Effects of plant flavonoids and selenium on pancreatic hormones and glucose homeostasis in autoimmune thyroiditis
Annotatsiya
Autoimmune thyroiditis (AIT) is a systemic autoimmune disorder that extends beyond thyroid dysfunction and is associated with disturbances in pancreatic endocrine secretion and glucose metabolism. The present study aimed to evaluate the effects of selected plant flavonoids-dihydroquercetin, chrysoeriol, luteolin, resveratrol, kaempferol, and thamiflaside-administered alone or in combination with selenium on pancreatic hormone secretion, glycemic control, and hepatic glycogen content in an experimental rat model of AIT. AIT was induced in male Wistar rats using thyroglobulin and Freund's adjuvant. After confirmation of autoimmune thyroiditis, animals received flavonoid treatment (20 mg/kg body weight), with or without selenium, for 14 days. Serum concentrations of insulin, glucagon, amylin, and somatostatin were determined by immunoassay. Glycated hemoglobin (HbA1c) was measured as an indicator of long-term glycemic control, and hepatic glycogen content was assessed in liver homogenates. AIT induction resulted in marked metabolic dysregulation characterized by reduced insulin and amylin secretion, elevated glucagon levels, impaired somatostatin regulation, increased HbA1c, and depletion of hepatic glycogen stores. Flavonoid treatment produced compound-specific corrective effects. Luteolin and kaempferol, particularly in combination with selenium, showed the strongest efficacy by restoring pancreatic hormone balance, reducing hyperglucagonemia, improving HbA1c levels, and replenishing hepatic glycogen toward physiological ranges. Dihydroquercetin and chrysoeriol exerted moderate protective effects, whereas resveratrol and thamiflaside showed limited efficacy. In conclusion, autoimmune thyroiditis induces significant disturbances in pancreatic endocrine function and hepatic glucose metabolism, while flavonoid-selenium combinations may represent promising strategies for correcting AIT-associated metabolic dysfunctions.