The present study was conducted to investigate the effects of decaffeinated and caffeinated coffee consumption, in a combination with atorvastatin, on selected lipidemic profle parametes, as well as liver and kidney function biomarkers in hyperlipidemia-induced rats. Major coffee constituents, including caffeine and chlorogenic acid, were extracted and quantified using HPLC-DAD. A total of 54 female Wistar rats were allocated into three main experimental groups: a standard diet group (SD), a high-fat diet-induced hyperlipidemic group (FD), and a high-fat diet-induced hyperlipidemic group treated with atorvastatin (FD+). Each main group was further subdivided into three subgroups: control, caffeinated coffee extract-supplemented, and decaffeinated coffee extract-supplemented. Biochemical analyses were performed to assess lipid profile parameters, liver function, and kidney function biomarkers. In the SD groups, significantly higher mean levels of non-high-density lipoprotein (non-HDL) and the atherogenic index of plasma (AIP) were observed in the SDeC group compared with the SCAF group (P<0.05). In contrast, within the FD groups, the FCAF group showed signfcantly higher mean non-HDL levels than the FDeC (21.41±2.31 vs 9.91±5.11 mg/dL, P<0.01). In the combination groups trated with atorvastatin (FD+), the FCAF+ demonstrated a significant reduction in mean non-HDL levels and AIP values compared with the FDeC+ (13.18±3.99 vs 16.25±5.77 mg/dL, P<0.05). These findings may suggest that decaffeinated coffee could be associated with less favorable lipid-modulating effects under certain experimental conditions. Overall, caffeinated coffee, when combined with atorvastatin, may provide greater benefits than decaffeinated coffee in improving specific cardiovascular risk-related parameters, particularly non-HDL cholesterol and AIP.
