Melatonin Modulates Hypophyseal-Thyroid Function through Differential Activation of MT1 and MT2 Receptors in Hypothyroid Mice

Abstract

Hypothyroidism is characterized by the low level of thyroid hormones in circulation, which affects the normal metabolic activities of organisms. Propylthiouracil (PTU) induced hypothyroid condition impairs the antioxidant defense system and therefore normal physiology alters. Melatonin influences most physiological activities and is also known for its antioxidative properties. Melatonin modulates physiological activities through receptor-mediated as well as non-receptor-mediated pathways. In this study, we evaluated the involvement of melatonin MT1 and MT2 receptors in the modulation of hypophyseal-thyroid function in PTU-induced hypothyroid mice. We have noted the decreased level of T3 and T4 and increased level of TSH hormone in PTU-treated mice. Melatonin treatment counteracted the PTU-caused changes in circulatory T3, T4, and TSH hormones. PTU treatment caused increased MT1 receptor protein expression in the thyroid as well as the pituitary gland while increased MT2 receptor protein in the pituitary gland. Melatonin treatment caused increased TSH receptor protein in the thyroid gland. Melatonin induced MT2 receptor protein expression in both the thyroid and pituitary glands whereas MT1 receptor proteins in the pituitary gland. This study may suggest that melatonin regulates hypophyseal-thyroid function through differential sensitization of MT1 and MT2 receptors on the pituitary and thyroid glands in hypothyroid mice.