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Mixed leachate from polylactic acid food containers exacerbates NAFLD in obese mice at environmentally relevant levels: cAMP-dependent acid lipolysis mechanism.
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Chemicals leaching from "eco-friendly" PLA plant-based food containers, at levels people realistically encounter, worsened fatty liver disease in obese mice by triggering fat cells to release more fat into the liver. The effect only showed up in obese mice, not normal-weight ones, suggesting these compostable plastic containers may carry hidden risks for people who are already overweight.
Although high-dose independent exposure to commercial microplastics or plastic additives triggers nonalcoholic fatty liver disease (NAFLD), the hepatotoxic effects of the mixed leachate from single-use food containers (SUFCs) at environmentally relevant concentrations remain poorly elucidated. In this study, mice were chronically exposed to the mixed leachate extracted from polylactic acid (PLA)-based SUFCs under realistic exposure scenarios. We found that PLA-SUFC leachate exacerbates hepatic lipid accumulation and promotes NAFLD progression in obese mice, while exerting negligible effects on normal-weight mice. Mechanistically, these effects are primarily mediated by enhanced hepatic uptake of free fatty acids (FFAs) along the epididymal white adipose tissue (eWAT)-liver axis. Remarkably, FFA liberation from eWAT adipocytes relies on lysosomal acid lipolysis rather than canonical cytoplasmic neutral lipolysis. Single-nucleus RNA sequencing and functional assays demonstrated that mixed leachate exposure increases cyclic adenosine monophosphate (cAMP) levels via inhibiting the insulin-like growth factor 1 (IGF1)-phosphatidylinositol 3-kinase (PI3K) pathway and activating adenylate cyclase 8. Elevated cAMP specifically upregulates lysosomal acid lipase activity via the exchange protein activated by cAMP (EPAC)/forkhead box O1 (FoxO1) pathway without altering adipose triglyceride lipase levels, thereby promoting lysosomal acid lipolysis in adipocytes. Collectively, these findings suggest that long-term consumption of PLA-SUFC might increase NAFLD risk in obese individuals, and further reveal cAMP-dependent acid lipolysis as a novel mechanism of NAFLD.
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