Adiponectin in eating disorders

Khalil, Rami Bou; Hachem, Claire El

doi:10.1007/s40519-013-0094-z

Cited by 32 publications

(29 citation statements)

References 58 publications

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“…One may argue whether similar central effects exist in humans (Pan et al 2006;Kos et al 2006). Consistent with potential central effects, human adiponectin levels were also shown to be altered in eating disorders such as anorexia nervosa, binge eating disorder and bulimia nervosa (reviewed in, e.g., Bou Khalil and El Hachem 2014). In particular, many studies demonstrated elevated adiponectin serum levels in female patients affected with anorexia nervosa (ModanMoses et al 2007;Pannacciulli et al 2003;Terra et al 2013), while binge eating disorder was related to decreased circulating adiponectin (Monteleone et al 2003;Carnier et al 2012).…”

Section: Introductionmentioning

confidence: 92%

Role of genetic variants in ADIPOQ in human eating behavior

et al. 2014

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The beneficial effects of adiponectin and its negative correlation with BMI are well described. Adiponectin serum levels are altered in eating disorders such as anorexia nervosa, bulimia nervosa or binge eating. Here, we tested the hypothesis that (1) adiponectin serum levels correlate with human eating behavior factors and (2) that genetic variants of the ADIPOQ locus influence both serum levels and eating behavior. We analyzed 11 SNPs within ADIPOQ and in the 5 0 UTR and measured serum adiponectin levels in 1,036 individuals from the German Sorbs population. The German version of the three-factor eating questionnaire (FEV) was completed by 548 Sorbs. For replication purposes, we included an independent replication cohort from Germany (N = 350). In the Sorbs, we observed positive correlations of restraint with adiponectin serum levels (P = 0.001; r = 0.148) which, however, did not withstand adjustment for covariates (P = 0.083; r = 0.077). In addition, four SNPs were nominally associated with serum adiponectin levels (all P \ 0.05). Of these, two variants (rs3774261; rs1501229, all P \ 0.05) were also related to disinhibition. Furthermore, three variants were exclusively associated with hunger (rs2036373, P = 0.049) and disinhibition (rs822396; rs864265, all P \ 0.05). However, none of these associations withstood Bonferroni corrections for multiple testing (all P [ 9.3 9 10 -4 ). In our replication cohort, we observed similar effect directions at rs1501229 for disinhibition and hunger. A meta-analysis resulted in nominal statistical significance P = 0.036 (Z score 2.086) and P = 0.017 (Z score 2.366), respectively. Given the observed relationship of the SNPs with adiponectin levels and eating behavior, our data support a potential role of adiponectin in human eating behavior. Whether the relationship with eating behavior is mediated by the effects of circulating adiponectin warrants further investigations.

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Section: Introductionmentioning

confidence: 92%

Role of genetic variants in ADIPOQ in human eating behavior

et al. 2014

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“…Research has also shown an association between appetite hormones and eating disorders, specifically binge‐eating disorder (BED) and BN. For example, adiponectin and leptin are appetite‐regulatory hormones that can act as an appetite suppressant that shows associations with both such that adiponectin is decreased in adults with BED and BN, albeit associations with BN are somewhat inconsistent (Khalil & El Hachem, ). On the other hand, leptin is increased in adults with BED and BN (Adami, Campostano, Cella, & Scopinaro, ; Monteleone, Di Lieto, Tortorella, Longobardi, & Maj, ).…”

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confidence: 99%

Reproductive and Appetite Hormones and Bulimic Symptoms during Midlife

Baker

Peterson

Thornton

et al. 2017

Euro Eating Disorders Rev

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Eating disorders and related symptoms occur during midlife; however, little is known about their etiology. It has been hypothesized that perimenopause represents a window of vulnerability for the development or exacerbation of eating disorder symptomatology because, like puberty, perimenopause is a period of reproductive hormone change. We compared symptoms of bulimia nervosa (bulimic symptomatology) assessed via mean scores on a self-report questionnaire in premenopausal and perimenopausal women. We also examined the association between hormone concentrations (reproductive/appetite) and bulimic symptomatology. No mean differences in bulimic symptomatology were observed between premenopause and perimenopause. However, there was a significant positive association between leptin and binge eating. Although no significant associations between reproductive hormones and bulimic symptomatology were observed, additional research is needed to provide definitive information. It is essential to learn more about the etiology of eating disorders and related symptomatology across the lifespan in order to develop age-relevant treatment and prevention programs.

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“…There are 212 variants within Adipor2 that distinguish the D2J strain from the B6J strain (https://www.sanger.ac.uk), including one 5' UTR SNP, three, 3' UTR SNPs, and over 60 nmd intronic variants (see "high impact variants" in Supplementary Table 1). Serum levels of adiponectin are inversely correlated with BMI and risk for diabetes and are decreased in patients with BED and increased in patients with AN (Khalil and El Hachem 2014).…”

Section: Discussionmentioning

confidence: 99%

Systems genetic analysis of binge-like eating in a C57BL/6J x DBA/2J-F2 cross

Yao

Babbs

Kelliher

et al. 2020

Preprint

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Word count in abstract: 247 Word count in main text: 4410 ACKNOWLEDGEMENTS This work was funded by R21DA038738 (C.D.B.), R01DA039168 (C.D.B.), and R01CA221260 (M.I.D., C.D.B.) ABSTRACTObjective. Binge eating is a heritable quantitative trait associated with eating disorders (ED) and refers to the rapid consumption of a large quantity of energy-dense food that is associated with loss of control, anxiety, and depression. Binge Eating Disorder is the most common ED in adults in the US; however, the genetic basis is unknown. We previously identified robust mouse inbred strain differences between C57BL/6J and DBA/2J in binge-like eating (BLE) of sweetened palatable food (PF) in an intermittent access, conditioned place preference paradigm. Methods.To map the genetic basis of BLE, we phenotyped and genotyped 128 C57BL/6J x DBA/2J-F2 mice.Results. We identified a quantitative trait locus (QTL) on chromosome 13 influencing progressive changes in body weight across training days (LOD = 5.5; 26-39 cM). We also identified two sex-combined QTLs influencing PF intake on chromosome 5 (LOD = 5.6; 1.5-LOD interval = 21-28 cM) and 6 (LOD = 5.3; 1.5-LOD interval = 50-59 cM). Furthermore, sex-specific analyses revealed that the chromosome 6 locus was driven by males (1.5-LOD interval: 52-59 cM) and identified a female-selective QTL for BLE on chromosome 18 (LOD = 4.1; 1.5-LOD interval: 23-35 cM). Systems genetic analysis of the chromosome 6 locus for BLE using GeneNetwork legacy trait datasets from BXD recombinant inbred strains identified Adipor2 and Plxnd1 as two positional, functional, biological candidate genes.Discussion. We identified genetic loci influencing BLE. Future studies will phenotype BXD recombinant inbred strains to fine map loci and support candidate gene nomination and validation.

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Adiponectin in eating disorders

Abstract: The potential role that plays adiponectin in the pathogenesis of eating disorders needs to be elucidated by further studies.

Cited by 32 publications

References 58 publications

Role of genetic variants in ADIPOQ in human eating behavior

Role of genetic variants in ADIPOQ in human eating behavior

Reproductive and Appetite Hormones and Bulimic Symptoms during Midlife

Systems genetic analysis of binge-like eating in a C57BL/6J x DBA/2J-F2 cross

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