{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,14]],"date-time":"2026-10-14T12:53:18Z","timestamp":1791982398806,"version":"4.4.0"},"reference-count":34,"publisher":"American Association for the Advancement of Science (AAAS)","issue":"5900","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Science"],"published-print":{"date-parts":[[2008,10,17]]},"abstract":"<jats:p>\n                    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\n                    <jats:italic>Taq<\/jats:italic>\n                    IA restriction fragment length polymorphism, which is associated with dopamine D2 receptor (\n                    <jats:italic>DRD2<\/jats:italic>\n                    ) 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.\n                  <\/jats:p>","DOI":"10.1126\/science.1161550","type":"journal-article","created":{"date-parts":[[2008,10,16]],"date-time":"2008-10-16T17:04:23Z","timestamp":1224176663000},"page":"449-452","source":"Crossref","is-referenced-by-count":690,"title":["Relation Between Obesity and Blunted Striatal Response to Food Is Moderated by\n                    <i>Taq<\/i>\n                    IA A1 Allele"],"prefix":"10.1126","volume":"322","author":[{"given":"E.","family":"Stice","sequence":"first","affiliation":[{"name":"Oregon Research Institute, 1715 Franklin Boulevard, Eugene, OR 97403, USA."},{"name":"Department of Psychology, University of Texas, Austin, TX 78712, USA."},{"name":"Department of Psychology, University of Oregon, Eugene, OR 97403, USA."},{"name":"The John B. Pierce Laboratory, New Haven, CT 06519, USA."},{"name":"Department of Psychiatry, Yale University School of Medicine, New Haven, CT 06511, USA."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"S.","family":"Spoor","sequence":"additional","affiliation":[{"name":"Oregon Research Institute, 1715 Franklin Boulevard, Eugene, OR 97403, USA."},{"name":"Department of Psychology, University of Texas, Austin, TX 78712, USA."},{"name":"Department of Psychology, University of Oregon, Eugene, OR 97403, USA."},{"name":"The John B. Pierce Laboratory, New Haven, CT 06519, USA."},{"name":"Department of Psychiatry, Yale University School of Medicine, New Haven, CT 06511, USA."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"C.","family":"Bohon","sequence":"additional","affiliation":[{"name":"Oregon Research Institute, 1715 Franklin Boulevard, Eugene, OR 97403, USA."},{"name":"Department of Psychology, University of Texas, Austin, TX 78712, USA."},{"name":"Department of Psychology, University of Oregon, Eugene, OR 97403, USA."},{"name":"The John B. Pierce Laboratory, New Haven, CT 06519, USA."},{"name":"Department of Psychiatry, Yale University School of Medicine, New Haven, CT 06511, USA."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"D. 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