Interleukin-16 is increased in obesity and alters adipogenesis and inflammation in vitro
Reyes-Farias, Marjorie (Universitat de Barcelona. Departament de Bioquímica i Fisiologia)
Fernández-García, Pablo (Universidad Rey Juan Carlos)
Corrales, Patricia (Universidad Rey Juan Carlos)
González, Lorena (Institut Germans Trias i Pujol)
Soria-Gondek, Andrea (Institut Germans Trias i Pujol. Hospital Universitari Germans Trias i Pujol)
Martínez, Ester (Universidad Rey Juan Carlos)
Pellitero, Silvia (Institut Germans Trias i Pujol. Hospital Universitari Germans Trias i Pujol)
Tarascó, Jordi (Institut Germans Trias i Pujol. Hospital Universitari Germans Trias i Pujol)
Moreno, Pau (Institut Germans Trias i Pujol. Hospital Universitari Germans Trias i Pujol)
Sumoy, Lauro (Institut Germans Trias i Pujol)
Medina-Gómez, Gema (Department of Basic Health Sciences. University Rey Juan Carlos)
Sánchez-Infantes, David (Instituto de Salud Carlos III)
Herrero, Laura (Instituto de Salud Carlos III)

Fecha:	2024
Resumen:	Introduction: Obesity is a chronic condition associated with low-grade inflammation mainly due to immune cell infiltration of white adipose tissue (WAT). WAT is distributed into two main depots: subcutaneous WAT (sWAT) and visceral WAT (vWAT), each with different biochemical features and metabolic roles. Proinflammatory cytokines including interleukin (IL)-16 are secreted by both adipocytes and infiltrated immune cells to upregulate inflammation. IL-16 has been widely studied in the peripheral proinflammatory immune response; however, little is known about its role in adipocytes in the context of obesity. Aim & Methods: We aimed to study the levels of IL-16 in WAT derived from sWAT and vWAT depots of humans with obesity and the role of this cytokine in palmitate-exposed 3T3-L1 adipocytes. Results: The results demonstrated that IL-16 expression was higher in vWAT compared with sWAT in individuals with obesity. In addition, IL-16 serum levels were higher in patients with obesity compared with normal-weight individuals, increased at 6 months after bariatric surgery, and at 12 months after surgery decreased to levels similar to before the intervention. Our in vitro models showed that IL-16 could modulate markers of adipogenesis (Pref1), lipid metabolism (Plin1, Cd36, and Glut4), fibrosis (Hif1a, Col4a, Col6a, and Vegf), and inflammatory signaling (IL6) during adipogenesis and in mature adipocytes. In addition, lipid accumulation and glycerol release assays suggested lipolysis alteration. Discussion: Our results suggest a potential role of IL-16 in adipogenesis, lipid and glucose homeostasis, fibrosis, and inflammation in an obesity context.
Ayudas:	Ministerio de Economía y Competitividad CP15/00106 Instituto de Salud Carlos III PI17/01455 Instituto de Salud Carlos III PI20/00807 Agencia Estatal de Investigación PID2020-114953RB-C21 Agencia Estatal de Investigación IJC2018-037142-I Agència de Gestió d'Ajuts Universitaris i de Recerca 2021/SGR-00367
Nota:	The author(s) declare financial support was received for the research, authorship, and/or publication of this article. This study was supported by the Instituto de Salud Carlos III (grants CP15/00106, PI17/01455, PI20/00807 to DS-I.) and the Spanish Ministry of Science and Innovation (MCIN/AEI) (grant PID2020-114953RB-C21 to LH, grant IJC2018-037142-I to RC) co-funded by the European Regional Development Fund [ERDF], the Biomedical Research Centre in Pathophysiology of Obesity and Nutrition (CIBEROBN) (Grant CB06/03/0001 to LH), the Merck Health Foundation (to LH), and the Government of Catalonia (2021SGR00367 to LH). RC is a Serra Húnter Fellow. MR-F is a recipient of a CONICYT-ANID Chile doctoral fellowship. Acknowledgments
Derechos:	Aquest document està subjecte a una llicència d'ús Creative Commons. Es permet la reproducció total o parcial, la distribució, la comunicació pública de l'obra i la creació d'obres derivades, fins i tot amb finalitats comercials, sempre i quan es reconegui l'autoria de l'obra original.
Lengua:	Anglès
Documento:	Article ; recerca ; Versió publicada
Publicado en:	Frontiers in endocrinology, Vol. 15 (2024) , p. 1346317, ISSN 1664-2392

DOI: 10.3389/fendo.2024.1346317
PMID: 38544694

11 p, 2.4 MB

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