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Ghrelin concentration as an indicator of eating-disorder risk in obese women

Abstract : Aim. - Eating disorders (EDs), disordered eating (DE) and obesity are thought to have overlapping aetiological processes. DE in obesity can jeopardize weight-loss results, and acyl ghrelin (AG) is a hormone that stimulates food intake and reward processes. The main study objective was to determine whether higher-than-expected concentrations of AG in common obesity are associated with DE symptoms. Methods. - The study population included 84 women, aged 20-55 years, free of established EDs: 55 were severely obese (OB) and 29 were of normal weight (NW). OB participants were stratified into two groups according to their median concentration of fasting AG distribution. The OB women with a high fasting plasma ghrelin concentration (HGC) were compared with both OB women with a low fasting plasma ghrelin concentration (LGC) and NW women. Participants were assessed by the Eating Disorder Inventory (EDI-2), Three-Factor Eating Questionnaire (TFEQ) and Hospital Anxiety and Depression Scale (HADS). Fasting glucose, insulin, leptin and ghrelin plasma concentrations were also quantified. Results. - Between the two AG groups of OB women, there was no statistical difference in either anthropometric or metabolic parameters, HADS, TFEQ or fasting hunger scores. However, the HGC group scored significantly higher than the LGC group on the drive-for-thinness subscale of EDI-2 (9.30 +/- 0.99 vs. 6.46 +/- 0.83, respectively; P = 0.033). Conclusion. - Results support the hypothesis of a potential relationship between fasting plasma AG concentrations and ED risk, regardless of mood and anxiety. AG may be considered a potential biomarker of vulnerability for developing EDs. (C) 2018 Elsevier Masson SAS. All rights reserved.
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Submitted on : Tuesday, February 4, 2020 - 1:57:36 PM
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S. Iceta, B. Julien, K. Seyssel, S. Lambert-Porcheron, B. Segrestin, et al.. Ghrelin concentration as an indicator of eating-disorder risk in obese women. Diabetes & metabolism, 2019, 45 (2), pp.160--166. ⟨10.1016/j.diabet.2018.01.006⟩. ⟨hal-02466326⟩

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