Adra1b, encoding the alpha-1b adrenergic receptor, is a key component in the adrenergic signaling pathway. These receptors are widely distributed in the peripheral and central nervous systems and are involved in various physiological processes such as vasoconstriction, energy and glucose homeostasis, and neurotransmitter regulation [1,2,3]. Genetic models, especially gene-knockout (KO) and conditional-knockout (CKO) mouse models, have been crucial in dissecting its functions.

In a CKO mouse model where Adra1b was selectively deleted in hepatocytes, it was found that loss of Adra1b exacerbated diet-induced obesity, insulin resistance, and glucose intolerance in female mice but not in male mice. This reveals a sex-dependent role of Adra1b in the sympathetic nervous system's regulation of energy and glucose homeostasis [1]. In addition, in a study on neuroblastoma, genetic knockout of ADRA1B or its blockade using antagonists sensitized MYCN-amplified NB cells to cell viability reduction and neural differentiation induced by 13-cis retinoic acid, suggesting its potential as a pharmacologic target in neuroblastoma treatment [4].

In conclusion, Adra1b plays important roles in energy and glucose homeostasis, as well as in the context of certain diseases like neuroblastoma. The use of Adra1b KO/CKO mouse models has provided valuable insights into its sex-specific metabolic functions and potential as a therapeutic target in neuroblastoma, highlighting its significance in understanding both normal physiological processes and disease mechanisms.