LEPRLeptin Receptor
LEPRLibrary of Experimental Phase Relations (web-based database)
LEPRLaser Electron Paramagnetic Resonance
Copyright 1988-2018 AcronymFinder.com, All rights reserved.
References in periodicals archive ?
(Nasdaq:RYTM), a biopharmaceutical company focused on the development and commercialization of therapeutics for the treatment of rare genetic disorders of obesity, today announced positive topline results from two pivotal, Phase 3 clinical trials evaluating setmelanotide, the company's melanocortin-4 receptor (MC4R) agonist, for the treatment of pro-opiomelanocortin (POMC) and leptin receptor (LEPR) deficiency obesities.
The company said both studies met their primary endpoints and all key secondary endpoints, showing a statistically significant and clinically meaningfully effect on weight loss and reductions in insatiable hunger in patients with POMC and LEPR deficiency obesities.
To reveal the role of leptin and Lepr in vivo, two mutant mouse strains with ligand (ob/ob mice) or receptor deficiency (db/db mice) have been widely used as obesity and type 2 diabetes animal models, respectively [10].
The purpose of this study is to investigate the genotype distribution and the allele frequency of LEPR Q223R polymorphism in OSAS patients and to estimate the effect of this polymorphism on metabolic and anthropometric traits.
Immunoreactive LEPR levels were semi-quantitatively assessed using the subsequent intensity categories: 0, no staining; [1.sup.+], weak but visible staining; [2.sup.+], moderate or distinct staining; and [3.sup.+], strong staining.
Accumulating evidence demonstrates that the effects of leptin to regulate the onset of puberty are thought to be mediated mainly by its receptor LEPR action on hypothalamic neurons (Bellefontaine et al., 2014; de Luque et al., 2007; Sanchez-Garrido and TenaSempere, 2013; Sheffer-Babila et al., 2013).
Both POMC and LepR deficiency obesity are rare genetic disorders associated with severe, early-onset obesity and unrelenting hyperphagia.
Results: There was statistically significant difference between the LEPR genotypes of acromegalic patients (GG 11.4%, GA 52.3%, and AA 36.4%) and controls (GG 33.3%, GA 50%, and AA 16.7%) although their LEP genotype distribution was similar.
Subjects with the LEPR rs1137101 allele A presented higher LDL cholesterol concentrations than G homozygous alleles that were only marginally significant (P = 0.017).
The goals of the study are (i) to characterize cellular immunolocalization (immunohistochemistry) and expression profile (mRNA and protein levels) of LEP, LEPR, GHR, and Ghr-R1A throughout the luteal phase; (ii) to evaluate the role of the hormones LEP and GHR in secretory activity (progesterone ([P.sub.4]) prostaglandin (PG) [E.sub.2] and [PGF.sub.2[alpha]], nitric oxide (nitrite), tumor necrosis factor [alpha] (TNF), and macrophage migration inhibitory factor (MIF, a proangiogenic factor)) and angiogenic activity (using bovine aortic endothelial cells proliferation assay) during CL establishment and maintenance.
Int J Lepr Other Mycobact Dis 2001;69(2 Suppl):S19-29.