Antioxidants, Redox Biology and Toxicology Research Group, Department of Medical Biochemistry, College of Health Sciences, Nile University of Nigeria, Abuja, Nigeria.
Arch Physiol Biochem. 2020 May;126(2):107-115. doi: 10.1080/13813455.2018.1498901. Epub 2018 Oct 5.
This study investigated the influence of betulinic acid on high-fructose diet-induced metabolic syndrome in rats. Oral administration of betulinic acid significantly reversed high-fructose diet-mediated increase in body mass index and blood glucose. Furthermore, betulinic acid restored high-fructose diet-mediated alterations in metabolic hormones (insulin, leptin and adiponectin). Betulinic acid-mediated upregulation of protein kinase B (Akt) and phosphoinositde-3 kinase (PI3K) anulled high-fructose diet mediated depletion. Also, elevated tumour necrosis factor-α, interleukin-6 and -8 were significantly lowered. Administration of betulinic acid restored high-fructose diet-mediated increase in the levels of lipid profile parameters and indices of atherosclerosis, cardiac and cardiovascular diseases. High-fructose diet-mediated decrease in activities of antioxidant enzymes (superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase and glucose 6-phosphate dehydrogenase) and increase in oxidative stress biomarkers (reduced glutathione, lipid peroxidation products, protein oxidation and fragmented DNA) were significantly restored by the phenolic acids. Conclusively, betulinic acid improves insulin sensitivity, elevated blood glucose, inflammation and dyslipidaemia and oxidative stress in high-fructose diet-induced metabolic syndrome through the PI#Kand Akt pathways .
本研究探讨了白桦脂酸对高果糖饮食诱导的大鼠代谢综合征的影响。白桦脂酸的口服给药显著逆转了高果糖饮食介导的体重指数和血糖升高。此外，白桦脂酸恢复了高果糖饮食介导的代谢激素（胰岛素、瘦素和脂联素）的改变。白桦脂酸介导的蛋白激酶 B（Akt）和磷酸肌醇-3 激酶（PI3K）的上调消除了高果糖饮食介导的消耗。此外，肿瘤坏死因子-α、白细胞介素-6 和白细胞介素-8 的水平也显著降低。白桦脂酸的给药恢复了高果糖饮食介导的脂质谱参数和动脉粥样硬化、心脏和心血管疾病指数的增加。高果糖饮食介导的抗氧化酶（超氧化物歧化酶、过氧化氢酶、谷胱甘肽过氧化物酶、谷胱甘肽还原酶和葡萄糖 6-磷酸脱氢酶）活性降低和氧化应激生物标志物（还原型谷胱甘肽、脂质过氧化产物、蛋白质氧化和断裂的 DNA）增加，被酚酸显著恢复。总之，白桦脂酸通过 PI#K 和 Akt 途径改善了高果糖饮食诱导的代谢综合征中的胰岛素敏感性、血糖升高、炎症和血脂异常以及氧化应激。
