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Loss of a Neural AMP-Activated Kinase Mimics the Effects of Elevated Serotonin on Fat, Movement, and Hormonal Secretions


While it is well appreciated that food availability has profound effects on behavior, physiology, and metabolism, the molecular systems that link these complex processes together still remain poorly understood. An ancient cellular sensor of energy is AMP-activated protein kinase, AMPK. Here we show that in the genetically tractable C. elegans, loss of AMPK in the nervous system mimics many of the outcomes also seen upon elevated serotonin signaling, a neural indicator of food availability. We show that similar to elevated serotonin signaling, loss of neural AMPK causes reduced movement while enhancing fat metabolism and secretions of neuroendocrine hormones known to be systemic regulators of energy balance, development and aging. While AMPK is generally considered a mediator of hormonal signaling, our findings indicate that it also regulates their release. Our findings suggest that some previous results attributed to roles of AMPK in the regulation of peripheral metabolism may in fact be due to the roles of this kinase complex in the nervous system as a mediator of serotonin signaling.


Vyšlo v časopise: Loss of a Neural AMP-Activated Kinase Mimics the Effects of Elevated Serotonin on Fat, Movement, and Hormonal Secretions. PLoS Genet 10(6): e32767. doi:10.1371/journal.pgen.1004394
Kategorie: Research Article
prolekare.web.journal.doi_sk: https://doi.org/10.1371/journal.pgen.1004394

Souhrn

While it is well appreciated that food availability has profound effects on behavior, physiology, and metabolism, the molecular systems that link these complex processes together still remain poorly understood. An ancient cellular sensor of energy is AMP-activated protein kinase, AMPK. Here we show that in the genetically tractable C. elegans, loss of AMPK in the nervous system mimics many of the outcomes also seen upon elevated serotonin signaling, a neural indicator of food availability. We show that similar to elevated serotonin signaling, loss of neural AMPK causes reduced movement while enhancing fat metabolism and secretions of neuroendocrine hormones known to be systemic regulators of energy balance, development and aging. While AMPK is generally considered a mediator of hormonal signaling, our findings indicate that it also regulates their release. Our findings suggest that some previous results attributed to roles of AMPK in the regulation of peripheral metabolism may in fact be due to the roles of this kinase complex in the nervous system as a mediator of serotonin signaling.


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