Previous studies could prove a fundamental role of the Fat mass and obesity associated gene (Fto) within obesity; however, its functional role within different cell types is less understood.
FTOrs9939609 and rs9935401 and MC4R rs12970134 and rs17782313 interactions were analysed through generalized multifactor dimensionality reduction, and logistic regression models were used to calculate the risk of the relationship between genotypes and obesity.
The fat mass and obesity-associated gene (FTO) rs9939609 A-allele is associated with higher acyl-ghrelin (AG) concentrations, higher energy intake, and obesity, although exercise may mitigate rs9939609 A-allele-linked obesity risk.
More importantly, this study revealed that the association between having a risk allele of the FTO gene and BMI (and obesity status) is largely concentrated among individuals who were heavier at birth.
The aim of this study is to investigate whether the genetic risk score (GRS) based on previously associated obesity polymorphisms (SNP) rs9939609 (fat mass and obesity-associated (FTO)), rs6548238 (transmembrane protein 18 (TMEM18)) and rs16835198 (fibronectin type III domain containing 5 (FNDC5)) could serve as a predictor for anthropometric characteristics in a sample of Brazilian children and adolescents.
FTO genotypes associated with risk for obesity and loss of control of eating, specifically rs1421085, may interact with insecure attachment in a way that may exacerbate binge eating among women with BED.
Altered postprandial responses in hunger hormones and metabolic flexibility may not be a mechanism by which FTO is associated with higher BMI and obesity in healthy, normal-weighted individuals.
Of interest, a markedly lower frequency of the FTOrs9939609obesity risk A-allele was found in BED patients (0.290) in relation to the control group (0.402).
Genetic variations of the FTO gene were associated with obesity and type 2 diabetes determinants in the European population, notably raised blood levels of insulin and glucose.
Our findings confirm the role of the FTO gene as a high-potential risk factor for obesity and indicate a value for predicting a weight gain induced by second-generation antipsychotics.
Mounting evidence indicated that FTO plays a critical role in occurrence, progression and treatment of various cancers, even acting as a cancer oncogene in acute myeloid leukaemia, research on which is no longer restricted to metabolic diseases such as obesity and diabetes.
This study aimed to investigate whether the association of changes in general and central obesity with added sugar and TFA intakes is modified by common fat mass and obesity-associated gene (FTO) polymorphisms, in isolation or in a combined-form genetic risk score (GRS).
Furthermore, FTO fails to bind to its own promoter that promotes FTO expression in the hypothalamus of high-fat diet-induced obese and 48-h fasting mice, suggesting a disruption of the stable expression of this gene.