Preventive Effect of Molecular Iodine in Pancreatic Disorders from Hypothyroid Rabbits

Pancreatic alterations such as inflammation and insulin resistance accompany hypothyroidism. Molecular iodine (I(2)) exerts antioxidant and differentiation actions in several tissues, and the pancreas is an iodine-uptake tissue. We analyzed the effect of two oral I(2) doses on pancreatic disorders in a model of hypothyroidism for 30 days. Adult female rabbits were divided into the following groups: control, moderate oral dose of I(2) (0.2 mg/kg, M-I(2)), high oral dose of I(2) (2.0 mg/kg, H-I(2)), oral dose of methimazole (MMI; 10 mg/kg), MMI + M-I(2,), and MMI + H-I(2). Moderate or high I(2) supplementation did not modify circulating metabolites or pancreatic morphology. The MMI group showed reductions of circulating thyroxine (T4) and triiodothyronine (T3), moderate glucose increments, and significant increases in cholesterol and low-density lipoproteins. Acinar fibrosis, high insulin content, lipoperoxidation, and overexpression of GLUT4 were observed in the pancreas of this group. M-I(2) supplementation normalized the T4 and cholesterol, but T3 remained low. Pancreatic alterations were prevented, and nuclear factor erythroid-2-related factor-2 (Nrf2), antioxidant enzymes, and peroxisome proliferator-activated receptor gamma (PPARG) maintained their basal values. In MMI + H-I(2,) hypothyroidism was avoided, but pancreatic alterations and low PPARG expression remained. In conclusion, M-I(2) supplementation reestablishes thyronine synthesis and diminishes pancreatic alterations, possibly related to Nrf2 and PPARG activation.