Relation between obesity and blunted striatal response to food is moderated by TaqIA A1 allele

Abstract

The dorsal striatum plays a role in consummatory food reward, and striatal dopamine receptors are reduced in obese individuals, relative to lean individuals, which suggests that the striatum and dopaminergic signaling in the striatum may contribute to the development of obesity. Thus, we tested whether striatal activation in response to food intake is related to current and future increases in body mass and whether these relations are moderated by the presence of the A1 allele of the TaqIA restriction fragment length polymorphism, which is associated with dopamine D2 receptor (DRD2) gene binding in the striatum and compromised striatal dopamine signaling. Cross-sectional and prospective data from two functional magnetic resonance imaging studies support these hypotheses, which implies that individuals may overeat to compensate for a hypofunctioning dorsal striatum, particularly those with genetic polymorphisms thought to attenuate dopamine signaling in this region.

Figures

Fig 1

A. Coronal section of weaker activation in the left caudate nucleus (−15, 18, 12, T = 3.65, p

Fig 2

Coronal section of weaker activation bilaterally in the putamen (−30, 0, 6, T = 3.98, p

Fig 3

A. Sagittal section of weaker activation in the left caudate nucleus (−12, −3, 24, T = 4.00, p

Fig 4

A. Activation in the caudate nucleus was negatively related to future weight gain for participants with the A1 allele, but positively related to future weight gain for participants without the A1 allele (Study 1). B. Activation in the putamen was negatively related to future weight gain for participants with the A1 allele, but positively related to future weight gain for participants without the A1 allele (Study 2).