Human studyVariant alleles of the D2 dopamine receptor gene and obesity
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Cited by (61)
Associations between dopamine D2 receptor availability and BMI depend on age
2016, NeuroImageCitation Excerpt :Within the dopamine system, the dopamine D2/3 receptor subtypes (DRD2/3) have been the most widely studied biomarker in relation to obesity. The Taq1A minor (A1) allele of the DRD2/3 gene is associated with lower DRD2/3 density and has been found to exist in higher frequencies in obese subjects (Noble et al., 1994; Blum et al., 1996; Spitz et al., 2000; Barnard et al., 2009). A landmark study in 2001 reported that striatal DRD2/3 availability was reduced in extremely obese subjects relative to control subjects and that striatal DRD2/3 availability correlated negatively with BMI in obese subjects (Wang et al., 2001).
Neuroimaging and neuromodulation approaches to study eating behavior and prevent and treat eating disorders and obesity
2015, NeuroImage: ClinicalCitation Excerpt :Most of them are functional magnetic resonance imaging (fMRI) studies. Most genetic fMRI studies investigating food reward have taken into account a common variation (i.e. polymorphism) referred to as TaqIA, of which the A1 allele has been positively associated with BMI in several early genetic studies (Noble et al., 1994; Jenkinson et al., 2000; Spitz et al., 2000; Thomas et al., 2001; Southon et al., 2003). The TaqIA polymorphism is located in the ANKK1 gene, ~10 kb downstream of the DRD2 gene (Neville et al., 2004).
The neurobiological underpinnings of obesity and binge eating: A rationale for adopting the food addiction model
2013, Biological PsychiatryCitation Excerpt :Much of these findings appear to be modified by a genetic profile affecting dopamine pathways, placing individuals at greater susceptibility for reward system dysfunction. Due to its role in dopamine receptor availability, the A1 allele of the Taq1A gene has been a target for drug and alcohol research over the last 20 years (64) and more recently in hyperphagia leading to obesity (64–66). Presence of the A1 allele can cause a 30% to 40% reduction in striatal D2 receptors (67) and has been implicated in corresponding deficits in glucose metabolism in the OFC, frontal and temporal gyri, insula, hippocampus, and dorsal and ventral striatum (68).