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. 2024 Mar 8;236(5):269–279. [Article in German] doi: 10.1055/a-2251-5382

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The Author(s). This is an open access article published by Thieme under the terms of the Creative Commons Attribution-NonDerivative-NonCommercial-License, permitting copying and reproduction so long as the original work is given appropriate credit. Contents may not be used for commercial purposes, or adapted, remixed, transformed or built upon. (https://creativecommons.org/licenses/by-nc-nd/4.0/).

This is an open-access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivatives License, which permits unrestricted reproduction and distribution, for non-commercial purposes only; and use and reproduction, but not distribution, of adapted material for non-commercial purposes only, provided the original work is properly cited.

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Abb. 3 — Varianten in BBS-Genen können die LEPR-Signalübertragung stören und die Aktivierung nachgeschalteter MC4R-exprimierender Neuronen beeinträchtigen, was zu Hyperphagie und früh einsetzender, schwerer Adipositas führt. Abb. basiert auf Daten aus ³⁹ ⁴⁰ ⁴¹ ⁴² ⁴³ ⁴⁴ ⁴⁵ ⁴⁶ ⁴⁷ . Legende: AgRP: Agouti-related Peptid; BBS: Bardet-Biedl-Syndrom; BBSome: Komplex von 8 Bardet-Biedl-Ssyndrom Proteinen; LEPR: Leptin Rezeptor; MC4R: Melanocortin-4 Rezeptor; MSH: Melanozyten stimulierendes Hormon; POMC: Proopiomelanocortin.