Discussing the Putative Role of Obesity-Associated Genes in the Etiopathogenesis of Eating Disorders

Gervasini, Guillermo; Gamero-Villarroel, Carmen

doi:10.2217/pgs.15.77

Cited by 13 publications

(8 citation statements)

References 189 publications

(231 reference statements)

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“…But, what would be the precise mechanism linking this gene to these behaviors and specifically to ED? These personality features are expressed by the involvement of a pattern of neuronal adaptations induced by central genes such as dopamine or serotonin, which has been consistently associated with ED‐coupled personality dimensions (Gervasini & Gamero‐Villarroel, 2015). Dopaminergic and serotonergic genes in the midbrain have AP‐2 binding sites; therefore it is likely that these transcription factors, aside from its established role during development, can also influence mood and personality in adults through this neurotransmitter system (Damberg, 2005; Damberg et al., 2001).…”

Section: Discussionmentioning

confidence: 99%

“…Genetic alterations in the complex neural system aimed to keep energy balance by food intake are known to trigger and maintain obesity, but the genes involved in the neuronal control of weight regulation might also be relevant for ED (Day, Ternouth, & Collier, 2009; Gervasini & Gamero‐Villarroel, 2015). Indeed, we and others have shown that variability in these genes is also associated with ED‐related behaviors (Gamero‐Villarroel et al., 2014, 2015; Muller et al., 2012; Rybakowski et al., 2007).…”

Section: Introductionmentioning

confidence: 99%

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Influence of TFAP2B and KCTD15 genetic variability on personality dimensions in anorexia and bulimia nervosa

et al. 2017

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Introduction TFAP2B and KCTD15 are obesity‐related genes that interact to regulate feeding behavior. We hypothesize that variability in these loci, isolated or in combination, could also be related to the risk of eating disorders (ED) and/or associated psychological traits.MethodsWe screened 425 participants (169 ED patients, 75 obese subjects, and 181 controls) for 10 clinically relevant and tag single‐nucleotide polymorphisms (SNPs) in KCTD15 and TFAP2B by the Sequenom MassARRAY platform and direct sequencing. Psychometric evaluation was performed with EDI‐2 and SCL‐90R inventories.ResultsThe KCTD15 rs287103 T variant allele was associated with increased risk of bulimia nervosa (BN) (OR = 4.34 [1.47–29.52]; p = .003) and with scores of psychopathological scales of these patients. Haplotype *6 in KCTD15 was more frequent in controls (OR = 0.40 [0.20–0.80], p = .009 for anorexia nervosa), while haplotype *4 in TFAP2B affected all three scales of the SCL‐90R inventory in BN patients (p ≤ .01). Epistasis analyses revealed relevant interactions with body mass index of BN patients (p < .001). Genetic profiles in obese patients did not significantly differ from those found in ED patients.ConclusionsThis is the first study that evaluates the combined role of TFAP2B and KCTD15 genes in ED. Our preliminary findings suggest that the interaction of genetic variability in these loci could influence the risk for ED and/or anthropometric and psychological parameters.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Influence of TFAP2B and KCTD15 genetic variability on personality dimensions in anorexia and bulimia nervosa

et al. 2017

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“…However, plasma levels of NPY (part of the orexigenic system) are anomalously low [96]. Abnormalities within the hormonal regulation of the homeostatic system have also been reported for BN [111] and BED [112].…”

Section: Neural Circuits and Neurotransmittersmentioning

confidence: 99%

Psychopharmacological advances in eating disorders

Himmerich

Treasure

2017

Expert Review of Clinical Pharmacology

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Anorexia nervosa (AN), bulimia nervosa (BN) and binge eating disorder (BED) are the primary eating disorders (EDs). The only psychopharmacological treatment options for EDs with approval in some countries include fluoxetine for BN and lisdexamfetamine for BED. Given the high comorbidity and genetic correlations with other psychiatric disorders, it seems possible that novel medications for these conditions might also be effective in EDs. Areas covered: The current scientific literature has increased our understanding of how medication could be beneficial for patients with EDs on a molecular, functional and behavioral level. On the basis of theoretical considerations about neurotransmitters, hormones and neural circuits, possible drug targets for the treatment of EDs may include signal molecules and receptors of the self-regulatory system such as serotonin, norepinephrine and glutamate, the hedonic system including opioids, cannabinoids and dopamine and the hypothalamic homeostatic system including histamine, ghrelin, leptin, insulin, and glucagon-like peptide-1. Expert commentary: The latest research points to an involvement of both the immune and the metabolic systems in the pathophysiology of EDs and highlights the importance of the microbiome. Therefore, the next few years may unveil drug targets for EDs not just inside and outside of the brain, but possibly even outside of the human body.

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“…MC4R and BDNF were found to be highly expressed in the hypothalamus, which suggests that they may play important roles in the central nervous system in eating behavior [15, 16]. Golden et al reported that the BDNF level was inversely correlated with adiponectin in adult males [17].…”

Section: Introductionmentioning

confidence: 99%

Associations of Two Obesity-Related Single-Nucleotide Polymorphisms with Adiponectin in Chinese Children

Gao

Zhao

et al. 2017

International Journal of Endocrinology

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Purpose. Genome-wide association studies have found two obesity-related single-nucleotide polymorphisms (SNPs), rs17782313 near the melanocortin-4 receptor (MC4R) gene and rs6265 near the brain-derived neurotrophic factor (BDNF) gene, but the associations of both SNPs with other obesity-related traits are not fully described, especially in children. The aim of the present study is to investigate the associations between the SNPs and adiponectin that has a regulatory role in glucose and lipid metabolism. Methods. We examined the associations of the SNPs with adiponectin in Beijing Child and Adolescent Metabolic Syndrome (BCAMS) study. A total of 3503 children participated in the study. Results. The SNP rs6265 was significantly associated with adiponectin under an additive model (P = 0.02 and 0.024, resp.) after adjustment for age, gender, and BMI or obesity statuses. The SNP rs17782313 was significantly associated with low adiponectin under a recessive model. No statistical significance was found between the two SNPs and low adiponectin after correction for multiple testing. Conclusion. We demonstrate for the first time that the SNP rs17782313 near MC4R and the SNP rs6265 near BDNF are associated with adiponectin in Chinese children. These novel findings provide important evidence that adiponectin possibly mediates MC4R and BDNF involved in obesity.

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Discussing the Putative Role of Obesity-Associated Genes in the Etiopathogenesis of Eating Disorders

Cited by 13 publications

References 189 publications

Influence of TFAP2B and KCTD15 genetic variability on personality dimensions in anorexia and bulimia nervosa

Influence of TFAP2B and KCTD15 genetic variability on personality dimensions in anorexia and bulimia nervosa

Psychopharmacological advances in eating disorders

Associations of Two Obesity-Related Single-Nucleotide Polymorphisms with Adiponectin in Chinese Children

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