Key result
Oral administration of 6PPDQ in mice induced metabolic syndrome and cognitive impairment via PI3K-AKT pathway inhibition, which was partially alleviated by the agonist SC79.
Why the study?
6PPD-quinone (6PPDQ) has been implicated in environmental and public health risks, prompting exploration of its impact on metabolic and cognitive functions.
Warrants caution on environmental 6PPDQ exposure for metabolic health; leaves open human cardiometabolic relevance pending translational studies.
6PPD-quinone (6PPDQ), a derivative of the antioxidant 6PPD used in the rubber industry, has been implicated in environmental and public health risks. To explore its impact on metabolic and cognitive functions, we orally administered 6PPDQ to mice and assessed its effects. Our results show that 6PPDQ induces a dose-dependent increase in body weight, elevated fasting blood glucose, insulin resistance, and other hallmarks of metabolic syndrome. Furthermore, cognitive tests revealed significant impairments in learning and memory in 6PPDQ-treated mice. Transcriptomic and Western blot analyses suggest that 6PPDQ disrupts insulin signaling through inhibition of the PI3K-AKT pathway, leading to metabolic and cognitive dysfunction. Notably, treatment with the PI3K-AKT agonist SC79 partially alleviated these effects. These findings highlight the health risks of 6PPDQ exposure and suggest potential avenues for preventive and therapeutic strategies.
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Wang et al. (2025) studied Metabolic syndrome and cognitive impairment. 6PPDQ was evaluated on Metabolic and cognitive functions. Oral administration of 6PPDQ in mice induced metabolic syndrome and cognitive impairment via PI3K-AKT pathway inhibition, which was partially alleviated by the agonist SC79.
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