Eddie Vedder
2008-10-17, 06:01
Från senaste numret av den vetenskapliga tidsskriften Science.
Man har undersökt olika människors respons för njutning efter intag av chokladdryck och upptäckt skillnader i dopaminrespons från striatum bland överviktiga och smala.
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.
http://www.sciencemag.org/cgi/content/full/322/5900/449
Relation Between Obesity and Blunted Striatal Response to Food Is Moderated by TaqIA A1 Allele. Science 17 October 2008: Vol. 322. no. 5900, pp. 449 - 452
Det förefaller alltså svårare att finna njutning för vissa personer vid ett visst intag av något gott, överviktiga människor tenderar att behöva mer och personer med samma "problem" antas kunna ligga i riskzonen för övervikt.
Från diskussionen:
Collectively, results from these two studies are consistent with the hypothesis that the dorsal striatum is less responsive to food reward in obese, relative to lean, individuals, potentially because the former have reduced D2 receptor density and compromised dopamine signaling, which may prompt them to overeat in an effort to compensate for this reward deficit. We did not observe effects (positive or negative) in the ventral striatum or midbrain, even when we reduced the significance threshold. Because we measured BOLD response, we can only speculate that the effects reflect reduced dopaminergic signaling. However, this interpretation seems reasonable because the presence of the A1 allele, which has been associated with reduced dopaminergic signaling in six studies (21–26), significantly moderated the observed BOLD effects, and because prior work has found that this region shows increased blood flow and increased dopamine release in response to ingestion of palatable food (2, 4). Our findings converge with evidence that obese, relative to lean, humans have fewer D2 receptors in the striatum (10, 11), and obese, relative to lean, rats have lower basal dopamine levels and reduced D2 receptor density (12, 13). Our findings extend these results by showing that response in the dorsal striatum is blunted during ingestion of palatable food. Our findings also extend work implicating the A1 allele in obesity (30) by providing evidence that the negative relation between striatal response to food receipt and BMI was significantly stronger for individuals with the A1 allele, presumably because these individuals have reduced dopamine signaling capacity in the striatum. Most important, although striatal activation in response to food intake was positively related to weight gain for those without the A1 allele, it was negatively related to weight gain for those with the A1 allele, which provides evidence that blunted dorsal striatal response to food intake temporally precedes weight gain for those with this allele. This finding is consistent with the theory that it represents a vulnerability factor for obesity (31).
Även DN skriver om studien idag:
http://www.dn.se/DNet/jsp/polopoly.jsp?d=597&a=841001
Man har undersökt olika människors respons för njutning efter intag av chokladdryck och upptäckt skillnader i dopaminrespons från striatum bland överviktiga och smala.
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.
http://www.sciencemag.org/cgi/content/full/322/5900/449
Relation Between Obesity and Blunted Striatal Response to Food Is Moderated by TaqIA A1 Allele. Science 17 October 2008: Vol. 322. no. 5900, pp. 449 - 452
Det förefaller alltså svårare att finna njutning för vissa personer vid ett visst intag av något gott, överviktiga människor tenderar att behöva mer och personer med samma "problem" antas kunna ligga i riskzonen för övervikt.
Från diskussionen:
Collectively, results from these two studies are consistent with the hypothesis that the dorsal striatum is less responsive to food reward in obese, relative to lean, individuals, potentially because the former have reduced D2 receptor density and compromised dopamine signaling, which may prompt them to overeat in an effort to compensate for this reward deficit. We did not observe effects (positive or negative) in the ventral striatum or midbrain, even when we reduced the significance threshold. Because we measured BOLD response, we can only speculate that the effects reflect reduced dopaminergic signaling. However, this interpretation seems reasonable because the presence of the A1 allele, which has been associated with reduced dopaminergic signaling in six studies (21–26), significantly moderated the observed BOLD effects, and because prior work has found that this region shows increased blood flow and increased dopamine release in response to ingestion of palatable food (2, 4). Our findings converge with evidence that obese, relative to lean, humans have fewer D2 receptors in the striatum (10, 11), and obese, relative to lean, rats have lower basal dopamine levels and reduced D2 receptor density (12, 13). Our findings extend these results by showing that response in the dorsal striatum is blunted during ingestion of palatable food. Our findings also extend work implicating the A1 allele in obesity (30) by providing evidence that the negative relation between striatal response to food receipt and BMI was significantly stronger for individuals with the A1 allele, presumably because these individuals have reduced dopamine signaling capacity in the striatum. Most important, although striatal activation in response to food intake was positively related to weight gain for those without the A1 allele, it was negatively related to weight gain for those with the A1 allele, which provides evidence that blunted dorsal striatal response to food intake temporally precedes weight gain for those with this allele. This finding is consistent with the theory that it represents a vulnerability factor for obesity (31).
Även DN skriver om studien idag:
http://www.dn.se/DNet/jsp/polopoly.jsp?d=597&a=841001