Adipokines, cortisol and cytokine alterations in recent onset anorexia nervosa. A case–control study

• Published in: Endocrinología, diabetes y nutrición diabetes y nutrición, 2019-11, Vol.66 (9), p.571-578
• Main Authors: Elegido, Ana, Gheorghe, Alina, Sepúlveda, Ana R, Andrés, Patricia, Díaz-Prieto, Ligia E, Graell, Montserrat, Marcos, Ascensión, Nova, Esther
• Format: Article
• Language: English
• ISSN: 2530-0164; 2530-0180
• DOI: 10.1016/j.endinu.2019.02.003

Abstract Introduction Psychological and neuroendocrine alterations are typical characteristics in anorexia nervosa patients. The role of adipokines and cytokines as mediators of body systems’ adaptations to the patients’ abnormal eating behavior is not well understood. The duration of disease seems to be a determinant of nutritional status and associated hormone changes. We aimed to assess whether alterations in adipokines, cytokines and cortisol do already exist in patients with a recent disease onset by means of a case–control study. Methods Forty-one adolescent female patients on their first-episode and diagnosed with anorexia nervosa, were matched by age and socioeconomic status (SES) (1:1) with healthy girls. Leptin, soluble leptin receptor (sOB-R), adiponectin, cortisol, and the cytokines IL-1β, IL-2, IL-6 and TNF-α were examined. Results The results showed reduced leptin and increased sOB-R and cortisol levels in AN patients. Adiponectin was also increased but opposite to the previous biomarkers did not correlate with BMI Z -score. Serum TNF-α and IL-2 showed significantly lower and higher values, respectively, in the AN patients than in the controls. Cortisol showed the strongest correlation with sOB-R ( r = 0.436; P = 0.005). Conclusions Our study confirms previous findings on adipokine and cortisol alterations in AN patients, while overall cytokine results did not show a clear disruption in AN patients with short disease duration. The results highlight the need to disentangle the role of the sOB-R in the interactions between leptin and cortisol secretion.