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. 2019 Oct 11;9:14695. doi: 10.1038/s41598-019-51193-x

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© The Author(s) 2019

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 license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license 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 license, visit http://creativecommons.org/licenses/by/4.0/.

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A working model for the role of the enzyme AMPK in regulating lipid metabolism during P. chabaudi infection. P. chabaudi infection induces a decrease in active hepatic AMPK, which leads to the activation of ACC and SREBP-1c and subsequent stimulation of gene transcription and expression of proteins involved in lipid biosynthesis, such as the enzyme FAS. Concomitantly, there is a reduction of β-oxidation due to the inhibition of the β-oxidation-limiting enzyme CPT1-A and decreased expression of PPAR-α and PGC-1α. Pretreatment with metformin elicits the activation of hepatic AMPK, reversing the lipid metabolism perturbations observed following Plasmodium infection and preventing the efficiency of Plasmodium infection of mice.