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- W2897037794 abstract "Significance The age of puberty in humans is changing via unknown mechanisms, although metabolic alterations in childhood are blamed as a major contributing factor. Perturbations in pubertal timing are posed with increased risk of later cardiometabolic diseases and reduced life expectancy, urging a better understanding of the molecular basis for these phenomena. We describe a mechanism whereby the main cellular energy sensor, AMPK, operates in a population of hypothalamic neurons, named Kiss1, which produce the puberty-activating signal, kisspeptin, to metabolically control puberty onset. This neuroendocrine circuit provides a molecular link between conditions of negative energy balance and delayed pubertal timing, via a repressive AMPK–Kiss1 pathway, which may become a druggable target in conditions of disordered puberty, especially of metabolic origin." @default.
- W2897037794 created "2018-10-26" @default.
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- W2897037794 date "2018-10-22" @default.
- W2897037794 modified "2023-10-15" @default.
- W2897037794 title "Metabolic regulation of female puberty via hypothalamic AMPK–kisspeptin signaling" @default.
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- W2897037794 doi "https://doi.org/10.1073/pnas.1802053115" @default.
- W2897037794 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6233121" @default.
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- W2897037794 hasPublicationYear "2018" @default.
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