The metabolic toxicity of Fumonisin B (FB) converges at the accumulation of sphingoid bases and reduced ceramide levels. Several studies have alluded to a hypercholesterolemic endpoint after FB exposure, yet the molecular mechanisms remain elusive. Cell surface receptors are important regulators of cholesterol metabolism by regulating influx of lipids and efflux of cholesterol. Western blot analysis showed that FB elevates the expression of ABCA1 (a cholesterol efflux promoter) in an LXR dependent mechanism. We further highlight the potential role of PCSK9 in the degradation of LDL receptor. These data provide important evidence for the mechanism underlying hypercholesterolemia in FB treated models. The disruption of lipid homeostasis by FB is beginning to shift away from canonical ceramide synthase inhibition, and this changed perspective may shed light on diseases caused by dysregulated cholesterol metabolism such as cancer initiation and promotion.
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| http://dx.doi.org/10.1016/j.toxicon.2020.12.011 | DOI Listing |
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