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Similarly, PPAR- has been shown to activate by PFAS in both animal and cell experiments, driving mesenchymal stem cells towards adipogenesis rather than osteogenesis and pre-adipocyte differentiation into adipocytes, thus resulting in imbalances in skeletal and adipose development and significant elevations in triglyceride levels [79,80,81,82]

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These findings provide a mechanistic framework linking KP dysregulation to the elevated cardiovascular morbidity and metabolic dysfunction frequently comorbid with MDD [153]