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- The market for dietary supplements has significantly grown due to their envisaged health benefits. These bioactive compounds are actively explored for their therapeutic benefits against vast metabolic complications due to their abundant antioxidant properties. Nuclear factor erythroid 2-related factor 2 (Nrf2) modulation as a cytoprotective mechanism against oxidative stress-induced metabolic stress has garnered interest, particularly through its regulation by many dietary supplements. This review aims to evaluate and critically discuss the available evidence on the potential therapeutic effects of dietary supplements, including prominently used nutraceuticals against dyslipidemia-associated cardiovascular complications. Notably, this review highlights the potential of these bioactive compounds to modulate the Nrf2 pathway, enhancing intracellular antioxidants and providing protection against oxidative stress-induced complications. Beyond the value of preclinical evidence on the ability of these supplements to regulate the Nrf2 pathway and counteract oxidative damage, this review also incorporates clinical evidence supporting their therapeutic benefits in dyslipidemia-related cardiovascular conditions. Fundamental pharmacological aspects such as bioavailability and relevant biological properties are also discussed to inform further development of these bioactive compounds as potential nutraceuticals against metabolic diseases.
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- This study investigates the effects of prolonged simvastatin exposure on coenzyme Q9/10 (CoQ9/10) levels, an essential component of antioxidant defense, in cultured cardiac cells. Statins, commonly used to manage dyslipidemia and reduce cardiovascular risk, may impair mitochondrial function, but their impact on CoQ10 depletion and oxidative stress is not well understood. We examined the influence of simvastatin on mitochondrial oxidative capacity, reactive oxygen species (ROS) production, and CoQ9/10 status at concentrations of 0.3, 0.6, 1.25, 2.5, 5, 10, and 20 μM, over durations of 24, 48, and 72 h. Using an in vitro model of cultured H9c2 cardiomyoblasts, our results showed that short-term exposure (24 h) at lower concentrations (<5 μM) enhanced cytosolic and mitochondrial ROS levels without affecting mitochondrial function or CoQ9/10 status. However, prolonged exposure to higher concentrations (≥10 μM for >48 h) resulted in impaired mitochondrial oxidative capacity, indicated by increased proton leak and elevated ROS levels, which were followed by significantly reduced cell viability. These findings suggest that prolonged, high-dose simvastatin exposure may disrupt the oxidative balance of CoQ9/10, leading to myocardial injury. This research addresses a gap in understanding the long-term effects of statins on mitochondrial health and underscores the need for further studies to optimize statin therapy and minimize adverse effects on myocardial function.
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- Aspalathin is a rooibos flavonoid with established blood glucose lowering properties, however, its efficacy to moderate complications associated with hepatic insulin resistance is unknown. To study such effects, C3A liver cells exposed to palmitate were used as a model of hepatic insulin resistance. These hepatocytes displayed impaired substrate metabolism, including reduced glucose transport and free fatty acid uptake. These defects included impaired insulin signaling, evident through reduced phosphatidylinositol-4,5-bisphosphate 3-kinase/ protein kinase B (PI3K/AKT) protein expression, and mitochondrial dysfunction, depicted by a lower mitochondrial respiration rate. Aspalathin was able to ameliorate these defects by correcting altered substrate metabolism, improving insulin signaling and mitochondrial bioenergetics. Activation of 5´-adenosine monophosphate-activated protein kinase (AMPK) may be a plausible mechanism by which aspalathin increases hepatic energy expenditure. Overall, these results encourage further studies assessing the potential use of aspalathin as a nutraceutical to improve hepatocellular energy expenditure, and reverse metabolic disease-associated complications.
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