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Background: Eating disorders (EDs) lead to multiple psychiatric and somatic complications and thus constitute a major public health concern., Objectives: The aim of this study was to give an exhaustive view of the studies reporting the prevalence of the different EDs or total EDs and to study their evolution., Methods: A literature search following PRISMA Guidelines and limited to studies in English or French published between 2000 and 2018 was performed and relevant studies were included in this systematic review on the prevalence of EDs. The literature search revealed 94 studies with accurate ED diagnosis and 27 with broad ED diagnosis., Results: In 94 studies with accurate ED diagnosis, the weighted means (ranges) of lifetime ED were 8.4% (3.3-18.6%) for women and 2.2% (0.8-6.5%) for men. The weighted means (ranges) of 12-month ED prevalence were 2.2% (0.8-13.1%) for women and 0.7% (0.3-0.9%) for men. The weighted means (ranges) of point prevalence were 5.7% (0.9-13.5%) for women and 2.2% (0.2-7.3%) for men. According to continents, the weighted means (ranges) of point prevalence were 4.6% (2.0-13.5%) in America, 2.2% (0.2-13.1%) in Europe, and 3.5% (0.6-7.8%) in Asia.In addition to the former, 27 other studies reported the prevalence of EDs as broad categories resulting in weighted means (ranges) of total point prevalence of any EDs of 19.4% (6.5-36.0%) for women and 13.8% (3.6-27.1%) for men., Conclusions: Despite the complexity of integrating all ED prevalence data, the most recent studies confirm that EDs are highly prevalent worldwide, especially in women. Moreover, the weighted means of point ED prevalence increased over the study period from 3.5% for the 2000-2006 period to 7.8% for the 2013-2018 period. This highlights a real challenge for public health and healthcare providers., (Copyright © American Society for Nutrition 2019.)

Specific peptide molecules classified as hormones, neuropeptides and cytokines are involved in intercellular signaling regulating various physiological processes in all organs and tissues. This justifies the peptidergic signaling as an attractive pharmacological target. Recently, a protein mimetic of a peptide hormone has been identified in Escherichia coli suggesting the potential use of specific bacterial proteins as a new type of peptide-like drugs. We review the scientific rational and technological approaches leading to the identification of the E. coli caseinolytic protease B (ClpB) homologue protein as a conformational mimetic of α-melanocyte-stimulating hormone (α-MSH), a melanocortin peptide critically involved in the regulation of energy homeostasis in humans and animals. Theoretical and experimental backgrounds for the validation of bacterial ClpB as a potential drug are discussed based on the known E. coli ClpB amino acid sequence homology with α-MSH. Using in silico analysis, we show that other protein sources containing similar to E. coli ClpB α-MSH-like epitopes with potential biological activity may exist in Enterobacteriaceae and in some Brassicaceae. Thus, the original approach leading to the identification of E. coli ClpB as an α-MSH mimetic protein can be applied for the identification of mimetic proteins of other peptide hormones and development of a new type of peptide-like protein-based drugs., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)

Obese subjects display elevated plasma levels of leptin reflecting the phenomenon of leptin resistance. Here, we aimed to determine whether leptin-reactive immunoglobulins (Ig) are present in obese and type 2 diabetes (T2D) patients and whether their plasma levels and affinity kinetics may correlate with obesity and diabetes markers. We show that leptin levels are increased in obese patients with and without T2D. Although mean plasma levels of leptin-reactive IgG were similar between study groups, IgG in obese non-diabetic patients had increased dissociation rate and lower affinity (increased dissociation equilibrium constant value; KD). In controls and diabetic patients, the association rates of leptin IgG correlated negatively with obesity and diabetes markers, respectively. In contrast, KD values correlated positively with plasma leptin levels and obesity traits in our cohort, and with diabetes markers in both the total cohort and in the obese T2D group. Taken together, our data reveal that leptin-reactive IgG are present in healthy subjects, obese, and diabetic patients but display altered affinity kinetics in obesity. Increased IgG binding to leptin in healthy subjects associated with lower body mass index (BMI) suggests an enhancing role of IgG in leptin signaling. Accordingly, a decreased affinity of IgG for leptin, found in obese patients, can be relevant to leptin resistance.