口服单宁酸可减轻高脂肪和果糖饮食引起的肥胖大鼠的血脂异常、高血糖和氧化应激

Emmanuel Ejiofor, Ernest Agwamba, Chima Egedigwe-Ekeleme, Paul Nweje-Anyalowu, Hitler Louis, Innocent Abalake, Francis Imeh, Bliss Harold, Deborah Azuh, Maureen Ejiofor, Christian Okoro, Joan Ejiofor, Chidinma Ekwegbalu, Laurene Ekwugha
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引用次数: 0

摘要

肥胖症和糖尿病被认为是威胁生命的疾病,其特点是氧化应激增加、胰岛素抵抗、肝毒性、高血糖和高胆固醇血症。因此,我们研究了单宁酸对高脂肪和果糖饮食诱导的肥胖大鼠模型的影响。与高脂高糖组相比,200 和 400 mg/kg 剂量的单宁酸能显著降低空腹血糖浓度,逆转紊乱的血脂谱,降低肝酶活性,抑制氧化应激。组织病理学检查显示,服用鞣酸组的胰腺和肝脏结构得到了保护。单宁酸对α-淀粉酶、α-葡萄糖苷酶和胰脂肪酶的体外抑制活性显示出良好的抑制潜力。分子对接研究表明,单宁酸与肥胖症和糖尿病相关受体蛋白(α-淀粉酶、α-葡萄糖苷酶和胰脂肪酶)之间具有很高的结合亲和力和更多的氢键相互作用。总之,单宁酸可以防止氧化应激的发生,保护肝脏,并恢复高脂和果糖饮食诱导的肥胖大鼠的脂质分布。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Oral administration of tannic acid attenuates dyslipidemia, hyperglycemia, and oxidative stress in high-fat and fructose diet-induced obesity in rats

Oral administration of tannic acid attenuates dyslipidemia, hyperglycemia, and oxidative stress in high-fat and fructose diet-induced obesity in rats

Obesity and diabetes are considered life-threatening conditions, characterized by increased oxidative stress, insulin resistance, hepatotoxicity, hyperglycemia, and hypercholesterolemia. Therefore, we studied the effects of tannic acid in a high-fat and fructose-diet-induced rat model of obesity. Administration of tannic acid at doses of 200 and 400 mg/kg significantly reduced fasting blood glucose concentration, reversed disoriented lipid profile, decreased liver enzyme activities, and inhibited oxidative stress compared to the high-fat, high-sugar group. Histopathological examination showed preserved pancreas and liver architecture in the tannic acid-administered groups. The in vitro inhibitory activity of tannic acid against alpha-amylase, alpha-glucosidase, and pancreatic lipase showed good inhibitory potential. Molecular docking studies showed high binding affinity and more hydrogen bond interactions between tannic acid and receptor proteins (alpha-amylase, alpha-glucosidase, and pancreatic lipase) implicated in obesity and diabetes. In conclusion, tannic acid prevented the onset of oxidative stress, preserved the liver, and restored the disoriented lipid profile in high-fat and fructose diet-induced obesity in rats.

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