Further information took a bit to track down but I found it here: http://www.ssib.org/web/past_programs/SSIB_2010_Abstracts.pdf http://www.ssib.org/web/past_pro

Further information took a bit to track down but I found it here: http://www.ssib.org/web/past_programs/SSIB_2010_Abstracts.pdf http://www.ssib.org/web/past_programs/SSIB_2010_Abstracts.pd... The full article is available for purchase here: http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6WB2-5087F0J-19&_user=10&_coverDate=06%2F30%2F2010&_rdoc=1&_fmt=high&_orig=search&_sort=d&_docanchor=&view=c&_acct=C000050221&_version=1&_urlVersion=0&_userid=10&md5=d1ecda4fc9cdb9796fbe6992d14607d2 http://www.sciencedirect.com/science?_ob=ArticleURL&_udi... though I wasn't willing to buy it. From the abstract: -- Consumption of a high fat diet affects phasic dopamine release and reuptake in the nucleus accumbens J.J. CONE 1,∗ , H.A. ROBBINS 2 , J.D. ROITMAN 2 , M.F. ROITMAN 1,2 1 Program in Neuroscience, University of Illinois at Chicago, USA 2 Dept of Psychology, University of Illinois at Chicago, Chicago, IL, USA The rate of obesity has climbed dramatically over the past several decades as food high in fat content has become more read- ily accessible. In the US alone, approximately one third of adults are considered obese. Obesity has been correlated with changes in the mesolimbic dopamine (DA) system. Human imaging stud- ies have revealed that DA terminal regions differentially respond to food depending on body mass index. In animal subjects, high fat diet exposure reduces motivated behavior and responses to amphetamine. Thus, high fat diet exposure may lead to obesity, in part, through feed forward mechanisms that suppress mesolimbic DA signaling. Here, we determined the effects of different durations of high fat diet exposure on phasic DA release evoked by electrical stimulation of the ventral tegmental area. Rats were given ad libi- tum access to either a high fat diet (60% kcal/g from fat; HFD) or a low fat diet (10% kcal/gm from fat; LFD). After different durations on the diet (2, 4 or 6 weeks), rats were anesthetized with urethane. Phasic spikes in DA concentration were evoked once every 2 min by stimulating the VTA and measured using fast scan cyclic voltam- metry at a carbon fiber microelectrode in the nucleus accumbens. DA function was assessed by altering the number, frequency, and intensity of current pulses before and up to 1 h after cocaine injec- tion. Cocaine caused a dramatic increase in evoked DA in LFD rats. In contrast, cocaine caused a much smaller increase in evoked DA in HFD rats. The data were modeled to determine if baseline and cocaine potentiated differences in evoked DA between LFD and HFD rats were due to changes in DA release, reuptake or both. The results demonstrate that high fat diet exposure results in dramatic changes in phasic DA signaling. Given its established role in reward, rein- forcement and motivation, these changes in phasic DA signaling likely contribute to further imbalance between energy intake and energy expenditure. doi:10.1016/j.appet.2010.04.046 -- The abstract still doesn't say what kind of fat it was (saturated, pufas, etc) only that it was 60% kcal/g for high fat and 10% kcal/g for low fat. The linked summary also says nothing about how they measured the dopamine effects which turned out to be anesthetizing the rats, giving them cocaine, and then measuring their dopamine levels. The study seemed to show that cocaine caused a dramatic increase in the dopamine levels of the low fat diet rats and much less of an increase in the high fat diet rats. As far as I can tell from that abstract: Low fat diet = much higher dopamine response from cocaine High fat diet = lower dopamine response from cocaine So the authors are concluding that the lower response will lead to eating more fat in order to get the dopamine reward. Further reading on dopamine: http://scienceblogs.com/developingintelligence/2007/02/dopamine_for_dummies.php http://scienceblogs.com/developingintelligence/2007/02/dopam...