamic resistance of the neuropeptide Y system [A358_GEO_hypocells]

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Hypothalamic responses to reduced food intake in healthy animals and rats bearing small tumors

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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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