article · International Journal of Diabetes Management
Background: Cardiometabolic Syndrome (CMS) brought on by a High-Fat Diet (HFD) involves interrelated oxidative, inflammatory and metabolic pathways. Although coenzyme Q-10 (CoQ10) and Taurine (TAU) are mitochondrial modulators, their combined effects on many biomarker domains are still unknown. Methods: The 48 male Wistar rats were divided into six groups: HFD (16 weeks), HFD+TAU (200 mg/kg), HFD+CoQ10 (20 mg/kg), HFD+TAU+CoQ10 (100+10 mg/kg) and HFD+Atorvastatin (5 mg/kg). Thirty-seven biomarkers were measured, including those related to glucose homeostasis, lipid profile, cardiac injury (cTnI, NT-proBNP), inflammation (hs-CRP, IL-6, IL-10), oxidative stress (MDA, 8-OHdG), antioxidant enzymes (SOD, GPx), adipokines (adiponectin, leptin), hepatokines (FGF-21) and mitochondrial function (mtDNA copy number via qPCR). Results: Severe multi-system disruptions were caused by HFD. Partial improvements (20-45%) were obtained with TAU or CoQ10 alone. FBG (98 ± 4 mg/dL), HOMA-IR (2.7 ± 0.3), TC (86 ± 5 mg/dL), cTnI (0.48 ± 0.04 ng/mL, 75% reduction), NT-proBNP (201 ± 18 pg/mL, 76% reduction) and urine 8-OHdG (79% reduction) were all normalized by the TAU+CoQ10 combination. Antioxidant enzyme levels (SOD: 102 ± 6 vs. HFD 41 ± 4 U/mg) were restored. The cardiac mtDNA copy number rose from 42 ± 4% to 94 ± 7% of the control group (p<0.001). FGF-21 dropped by 72%, but adiponectin rose 3.2 times. Additive to synergistic effects were produced by the combination (combination index <0.9 for 28/37 biomarkers). Conclusion: Low-dose TAU+CoQ10 outperforms monotherapies and corresponding atorvastatin in reversing HFD-induced CMS across 37 validated biomarkers. These results lend credence to the clinical assessment of TAU+CoQ10 as a metabolic treatment that targets the mitochondria.
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DOI: 10.61797/ijdm.v5i1.725
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