Excess Iodine Consumption Induces Oxidative Stress and Pancreatic Damage Independently of Chemical Form in Male Wistar Rats: Participation of PPAR-γ and C/EBP-β

• Published in: Biology (Basel, Switzerland) Switzerland), 2024-06, Vol.13 (7), p.466
• Main Authors: Arbez-Evangelista, Cristian, Arroyo-Xochihua, Omar, Ortega-Ibarra, Ilse Haide, Ortega-Ibarra, Edú, De León-Ramírez, Yeimy Mar, Cuevas-Romero, Estela, Arroyo-Helguera, Omar
• Format: Article
• Language: English
• Subjects: Acids; AKT protein; Animal models; Antioxidants; Apoptosis; C/EBP-β; CCAAT/enhancer-binding protein; Diabetes; Diabetes mellitus (non-insulin dependent); Diet; Drinking water; Enzymes; Gene expression; Glucose; GLUT-4; Hormones; Hypertriglyceridemia; Insulin; Insulin resistance; Iodine; Laboratory animals; Lipids; Oxidants; Oxidative stress; Pancreas; pancreatic damage; Peroxisome proliferator-activated receptors; Potassium; Potassium iodide; PPAR-γ; Proteins; Public health; Thyroid gland; Thyroid hormones; Thyroid-stimulating hormone; Transcription factors; α-Amylase
• ISSN: 2079-7737; 2079-7737
• DOI: 10.3390/biology13070466

Human beings consume different chemical forms of iodine in their diet. These are transported by different mechanisms in the cell. The forms of iodine can be part of thyroid hormones, bind to lipids, be an antioxidant, or be an oxidant, depending on their chemical form. The excessive consumption of iodine has been associated with pancreatic damage and diabetes mellitus type 2, but the association between disease and the chemical form consumed in the diet is unknown. This research analyzes the effect of excessive iodine consumption as Lugol (molecular iodine/potassium iodide solution) and iodate on parameters of pancreatic function, thyroid and lipid profiles, antioxidant and oxidant status, the expression of IR/Akt/P-Akt/GLUT4, and transcription factors PPAR-γ and CEBP-β. Three groups of Wistar rats were treated with 300 μg/L of iodine in drinking water: (1) control, (2) KIO , and (3) Lugol. Lugol and KIO consumption increased total iodine levels. Only KIO increased TSH levels. Both induced high serum glucose levels and increased oxidative stress and pancreatic alpha-amylase activity. Insulin levels and antioxidant status decreased significantly. PPAR-γ and C/EBP-β mRNA expression increased. The pancreatic damage, hypertriglyceridemia, and oxidative stress were independent of the chemical form of iodine consumed. These effects depended on PPAR-γ, C/EBP-β, GLUT-4, and IR.