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
{"title":"Oral administration of tannic acid attenuates dyslipidemia, hyperglycemia, and oxidative stress in high-fat and fructose diet-induced obesity in rats","authors":"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","doi":"10.1002/fsh3.12081","DOIUrl":null,"url":null,"abstract":"<p>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.</p>","PeriodicalId":100546,"journal":{"name":"Food Safety and Health","volume":"3 2","pages":"250-263"},"PeriodicalIF":0.0000,"publicationDate":"2024-11-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/fsh3.12081","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Food Safety and Health","FirstCategoryId":"1085","ListUrlMain":"https://onlinelibrary.wiley.com/doi/10.1002/fsh3.12081","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
Abstract
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.