Olfactomedin 2 deficiency protects against diet-induced obesity.

Autor: González-García I; Department of Physiology, CiMUS, University of Santiago de Compostela, Instituto de Investigación Sanitaria (IDIS), Santiago de Compostela, Spain; CIBER de la Fisiopatología de la Obesidad y la Nutrición (CIBEROBN), Instituto de Salud Carlos III (ISCIII), Madrid, Spain. Electronic address: ismael.gonzalez@usc.es., Freire-Agulleiro Ó; Department of Physiology, CiMUS, University of Santiago de Compostela, Instituto de Investigación Sanitaria (IDIS), Santiago de Compostela, Spain; CIBER de la Fisiopatología de la Obesidad y la Nutrición (CIBEROBN), Instituto de Salud Carlos III (ISCIII), Madrid, Spain., Nakaya N; Section on Retinal Ganglion Cell Biology, Laboratory of Retinal Cell and Molecular Biology, National Eye Institute, National Institutes of Health, Bethesda, MD, USA., Ortega FJ; CIBER de la Fisiopatología de la Obesidad y la Nutrición (CIBEROBN), Instituto de Salud Carlos III (ISCIII), Madrid, Spain; Service of Diabetes, Endocrinology and Nutrition (UDEN), Institut d'Investigació Biomédica de Girona (IDIBGI), Girona, Spain., Garrido-Gil P; Laboratory of Cellular and Molecular Neurobiology of Parkinson's Disease (CiMUS), Department of Morphological Sciences, University of Santiago de Compostela, Instituto de Investigación Sanitaria (IDIS), Santiago de Compostela, Spain; Centro de Investigación Biomédica en Red sobre Enfermedades Neurodegenerativas (CIBERNED), Instituto de Salud Carlos III (ISCIII), Madrid, Spain., Liñares-Pose L; Department of Physiology, CiMUS, University of Santiago de Compostela, Instituto de Investigación Sanitaria (IDIS), Santiago de Compostela, Spain; CIBER de la Fisiopatología de la Obesidad y la Nutrición (CIBEROBN), Instituto de Salud Carlos III (ISCIII), Madrid, Spain., Fernø J; Hormone Laboratory, Haukeland University Hospital, Bergen, Norway., Labandeira-Garcia JL; Laboratory of Cellular and Molecular Neurobiology of Parkinson's Disease (CiMUS), Department of Morphological Sciences, University of Santiago de Compostela, Instituto de Investigación Sanitaria (IDIS), Santiago de Compostela, Spain; Centro de Investigación Biomédica en Red sobre Enfermedades Neurodegenerativas (CIBERNED), Instituto de Salud Carlos III (ISCIII), Madrid, Spain., Diéguez C; Department of Physiology, CiMUS, University of Santiago de Compostela, Instituto de Investigación Sanitaria (IDIS), Santiago de Compostela, Spain; CIBER de la Fisiopatología de la Obesidad y la Nutrición (CIBEROBN), Instituto de Salud Carlos III (ISCIII), Madrid, Spain., Sultana A; Section on Retinal Ganglion Cell Biology, Laboratory of Retinal Cell and Molecular Biology, National Eye Institute, National Institutes of Health, Bethesda, MD, USA., Tomarev SI; Section on Retinal Ganglion Cell Biology, Laboratory of Retinal Cell and Molecular Biology, National Eye Institute, National Institutes of Health, Bethesda, MD, USA., Fernández-Real JM; CIBER de la Fisiopatología de la Obesidad y la Nutrición (CIBEROBN), Instituto de Salud Carlos III (ISCIII), Madrid, Spain; Service of Diabetes, Endocrinology and Nutrition (UDEN), Institut d'Investigació Biomédica de Girona (IDIBGI), Girona, Spain., López M; Department of Physiology, CiMUS, University of Santiago de Compostela, Instituto de Investigación Sanitaria (IDIS), Santiago de Compostela, Spain; CIBER de la Fisiopatología de la Obesidad y la Nutrición (CIBEROBN), Instituto de Salud Carlos III (ISCIII), Madrid, Spain. Electronic address: m.lopez@usc.es.
Jazyk: angličtina
Zdroj: Metabolism: clinical and experimental [Metabolism] 2022 Apr; Vol. 129, pp. 155122. Date of Electronic Publication: 2022 Jan 11.
DOI: 10.1016/j.metabol.2021.155122
Abstrakt: Background and Aims: Olfactomedin 2 (OLFM2; also known as noelin 2) is a pleiotropic protein that plays a major role in olfaction and Olfm2 null mice exhibit reduced olfactory sensitivity, as well as abnormal motor coordination and anxiety-related behavior. Here, we investigated the possible metabolic role of OLFM2.
Methods: Olfm2 null mice were metabolically phenotyped. Virogenetic modulation of central OLFM2 was also performed.
Results: Our data showed that, the global lack of OLFM2 in mice promoted anorexia and increased energy expenditure due to elevated brown adipose tissue (BAT) thermogenesis and browning of white adipose tissue (WAT). This phenotype led to resistance to high fat diet (HFD)-induced obesity. Notably, virogenetic overexpression of Olfm2 in the lateral hypothalamic area (LHA) induced weight gain associated with decreased BAT thermogenesis.
Conclusion: Overall, this evidence first identifies central OLFM2 as a new molecular actor in the regulation of whole-body energy homeostasis.
(Copyright © 2022 Elsevier Inc. All rights reserved.)
Databáze: MEDLINE
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