ARTICLE IN PRESS 288
Abstracts / Appetite 49 (2007) 272–341
Taste receptor polymorphisms in the Old Order Amish: Associations with obesity and related traits C.D. DOTSONa,
A.E.T. ELSONa, H. SHAWb, X. SHIb, C.M. DAMCOTTb, A. NAJb, S. SNITKERb, N.I. STEINLEb, S.D. MUNGERa. a Department of Anatomy & Neurobiology, University of Maryland School of Medicine, Baltimore, MD, USA. b Department of Medicine, Division of Endocrinology, University of Maryland School of Medicine, Baltimore, MD, USA Nutritional intake contributes to the development of human disease mainly by influencing the development of obesity-related conditions such as diabetes and cardiovascular disease. Orosensory variation strongly affects ingestive behavior and nutrient intake, while genetic variation in taste receptors (TRs) strongly affects taste sensitivity and food preference. Moreover, the expression of TRs in the gastrointestinal tract suggests that they may be involved in the nutrient-dependent regulation of metabolism. Therefore, we hypothesized that genetic variation in TRs may impact the development of obesity-related disease. To investigate these possibilities, we genotyped 460 haplotypetagging single-nucleotide polymorphisms (SNPs) within 2 kB of all TAS1R and TAS2R genes in DNA samples from the Amish Family Diabetes Study. We identified candidate SNPs from the dbSNP and HapMap databases, and prioritized those with a minor allele frequency of X0.2 in the CEU cohort (Utah residents with ancestry from northern and western Europe). We then evaluated the effects of genotype on 39 obesity-related traits (with adjustments for age, sex, and BMI). Several SNPs were significantly associated with obesity-related traits, including diabetes, glucose and insulin levels during oral glucose-tolerance tests, weight, and eating behaviors. We conclude that common variation in taste receptor genes may influence food preference, metabolism and/or risk factors associated with obesity. Support: NIDCD, NHLBI, NIDDK, UMSOM. 10.1016/j.appet.2007.03.060
Effects of chocolate consumption on enhancing cognitive performance R. DRAKE, D. FELBAUM, C. HUNTLEY,
A. REED, L. MATTHEWS, B. RAUDENBUSH. Department of Psychology, Wheeling Jesuit University, Wheeling, WV, USA Previous research has found that the nutrient content of foods aids in glucose release and increased blood flow. These increases have subsequently been implicated in augmenting cognitive performance. The present study assessed the effects of various chocolate types on cognitive performance, mood, and task workload. In a within-subjects design, participants completed
the protocol under four conditions: 85 g milk chocolate (total fat 26 g, saturated fat 18 g, carbohydrates 50 g, fiber 2 g, sugar 44 g, protein 6 g), 85 g dark chocolate (total fat 34 g, saturated fat 20 g, carbohydrates 46 g, fiber 6 g, sugar 34 g, protein 4 g), 85 g carob (total fat 20 g, saturated fat 14 g, carbohydrates 45 g, fiber 11 g, sugar 40 g, protein 11 g), and a non-consumption control condition. After a 15 min digestive period, participants completed a variety of computer-based neuropsychological tests assessing word discrimination, verbal memory, design memory, attention span, reaction time, problem solving, and response variability. Mood and task workload were assessed via the Profile of Mood States (POMS) and the NASA-Task Load Index (NASA-TLX). Gender and age served as co-variates for the analyses. Composite scores for verbal and visual memory were significantly higher for milk chocolate than the other conditions. Consumption of milk or dark chocolate showed improved impulse control and reaction time. These findings provide support for nutrient release via chocolate consumption to enhance cognitive performance. 10.1016/j.appet.2007.03.061
Cannabinoid agonist antagonizes cFos induced by intraperitoneal cholecystokinin G.L. EDWARDS, D.R. GADDAM,
K.G. FREEMAN. Department of Physiology & Pharmacology, College of Veterinary Medicine, University of Georgia, Athens, GA 30602 Cannabinoid agonist is reported to increase intake of highly palatable foods when injected into the fourth cerebroventricle [(2004). Physiological Behavior, 80, 611]. One possible mechanism for enhanced intake by cannabinoid agonists is attenuation of visceral signals from the gut. Our initial attempts to address this question have focused on induction of cFos by intraperitoneal cholecystokinin (CCK). It is well recognized the CCK induces cFos immunoreactivity in neurons of the caudal nucleus of the solitary tract (NTS) and area postrema (AP). We hypothesized that cannabinoid agonist will attenuate CCK-induced cFos in the hindbrain. We found that CCK induced a significant increase in cFos-immunoreactive neurons in the NTS and AP. The number of cFos-immunoreactive neurons was decreased significantly by prior application of the cannabinoid agonist CP55940. This reduction in cFos-immunoreactive neurons by CP 55940 was blocked by the CB1 receptor antagonist SR141716. Moreover, treatment with cannabinoid antagonist alone does not appear to significantly elevate cFos in the NTS. These observations suggest that cannabinoids may work in the NTS to blunt inhibitory signals from the gut resulting in elevated food intake. (Supported by the Department of Physiology & Pharmocology, University of Georgia). 10.1016/j.appet.2007.03.062