Behavioural Neuroscience/Neuropharmacology Unit, Department of Pharmacology, Ladoke Akintola University of Technology, Ogbomosho, Oyo State,Nigeria.
Behavioural Neuroscience/Neuropharmacology Unit, Department of Pharmacology, Ladoke Akintola University of Technology, Ogbomosho, Oyo State,Nigeria | Department of Pharmacology, Therapeutics and Toxicology, Faculty of Basic Clinical Sciences, College of Medicine, Lagos State University, Ikeja, Lagos State, Nigeria.
Antiinflamm Antiallergy Agents Med Chem. 2021;20(4):380-388. doi: 10.2174/1871523020666210427111328.
The dietary model of metabolic syndrome has continued to aid our understanding of its pathogenesis and possible management interventions. However, despite progress in research, therapy continues to be challenging for humans; hence, the search for newer treatment and prevention options continues.
The objective of this study was to evaluate the impact of dietary CQ10 supplementation on metabolic, oxidative, and inflammatory markers in a diet-induced mouse model of metabolic syndrome.
Mouse groups were fed a Standard Diet (SD), High-Fat High-Sugar (HFHS) diet, and SD or HFHS diet (with incorporated CQ10) at 60 and 120 mg/kg of feed. At the completion of the study (8 weeks), blood glucose levels, Superoxide Dismutase (SOD) activity, plasma insulin, leptin, adiponectin, TNF-α, IL-10, serum lipid profile, and Lipid Peroxidation (LPO) levels were assessed. The liver was either homogenised for the assessment of antioxidant status or processed for general histology.
Dietary CQ10 mitigated HFHS diet-induced weight gain, decreased glucose, insulin, and leptin levels, and increased adiponectin levels in mice. Coenzyme-Q10 improved the antioxidant status of the liver and blood in HFHS diet-fed mice while also decreasing lipid peroxidation. Lipid profile improved, level of TNF-α decreased, and IL-10 increased following CQ10 diet. A mitigation of HFHS diet-induced alteration in liver morphology was also observed with CQ10.
Dietary CQ10 supplementation mitigates HFHS diet-induced changes in mice, possibly through its anti-oxidant, anti-lipaemic, and anti-inflammatory potential.
代谢综合征的饮食模式继续帮助我们理解其发病机制和可能的管理干预措施。然而，尽管研究取得了进展，人类的治疗仍然具有挑战性；因此，人们仍在继续寻找新的治疗和预防方法。
本研究旨在评估饮食补充 CQ10 对饮食诱导的代谢综合征小鼠模型代谢、氧化和炎症标志物的影响。
将小鼠分为标准饮食（SD）组、高脂肪高糖（HFHS）饮食组、SD 或 HFHS 饮食（添加 CQ10）组，饲料中 CQ10 含量为 60 和 120mg/kg。研究结束时（8 周），检测血糖水平、超氧化物歧化酶（SOD）活性、血浆胰岛素、瘦素、脂联素、TNF-α、IL-10、血清脂质谱和脂质过氧化（LPO）水平。肝脏匀浆用于评估抗氧化状态，或用于一般组织学处理。
饮食 CQ10 减轻了 HFHS 饮食引起的体重增加，降低了小鼠的血糖、胰岛素和瘦素水平，增加了脂联素水平。辅酶 Q10 改善了 HFHS 饮食喂养小鼠的肝脏和血液的抗氧化状态，同时降低了脂质过氧化。CQ10 饮食还改善了血脂谱，降低了 TNF-α 水平，增加了 IL-10 水平。CQ10 还减轻了 HFHS 饮食引起的肝形态改变。
饮食补充 CQ10 可减轻 HFHS 饮食引起的小鼠变化，可能通过其抗氧化、抗脂肪和抗炎作用。
