Quinic acid attenuates arsenic-induced hepatic injury and hyperglycemia in mice via GLUT2 upregulation and suppression of oxidative stress and inflammation.

Chronic exposure to arsenic is associated with an increased risk of developing diabetes mellitus. Quinic acid (QA), a cyclic polyol compound with known antioxidant and anti-inflammatory properties, was evaluated for its protective effects against sodium arsenite (SA)-induced hyperglycemia and hepatotoxicity in mice. In this study, mice were divided into 6 groups: control, SA (10 mg/kg), QA (200 mg/kg), and three groups receiving SA + QA at doses of 50, 100, or 200 mg/kg. After 28 days of treatment, fasting blood glucose was measured, followed by a glucose tolerance test. On day 30, blood samples were collected for analysis of serum liver enzymes, triglycerides, and cholesterol. Hepatic oxidative stress markers, inflammatory markers, glucagon-like peptide-1 levels, and serum levels of gastric inhibitory polypeptide and insulin were also measured. Hepatic glucose transporter protein 2 (GLUT2) expression was assessed by Western blot. Histological analysis of liver and pancreatic tissues was also performed. Arsenic exposure resulted in impaired glucose tolerance, oxidative stress, inflammation, and liver injury. Treatment with QA significantly reduced these effects, restored antioxidant defenses, reduced inflammatory responses, and improved glycemic control. Western blot analysis showed that GLUT2 protein expression was decreased in the SA group, whereas QA increased hepatic GLUT2 expression in a dose-dependent manner.