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Adipokines,metabolic dysfunction and illness course in bipolar disorder
Affiliation:1. Laboratory of Pediatric Infectious Diseases, Felsenstein Medical Research Center, Petach Tikva 4941492, Israel;2. Laboratory of Biological Psychiatry, Felsenstein Medical Research Center, Petach Tikva 4941492, Israel;3. Department of Pediatrics A, Schneider Children''s Medical Center of Israel, Petach Tikva 4920235, Israel;4. Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv 6997801, Israel;5. Research Unit, Geha Mental Health Center, Petach Tikva 4941492, Israel;1. Department of Clinical Medicine, Londrina State University (UEL), Health Sciences Centre, Londrina, Paraná, Brazil;2. Center of Approach and Treatment for Smokers, University Hospital, Londrina State University, University Campus, Londrina, Paraná, Brazil;3. Health Sciences Graduation Program, Health Sciences Center, State University of Londrina, Londrina, Paraná, Brazil;4. CRC Scotland & London, London, UK;5. Department of Clinical and Toxicological Analysis, State University of Londrina, Londrina, Paraná, Brazil;6. Department of Adult Psychiatry, University of Lodz, Lodz, Poland;7. Department of Clinical Medicine and Translational Psychiatry Research Group, Faculty of Medicine, Federal University of Ceará, Fortaleza, CE, Brazil;8. Department of Psychiatry, Chulalongkorn University, Bangkok, Thailand;9. Department of Psychiatry, Plovdiv University, Plovdiv, Bulgaria;10. Revitalis, Waalre, The Netherlands;11. Impact Strategic Research Center, Deakin University, Geelong, Australia
Abstract:Replicated evidence indicates that individuals with BD are differentially affected by metabolic comorbidities and that its occurrence is a critical mediator and/or moderator of BD outcomes. This study aimed to explore the role of adipokines on bipolar disorder (BD) course and its relationship with metabolic comorbidities (i.e. type 2 diabetes mellitus, obesity). We measured plasma levels of adiponectin and leptin, as well as anthropometric and metabolic parameters of 59 patients with BD and 28 healthy volunteers. Our results showed that, in female participants, adiponectin was lower in individuals with BD, relative to healthy controls (p = 0.017). In the BD population, adiponectin levels were correlated with fasting glucose (r = −0.291, p = 0.047), fasting insulin (r = −0.332, p = 0.023), C-peptide (r = 0.040, p = 0.040), homeostatic model assessment-insulin resistance (r = −0.411, p = 0.004), HDL (r = 0.508, p < 0.001), VLDL (r = −0.395, p = 0.005) and triglycerides (r = −0.310, p = 0.030). After adjustment for age, gender and BMI, individuals with BD and low adiponectin levels (i.e. < 7.5 μg/ml), had a higher number of mood episodes (p < 0.001), lower number of psychiatric hospitalizations (p = 0.007), higher depressive symptoms (p < 0.001) and lower levels of functioning (p = 0.020). In conclusion, adiponectin levels, either directly or as a proxy of metabolic dysfunction, is independently associated with an unfavorable course of illness in BD.
Keywords:Bipolar disorder  Metabolism  Leptin  Adiponectin
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