with this genotype and, as mentioned previously, the magnitude of the reduction in D2 receptors is proportional to the increase in BMI in obese individuals with the A1 allele. Neuroimaging also allows comparisons of activation patterns between obese and normalweight individuals during the presentation of food cues. The promoter region of a gene is where the initial binding of transcription proteins takes place, so polymorphisms in this area are particularly influential on gene product availability. Increasing evidence suggests that genetics may play a role, with one potential explanation being variability in genes within the neurotransmitter dopamine pathway. Maob The A allele of an single nucleotide polymorphism (SNP) in the maob isoform of this gene (B-SNP13, rs1799836) correlates with higher dopamine levels in the brain. This observation may indicate a reduction in the rewarding aspects of food intake, which may lead to overeating in compensation. Furthermore, this information fits into the larger body of knowledge about weight gain leading to obesity, namely, that factors such as age, race, gender, physical activity, dietary intake, and medications can also contribute to increased weight. Keywords: dopamine, obesity, BMI, genetics, as the incidence of obesity continues to rise, clinicians and researchers alike are seeking explanations for why some people become obese while others do not.
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In summary, there is strong experimental evidence for the association between genes related to dopamine and changes in weight. While research has revealed some promising genetic associations regarding individuals responses to changes in physical activity and diet, most have had small effect sizes, and the inherent noise of this type of data also tempers their promise at this time. Although not explicitly illustrated by this model, genotype (and expression of that genotype) can influence an individuals unique response to changes in physical activity and diet. Dopamine Transporter Gene Neurotransmitter transporters are cell membrane portals that remove neurotransmitters from the synapse and regulate the strength and duration of neurotransmission. Table 1, neurogenetic Evidence for a Relationship Between Obesity and Dopamine. It appears likely that this polymorphism acts as a marker in linkage disequilibrium with another causal variant, perhaps rs4818 noted previously. This evidence indicates that the association occurs at multiple locations in dopamine production pathways and suggests that changes in weight could be genetically driven at any of these points. This same gene is also called DAT1.