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. 2021 Nov 4;11:21644. doi: 10.1038/s41598-021-00947-7

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© The Author(s) 2021

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.

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Mechanisms proposed for lactate to depolarize POMC neurons of the hypothalamus. In a high-energy condition, lactate modulates the activity of POMC neurons through two pathways: (1) directly through incorporation via MCT2 or indirectly by binding to HCAR1 in astrocytes. (A) In a classical mechanism of neuronal activation, lactate is taken up by neurons using MCT2 and serves as a suitable energetic substrate. The increase in the ATP/ADP ratio causes the closure of ATP-sensitive K⁺ channels, producing a depolarization. (B) The binding of lactate to HCAR1 in astrocytes activates a Gi/o-coupled pathway that, through an increase in intracellular calcium, leads to the release of glutamate onto POMC neurons. In this model, the activation of glutamate receptors will cause depolarization of POMC neurons. Dotted line shows a possible mechanism that has not been evaluated yet.