Adipokines as drug targets in diabetes and underlying disturbances.
Diabetes and obesity are worldwide health problems. White fat dynamically participates in hormonal and inflammatory regulation. White adipose tissue is recognized as a multifactorial organ that secretes several adipose-derived factors that have been collectively termed "adipokines." Adipokines are pleiotropic molecules that gather factors such as leptin, adiponectin, visfatin, apelin, vaspin, hepcidin, RBP4, and inflammatory cytokines, including TNF and IL-1β, among others. Multiple roles in metabolic and inflammatory responses have been assigned to these molecules. Several adipokines contribute to the self-styled "low-grade inflammatory state" of obese and insulin-resistant subjects, inducing the accumulation of metabolic anomalies within these individuals, including autoimmune and inflammatory diseases. Thus, adipokines are an interesting drug target to treat autoimmune diseases, obesity, insulin resistance, and adipose tissue inflammation. The aim of this review is to present an overview of the roles of adipokines in different immune and nonimmune cells, which will contribute to diabetes as well as to adipose tissue inflammation and insulin resistance development. We describe how adipokines regulate inflammation in these diseases and their therapeutic implications. We also survey current attempts to exploit adipokines for clinical applications, which hold potential as novel approaches to drug development in several immune-mediated diseases.
Laboratory of Transplantation Immunobiology, Department of Immunology, Institute of Biomedical Sciences IV, University of São Paulo, SP, Brazil.
Vinícius
0000-0002-0426-1828
V
Andrade-Oliveira
Laboratory of Transplantation Immunobiology, Department of Immunology, Institute of Biomedical Sciences IV, University of São Paulo, SP, Brazil ; Laboratory of Clinical and Experimental Immunology, Nephrology Division, Federal University of São Paulo, SP, Brazil.
Niels O S
0000-0001-5436-1248
NO
Câmara
Division of Endocrinology, Diabetes, and Metabolism, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, MA, USA.
Pedro M
PM
Moraes-Vieira
D054392:Adipokines / Q000378:metabolism* / Q000502:physiology; D052242:Adiponectin / Q000502:physiology; D000273:Adipose Tissue / Q000378:metabolism; D000818:Animals; D003920:Diabetes Mellitus / Q000188:drug therapy / Q000378:metabolism* / Q000401:mortality; D006801:Humans; D007249:Inflammation; D053583:Interleukin-1beta / Q000502:physiology; D020738:Leptin / Q000502:physiology; D051379:Mice; D054409:Nicotinamide Phosphoribosyltransferase / Q000502:physiology; D009765:Obesity / Q000150:complications* / Q000188:drug therapy; D054839:Retinol-Binding Proteins, Plasma / Q000502:physiology; D014409:Tumor Necrosis Factor-alpha / Q000502:physiology
D054392:Adipokines; D052242:Adiponectin; D053583:Interleukin-1beta; D020738:Leptin; C101326:RBP4 protein, human; D054839:Retinol-Binding Proteins, Plasma; D014409:Tumor Necrosis Factor-alpha; D054409:Nicotinamide Phosphoribosyltransferase