The Role of Autophagy in White Adipose Tissue Function: Implications for Metabolic Health
White adipose tissue (WAT) is a highly adaptive endocrine organ that continuously remodels in response to nutritional cues. WAT expands to store excess energy by increasing adipocyte number and/or size. Failure in WAT expansion has serious consequences on metabolic health resulting in altered lipid, glucose, and inflammatory profiles. Besides an impaired adipogenesis, fibrosis and low-grade inflammation also characterize dysfunctional WAT. Nevertheless, the precise mechanisms leading to impaired WAT expansibility are yet unresolved. Autophagy is a conserved and essential process for cellular homeostasis, which constitutively allows the recycling of damaged or long-lived proteins and organelles, but is also highly induced under stress conditions to provide nutrients and remove pathogens. By modulating protein and organelle content, autophagy is also essential for cell remodeling, maintenance, and survival. In this line, autophagy has been involved in many processes affected during WAT maladaptation, including adipogenesis, adipocyte, and macrophage function, inflammatory response, and fibrosis. WAT autophagy dysregulation is related to obesity and diabetes. However, it remains unclear whether WAT autophagy alteration in obese and diabetic patients are the cause or the consequence of WAT malfunction. In this review, current data regarding these issues are discussed, focusing on evidence from human studies. ; M.C.P. was a recipient of a post-doctoral grant Juan de la Cierva Formación (FJCI-2017-32194) from the Ministerio de Ciencia, Innovación y Universidades (Spain). R.E.B. is under a contract from the 'Nicolas Monarde' (C-0030-2016) program from the Servicio Andaluz de Salud, Regional Ministry of Health of the Andalusian Government, Andalusia, Spain. This research was funded by Centros de Investigación Biomédica en Red (CIBER, CB06/03/0018) from the ISCIII, Madrid (Spain); RIC-0539-2018 and PI-0092-2017 from Consejería de Salud (Junta de Andalucía), Spain; PI18/01160 from the ISCIII (Madrid, Spain), and co-funded by the Fondo Europeo de Desarrollo Regional (FEDER). ; Yes