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.