“…Alternatively, since BDNF has also a key role in the modulation of different neurotransmitters, it could indirectly participate in ANR and low MBMI through changes in these systems previously involved in ED. [2][3][4][5] The contribution of distinct susceptibility factors to the different ED subtypes, which is supported by other studies where differential personality and psychopathological traits were found between purging (ANBP or BN) and nonpurging ED (ANR), [20][21][22] Neither association was found in any ED group when the À270C/T SNP was considered, suggesting that it may not be involved in eating behavior alterations. Nevertheless, it would be necessary to test it in a larger sample because of its low frequency in the studied populations.…”
supporting
confidence: 65%
“…Under the hypothesis that BDNF may confer susceptibility to the ED subtypes in different ways and to reduce heterogeneity, our patients were subdivided into four main diagnostic groups that have been shown to differ in various biological and psychopathological features. [20][21][22] Thus, AN, ANR, ANBP and BN diagnoses were separately considered in the statistical analyses.…”
Several lines of evidence support a role for brain-derived neurotrophic factor (BDNF) alterations in the etiology of eating disorders (EDs). BDNF heterozygous knockout mice show alterations in eating behavior, increased body weight and adipocyte hypertrophy. BDNF also regulates the synaptic efficiency through the modulation of key neurotransmitter systems previously known to be involved in ED. These findings, together with the fact that this neurotrophin is expressed in the hypothalamus nuclei associated with weight regulation and feeding control, led us to propose BDNF as a candidate gene for ED. To investigate the possible involvement of this neurotrophin in eating behavior, we screened the BDNF gene in 95 ED patients and identified four sequence variants. Two of them, À374A/T and À256G/A, were found in two patients with anorexia nervosa (AN) and consisted of single-nucleotide mutations within the 5 0 untranslated region (5 0 UTR). The other two polymorphisms resulted in a C to T transition located at the 5 0 UTR of the BDNF gene and an amino-acid substitution within the BDNF precursor protein (Val66Met). We performed a case-control study for these two Single-nucleotide polymorphisms in a sample of 143 ED patients and 112 unrelated controls and found a strong association of restricting AN (ANR) with the Met allele of the Val66Met BDNF polymorphism (2p ¼ 0.002). There was also evidence for a significant effect of this sequence variant on the minimum body mass index (MBMI) (2p ¼ 0.006). These results suggest that the BDNF Met66 variant may be a susceptibility factor to ED, mainly to ANR and low MBMI. Keywords: anorexia; bulimia; brain-derived neurotrophic factor; BDNF; single-nucleotide polymorphism Eating disorders (EDs) are complex and multifactorial, with the involvement of both psychosocial and biological factors. 1-6 A genetic contribution in ED is widely accepted 6-9 and genes involved in eating behavior, weight regulation, satiety and metabolism, as well as those under hormonal control are considered candidate genes for their role in anorexia nervosa (AN) and bulimia nervosa (BN). Among these candidates, we propose brain-derived neurotrophic factor (BDNF), which encodes for a neurotrophic factor with an essential role in neuronal survival and differentiation, and is also involved in synaptic efficiency and neuronal plasticity. 10-13 BDNF maps to 11p13-p14 14 and, although the structure of the coding exon is well known, 15 the genomic organization of the 5 0 noncoding exons has not been described.Several lines of evidence indicate a role of this neurotrophin in eating behavior and suggest that alterations in its function or expression pattern could be considered susceptibility factors to ED. To test this hypothesis we have characterized the genomic structure of the human BDNF gene. BDNF is composed of, at least, four 5 0 nontranslated exons and a single 3 0 coding exon (exon 5; Figure 1b). Since mRNA transcripts were different at their 5 0 ends, we determined the existence of four 5 0 untranslated exons th...
“…Alternatively, since BDNF has also a key role in the modulation of different neurotransmitters, it could indirectly participate in ANR and low MBMI through changes in these systems previously involved in ED. [2][3][4][5] The contribution of distinct susceptibility factors to the different ED subtypes, which is supported by other studies where differential personality and psychopathological traits were found between purging (ANBP or BN) and nonpurging ED (ANR), [20][21][22] Neither association was found in any ED group when the À270C/T SNP was considered, suggesting that it may not be involved in eating behavior alterations. Nevertheless, it would be necessary to test it in a larger sample because of its low frequency in the studied populations.…”
supporting
confidence: 65%
“…Under the hypothesis that BDNF may confer susceptibility to the ED subtypes in different ways and to reduce heterogeneity, our patients were subdivided into four main diagnostic groups that have been shown to differ in various biological and psychopathological features. [20][21][22] Thus, AN, ANR, ANBP and BN diagnoses were separately considered in the statistical analyses.…”
Several lines of evidence support a role for brain-derived neurotrophic factor (BDNF) alterations in the etiology of eating disorders (EDs). BDNF heterozygous knockout mice show alterations in eating behavior, increased body weight and adipocyte hypertrophy. BDNF also regulates the synaptic efficiency through the modulation of key neurotransmitter systems previously known to be involved in ED. These findings, together with the fact that this neurotrophin is expressed in the hypothalamus nuclei associated with weight regulation and feeding control, led us to propose BDNF as a candidate gene for ED. To investigate the possible involvement of this neurotrophin in eating behavior, we screened the BDNF gene in 95 ED patients and identified four sequence variants. Two of them, À374A/T and À256G/A, were found in two patients with anorexia nervosa (AN) and consisted of single-nucleotide mutations within the 5 0 untranslated region (5 0 UTR). The other two polymorphisms resulted in a C to T transition located at the 5 0 UTR of the BDNF gene and an amino-acid substitution within the BDNF precursor protein (Val66Met). We performed a case-control study for these two Single-nucleotide polymorphisms in a sample of 143 ED patients and 112 unrelated controls and found a strong association of restricting AN (ANR) with the Met allele of the Val66Met BDNF polymorphism (2p ¼ 0.002). There was also evidence for a significant effect of this sequence variant on the minimum body mass index (MBMI) (2p ¼ 0.006). These results suggest that the BDNF Met66 variant may be a susceptibility factor to ED, mainly to ANR and low MBMI. Keywords: anorexia; bulimia; brain-derived neurotrophic factor; BDNF; single-nucleotide polymorphism Eating disorders (EDs) are complex and multifactorial, with the involvement of both psychosocial and biological factors. 1-6 A genetic contribution in ED is widely accepted 6-9 and genes involved in eating behavior, weight regulation, satiety and metabolism, as well as those under hormonal control are considered candidate genes for their role in anorexia nervosa (AN) and bulimia nervosa (BN). Among these candidates, we propose brain-derived neurotrophic factor (BDNF), which encodes for a neurotrophic factor with an essential role in neuronal survival and differentiation, and is also involved in synaptic efficiency and neuronal plasticity. 10-13 BDNF maps to 11p13-p14 14 and, although the structure of the coding exon is well known, 15 the genomic organization of the 5 0 noncoding exons has not been described.Several lines of evidence indicate a role of this neurotrophin in eating behavior and suggest that alterations in its function or expression pattern could be considered susceptibility factors to ED. To test this hypothesis we have characterized the genomic structure of the human BDNF gene. BDNF is composed of, at least, four 5 0 nontranslated exons and a single 3 0 coding exon (exon 5; Figure 1b). Since mRNA transcripts were different at their 5 0 ends, we determined the existence of four 5 0 untranslated exons th...
“…This disease group and 121 unrelated controls, Table 1 SNPs identified within the NTRK2 gene through a PCR-SSCP mutational screening in a total sample of 91 ED patients Under the hypothesis that NTRK2 may confer vulnerability to ED subtypes by different mechanisms and to reduce heterogeneity, ED patients were subdivided into three main diagnostic groups for statistical analyses: restricting AN (ANR), binge/ eating purging AN (ANP) and BN. [14][15][16] Consistent with the physical distance between SNPs, linkage disequilibrium (LD) analysis showed that À69G4C and IVS2 þ 40C4T, and IVS17À125T4 C and IVS18 þ 13G4A SNPs were in strong LD (D 0 ¼ 1; Table 2). All sequence variants were in Hardy-Weinberg equilibrium and showed statistical (Table 3).…”
Section: Ntrk2 and Eating Disorders M Ribases Et Almentioning
confidence: 53%
“…This hypothesis is supported by the fact that both purging clinic subtypes (ANP and BN) share different personality and psychopathological traits and by the positive association between the C-A-insC haplotype and high scores of Harm avoidance observed in the BN patients. [14][15][16] A strong relationship between ED and some personality traits has been described. [24][25][26] We report here that BN patients carrying the NTRK2 high-risk haplotype C-A-insC display high scores in Harm 27,28 These results support the involvement of NTRK2 in the development of ED, not only through a direct participation in food intake and body weight regulation, as suggested by animal models, but also through the modulation of different personality traits that may increase the risk of AN and BN, such as depression or anxiety.…”
Section: Ntrk2 and Eating Disorders M Ribases Et Almentioning
Anorexia nervosa (AN) and bulimia nervosa (BN) are eating disorders (ED) with complex genetic and environmental components. Genetic studies and animal models support the participation of brain-derived neurotrophic factor (BDNF) in the vulnerability to AN and BN. We investigated the genetic contribution of the BDNF-specific receptor neurotrophic tyrosine kinase receptor type 2 (NTRK2) to the susceptibility to ED. We have screened the entire NTRK2 gene in 91 patients with ED and have identified 14 single-nucleotide polymorphisms (SNPs). A population-based association study with six SNPs from the NTRK2 locus was performed in 164 ED patients and 121 controls. Significant evidence of association for markers -69C4G and IVS13 þ 40G4A was detected. We also observed a strong association between the C-A-insC haplotype (-69/IVS13 þ 40/2784-2785) and binge-eating/purging AN (ANP, P ¼ 0.006; OR ¼ 2.27), and a reduced frequency of haplotype G-A-delCl in BN patients (P ¼ 0.034; OR ¼ 0.6). The analysis of ED-related phenotypes revealed a clear association between NTRK2, high scores of Harm avoidance measured by the temperament and character inventory (TCI-R; P ¼ 0.003) and minimum body mass index (minBMI; Po0.001). Our data support a contribution of NTRK2 to the genetic susceptibility of ED, mainly ANP, and ED-related phenotypic traits, such as Harm avoidance and minBMI. Keywords: anorexia; bulimia; eating disorders; harm avoidance; BDNF; NTRK2 Eating disorders (ED) are complex psychiatric diseases characterized by alterations in eating behaviour, body shape perception and body weight regulation. Different genetic, psychological and environmental factors contribute to the vulnerability to both anorexia nervosa (AN) and bulimia nervosa (BN), but the pathophysiology of these disorders is still largely unknown. 1 Brain-derived neurotrophic factor (BDNF) encodes for a neurotrophic factor expressed in the hypothalamic nuclei that regulate eating behaviour and modulates synaptic efficiency and neuronal plasticity through the control of different neurotransmitter systems previously involved in ED.2,3 Intraventricular administration of Bdnf induces appetite suppression and body weight reduction in rats, while Bdnf knockout mice develop obesity associated to hyperphagia and serotonin dysfunctions.3-5 Moreover, we and others have previously reported a strong association between BDNF and both AN and BN in different populations. [6][7][8][9] Due to the strong association between BDNF and ED, we propose its high-affinity receptor neurotrophic tyrosine kinase receptor type 2 (NTRK2) as a candidate gene to participate in the aetiology of ED and suggest that alterations on its function or expression pattern could contribute to the development of AN and BN. Different lines of evidences support this hypothesis. NTRK2 is expressed in hypothalamic neurons that control food intake and energy expenditure. Infusion of the Ntrk2 specific ligands, Bdnf or Nt4/5, transiently reverse the eating behaviour and obesity of the Bdnf (7) knockout mice and the ...
“…Although eating disorders such as binge eating have been related to a greater risk of psychopathology, 18,19 relationships between eating behaviors and psychological functioning have not been clearly established. [20][21][22] Some adverse effects of dieting have been previously observed on mental well-being, 23 but these results have not been corroborated by the review published by the National Task Force on the Prevention and Treatment of Obesity in 2000. 24 As the relationship between obesity status and mental health is still under debate, it could be hypothesized that some characteristics of overweight and obese individuals, such as eating behaviors or dieting history, may be important correlates of psychological well-being.…”
Psychological correlates of obesity remain under controversy. As eating behaviors and dieting history have been previously related to obesity status, these dietary variables may contribute to identify overweight and obese individuals who are at higher risk of having an impaired psychological well-being. Objective: The main purpose of this cross-sectional study was to verify the hypothesis of a relationship between weight status and psychological well-being, and to examine whether cognitive dietary restraint, disinhibition, susceptibility to hunger and dieting history could be related to psychological well-being. Design and subjects: In a sample of 101 postmenopausal women, we performed anthropometric measurements (weight, height and body mass index (BMI)), and measured psychological well-being (PER Questionnaire). The Three-Factor Eating Questionnaire (TFEQ) and a questionnaire about dieting history (dieters: had already been on a diet; non-dieters: had never been on a diet) were also administrated. Results: A trend for a significant relationship was observed between BMI and psychological well-being (r ¼ À0.17; P ¼ 0.08). Significant negative relationships were observed for disinhibition, susceptibility to hunger and all their subscales with psychological well-being (À0.28prpÀ0.48), whereas no significant differences in psychological well-being were observed between dieters and non-dieters. Finally, women displaying a higher score for habitual susceptibility to disinhibition (which is the subscale of TFEQ that was the most closely related to psychological well-being) had a lower level of psychological wellbeing, regardless of their weight status.
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