SAT-561 Protective Effect of Moderated Dose of Iodine in Pancreatic Alterations during Hypothyroidism

Abstract

Pancreatitis and insulitis are known causes of type 2 diabetes mellitus, and recently it has been shown that hypothyroidism can exacerbate these alterations. Molecular iodine (I2) exerts antioxidant, anti-inflammatory, and anti-dyslipidemia effects in diverse tissues. The objective of this study was to evaluate the effect of the oral supplement of this halogen in the induction of prediabetic status in a model of pharmacological hypothyroidism. Adult virgin rabbits of the Chinchilla breed were divided into control (n = 6) and hypothyroid (methimazole, MMI n = 6, 10 mg/kg in drinking water) groups, supplemented with moderate (MMI + I2 0.2 mg/kg; n= 6) and high dose of I2 (MMI + I2 2 mg/kg, n= 6). The results showed that hypothyroidism (1 month) was accompanied by circulating elevations of total cholesterol, HDL, LDL (enzymatic methods) and sCD163 (Western blot). It also promoted pancreatitis (H & E, Masson's trichrome, and PAS stains, as well as western blot for CD163) and insulitis (PAS and Masson's trichrome stains). In the pancreas, hypothyroidism increased the beta-amyloid around vessels (Congo red stain); triglycerides (Folch method), lipoperoxidation (levels of malondialdehyde MDA, enzymatic method) and expression of insulin and GLUT4. A low cholesterol synthesis (Folch method and western blot for CYP51A1) and a decrease in the expression of PPARγ (immunohistochemistry and western blot) were also observed. High doses of I2 supplement (2 mg/kg) aggravated pancreatic damage, promoting even islet amyloidosis and fibrosis. In contrast, the moderate dose of I2 (0.2 mg / kg) was able to prevent alterations in circulating lipids and in the pancreatic tissue. This prevention was accompanied by a significant decrease in the lipoperoxidation and a great expression of PPARγ. These results describe for first time the anti-inflammatory and anti-dyslipidemia effect of the moderate dose of I2 in the pancreas and suggest the possible participation of PPARγ receptors. More studies are needed to analyze the therapeutic effect of iodine in chronic pancreatic diseases associated with inflammation. This work was partially supported by grants CONACyT 257549 and PAPIIT-UNAM 201516.