Trh, short for thyrotropin-releasing hormone, is a crucial endocrine agent. It is an important regulator of cells in the anterior pituitary, central and peripheral nervous systems. By controlling the synthesis and release of thyroid hormones, Trh is involved in multiple physiological functions, such as energy homeostasis. It exerts its effects mainly through G protein-coupled Trh receptors, which primarily signal via Gq/11 [1].

Trh knockout mice show characteristic phenotypes of tertiary hypothyroidism, indicating its key role in regulating the hypothalamus-pituitary-thyroid (HPT) axis. Hypophysiotropic Trh neurons in the hypothalamus act as energy sensors and control the synthesis and release of thyrotropin, which in turn activates the synthesis and secretion of thyroid hormones [2,4]. In rats, hypothalamic Trh mediates the anorectic effects of serotonin, suggesting its involvement in feeding regulation [3].

In conclusion, Trh is essential for regulating the HPT axis, energy homeostasis, and feeding behavior. The study of Trh knockout mouse models has provided valuable insights into its role in hypothyroidism and feeding-related disorders, helping us better understand the underlying biological mechanisms and potentially paving the way for new therapeutic strategies in these disease areas.