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Dietzsch, A.N.* ; Al-Hasani, H.* ; Altschmied, J.* ; Bottermann, K.* ; Brendler, J.* ; Haendeler, J.* ; Horn, S.* ; Kaczmarek, I.* ; Körner, A. ; Krause, K.* ; Landgraf, K.* ; Le Duc, D.* ; Lehmann, L.* ; Lehr, S.* ; Pick, S.* ; Ricken, A.* ; Schnorr, R.* ; Schulz, A.* ; Strnadová, M.* ; Velluva, A.* ; Zabri, H.* ; Schöneberg, T.* ; Thor, D.* ; Prömel, S.*

Dysfunction of the adhesion G protein-coupled receptor latrophilin 1 (ADGRL1/LPHN1) increases the risk of obesity.

Signal Transduct. Target. Ther. 9:103 (2024)
Verlagsversion DOI PMC
Creative Commons Lizenzvertrag
Obesity is one of the diseases with severe health consequences and rapidly increasing worldwide prevalence. Understanding the complex network of food intake and energy balance regulation is an essential prerequisite for pharmacological intervention with obesity. G protein-coupled receptors (GPCRs) are among the main modulators of metabolism and energy balance. They, for instance, regulate appetite and satiety in certain hypothalamic neurons, as well as glucose and lipid metabolism and hormone secretion from adipocytes. Mutations in some GPCRs, such as the melanocortin receptor type 4 (MC4R), have been associated with early-onset obesity. Here, we identified the adhesion GPCR latrophilin 1 (ADGRL1/LPHN1) as a member of the regulating network governing food intake and the maintenance of energy balance. Deficiency of the highly conserved receptor in mice results in increased food consumption and severe obesity, accompanied by dysregulation of glucose homeostasis. Consistently, we identified a partially inactivating mutation in human ADGRL1/LPHN1 in a patient suffering from obesity. Therefore, we propose that LPHN1 dysfunction is a risk factor for obesity development.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Korrespondenzautor
Schlagwörter Nervous-system Control; Human Adipose-tissue; Food-intake; Insulin-resistance; Alpha; Lipolysis; Neurons; Mice; Proopiomelanocortin; Inflammation
ISSN (print) / ISBN 2095-9907
e-ISSN 2059-3635
Zeitschrift Signal transduction and targeted therapy
Quellenangaben Band: 9, Heft: 1, Seiten: , Artikelnummer: 103 Supplement: ,
Verlag Nature Publishing Group
Verlagsort Campus, 4 Crinan St, London, N1 9xw, England
Nichtpatentliteratur Publikationen
Begutachtungsstatus Peer reviewed
Institut(e) Helmholtz Institute for Metabolism, Obesity and Vascular Research (HI-MAG)
Förderungen Deutsche Forschungsgemeinschaft (DFG, German Research Foundation)
Juergen Manchot Foundation
Medical Faculty, Leipzig University