MCH(human, mouse, rat)

MCH (human, mouse, rat) is a cyclic neuropeptide mainly synthesized by neurons in the lateral hypothalamic area. MCH (human, mouse, rat) also serves as an endogenous ligand for the melanin-concentrating hormone receptor (MHC receptor), with a binding IC₅₀ of 0.3 nM and 1.5 nM for human MCH-1R and MCH-2R, respectively; its functional EC₅₀ values are 3.9 nM and 88.7 nM. MCH (human, mouse, rat) acts not only as an orexigenic signal but also as a key integrating and regulatory hormone for energy homeostasis and sleep-wake cycles. MCH (human, mouse, rat) can be used in studies related to obesity, sleep disorders, and other associated conditions^[1][2][3][4]. IC50 & Target:Binding IC50: 0.3 nM (MCH1R)
IC50: 1.5 nM (MCH1R)^[1] In Vitro:MCH (human, mouse, rat) potently displaces the binding of [¹²⁵I]Phe¹³-Tyr¹⁹-MCH to MCH-2R on the membranes of transfected COS-7 and CHO cells, with an IC₅₀ of 1.5 nM^[2].
MCH (human, mouse, rat) (60 min) dose-dependently activates calcium mobilization in CHO cells stably expressing human MCH-2R, with an EC₅₀ of 0.1 nM^[2].
MCH (human, mouse, rat) (30 s) induces a robust, dose-dependent intracellular calcium response in HEK293-AEQ17 cells stably expressing human MCH-2R, with an EC₅₀ of 31 nM^[2].
MCH (human, mouse, rat) (1 h) potently stimulates inositol phosphate turnover in HEK293-AEQ17 cells stably expressing human MCH-2R, with an EC₅₀ of 2.7 nM^[2].
MCH (human, mouse, rat) reduces the release of α-MSH and secretion of CART in rodent hypothalamic tissue explants, and induces the release of NPY and AgRP^[3].
MCH (human, mouse, rat) induces dose-dependent GIRK currents in Xenopus laevis oocytes co-expressing SLC-1 receptors and GIRK channels^[4].
MCH (human, mouse, rat) induces calcium-mediated chloride currents in Xenopus laevis oocytes expressing the SLC-1 receptor by activating the phospholipase C pathway^[4].
MCH (human, mouse, rat) exerts inhibitory effects on primary cultured rat LH neurons, including reducing spontaneous firing frequency, suppressing glutamatergic synaptic transmission, and decreasing the amplitude of VDCC via a Gi/o-dependent pathway, with an IC₅₀ of 7.84 nM, and it does not induce GIRK currents^[4]. In Vivo:Administration of MCH (human, mouse, rat) (into the medial preoptic area) reduces the active maternal behavioral components in lactating rats^[1].
Levels of MCH (human, mouse, rat) are upregulated in fasted rats, leptin-deficient ob/ob obese mice, fa/fa rats, and diet-induced obese rats^[2].
form of MCH (human, mouse, rat) (administered intracerebroventricularly; acute single injection; chronic infusion) exerts orexigenic effects in Wistar rats and Sprague-Dawley rats, including increased acute food intake and obesity induced by chronic infusion^[3].
form of MCH (human, mouse, rat) (intracerebral/intracerebroventricular; chronic administration) increases food intake, body weight and obesity in mice, while overexpression of this substance in the lateral hypothalamus induces obesity and insulin resistance^[4].
form of MCH (human, mouse, rat) (administered intracerebrally; administered intracerebroventricularly; administered locally in the hypothalamus; acutely administered) stimulates food intake in rats^[4].
MCH (human, mouse, rat) regulates memory retention in rats^[4].