***TASK*** the task is to summarize an input biomedical literature in six sentences 
    ***INPUT*** the input is a biomedical literature 
    ***OUTPUT*** the output is the summary of an input biomedical literature in six sentences 
    ***DOCUMENTATION*** 
    ***EXAMPLES*** 
    Input: Background The A1 allele of the ANKK1 Taq IA polymorphism ( previously reported as located in the D2 dopamine receptor ( DRD2 ) gene ) is associated with reduced DRD2 density in the striatum and with clinical disorders , particularly addiction . It was hypothesized that impulsivity represents an endophenotype underlying these associations with the Taq IA and that environmental stress would moderate the strength of the gene-behavior relationship . Methods Taq IA genotyping was conducted on 72 healthy young adults who were r and omly allocated to either an acute psychosocial stress or relaxation induction condition .  Behavioral phenotypes of impulsivity were measured using a card-sorting index of reinforcement sensitivity and computerized response inhibition and delay discounting tasks . Results Separate analyses of variance revealed associations between the A1 allele and two laboratory measures of impulsivity . The presence of the Taq IA allele ( A1 + ) was associated with slower card-sorting in the presence of small financial reinforcers , but was overcome in a second administration after either a five-minute rest or psychosocial stress induction . A1 + participants also demonstrated significantly poorer response inhibition and faster response times on a computerized stop inhibition task , independent of acute stress exposure . Conclusion These findings indicate the A1 allele is associated with an endophenotype comprising both a " rash impulsive " behavioral style and reinforcement-related learning deficits . These effects are independent of stress Dopamine is known to regulate food intake by modulating food reward via the mesolimbic circuitry of the brain . The objective of this study was to compare the effects of high energy input ( i.v . glucose ) on striatal and thalamic dopamine release in overweight and lean individuals . We hypothesized that glucose would induce dopamine release and positive ratings ( e.g. , satiety ) in Behavioral Analog Scales , particularly in food-deprived lean subjects .  [(11)C]raclopride PET was performed for 12 lean ( mean BMI = 22 kg/m(2 ) ) and 12 overweight ( mean BMI = 33 kg/m(2 ) ) healthy subjects . Each subject was imaged twice in a blinded counter-balanced setting , after 300 mg/kg i.v . glucose and after i.v . placebo .  Dopamine D2 receptor binding potentials ( BPs ) were estimated . The voxel-based analysis of the baseline scans indicated lower striatal BPs in the overweight group and a negative correlation between BMI s and BPs . Intravenous glucose  did not have a significant effect on BPs in overweight or lean subjects ( male and female groups combined ) . However , BP changes were opposite in the two gender groups . In male subjects , significant BP reductions after glucose were seen in the right and left cau date nucleus , left putamen , and right thalamus . In female subjects , increases in BP secondary to glucose were seen in the right cau date nucleus and right and left putamen . The sexually dimorphic effect of glucose  was seen in both overweight and lean subjects . Although gender differences were not among the a priori hypotheses of the present study and , therefore , they must be considered to be preliminary findings , we postulate that this observation is a reflection of an interaction between glucose , sex steroids ( estrogen ) , leptin , and dopamine BACKGROUND Food reinforcement and dopaminergic activity may influence food consumption , but research on whether they interact has not been performed . OBJECTIVE We assessed the effects of food reinforcement and the interaction of food reinforcement with the dopamine transporter ( SLC6A3 ) genotype and the dopamine D(2 ) receptor ( DRD(2 ) ) genotype on energy consumption . DESIGN We studied food-consumption and reinforcing-value-of-food tasks in 88 smokers of European ancestry before they enrolled in smoking-cessation treatment . In the food-consumption task , subjects tasted and consumed 8 snack foods ad libitum . The reinforcing-value-of-food task assessed how hard subjects would work for food . RESULTS Significant interactions between dopamine genotypes and food reinforcement were observed . Subjects high in food reinforcement who lacked an SLC6A3 * 9 allele consumed significantly more calories ( > 150 kcal ; P = 0.015 ) than did subjects low in food reinforcement or those high in food reinforcement who carried at least one SLC6A3 * 9 allele . Similarly , subjects high in food reinforcement who carried at least one DRD(2)*A1 allele consumed > 130 kcal more ( P = 0.021 ) than did subjects low in food reinforcement or those high in food reinforcement who lacked a DRD(2)*A1 allele . There was also a main effect of food reinforcement on energy intake ( P = 0.005 ) , with subjects high in food reinforcement consuming 104 kcal ( or 30 % ) more than did subjects low in food reinforcement . CONCLUSIONS Food reinforcement has a significant effect on energy intake , and the effect is moderated by the dopamine loci SLC6A3 and DRD(2 ) OBJECTIVE Certain D2 dopamine receptor Taq 1A genotypes ( A1A1 , A1A2 ) have been associated with obesity and substance abuse . We hypothesized that their presence would be associated with reduced efficacy of  dietary interventions in individuals with type 2 diabetes . METHODS In the course of a r and omized clinical trial in an outpatient research center in which 93 adults with type 2 diabetes were assigned to a low-fat vegan diet or a diet following 2003 American Diabetes Association guidelines for 74 wk , Taq 1A genotype was determined . Nutrient intake , body weight , and hemoglobin A1c ( A1c ) were measured over 74 wk . RESULTS The A1 allele was highly prevalent , occurring in 47 % of white participants ( n = 49 ) , which was significantly higher than the 29 % prevalence previously reported in non-diabetic whites ( P = 0.01 ) . The A1 allele was found in 55 % of black participants ( n = 44 ) . Black participants with A1(+ ) genotypes had significantly greater mean body weight ( 11.2 kg heavier , P = 0.05 ) and greater intake of fat ( P = 0.002 ) , saturated fat ( P = 0.01 ) , and cholesterol ( P = 0.02 ) compared with A2A2 ( A1(- ) ) individuals ; dietary changes during the study did not favor one genotype group . Among whites , baseline anthropometric and nutrient differences between gene groups were small . However , among whites in the vegan group , A1(+ ) individuals reduced fat intake ( P = 0.04 ) and A1c ( P = 0.01 ) significantly less than did A1(- ) individuals . CONCLUSION The A1 allele appears to be highly prevalent among individuals with type 2 diabetes . Potential influences on diet , weight , and glycemic control merit further exploration OBJECTIVE To determine whether responsivity of reward circuitry to food predicts future increases in body mass and whether polymorphisms in DRD2 and DRD4 moderate these relations . DESIGN The functional magnetic resonance imaging ( fMRI ) paradigm investigated blood oxygen level dependent activation in response to imagined intake of palatable foods , unpalatable foods , and glasses of water shown in pictures . DNA was extracted from saliva sample s using st and ard salting-out and solvent precipitation methods . PARTICIPANTS Forty-four adolescent female high school students ranging from lean to obese . MAIN OUTCOME Future increases in body mass index ( BMI ) . RESULTS Weaker activation of the frontal operculum , lateral orbitofrontal cortex , and striatum in response to imagined intake of palatable foods , versus imagined intake of unpalatable foods or water , predicted future increases in body mass for those with the DRD2 TaqIA A1 allele or the DRD4 - 7R allele . Data also suggest that for those lacking these alleles , greater responsivity of these food reward regions predicted future increases in body mass . DISCUSSION This novel prospect i ve fMRI study indicates that responsivity of reward circuitry to food increases risk for future weight gain , but that genes that impact dopamine signaling capacity moderate the predictive effects , suggesting two qualitatively distinct pathways to unhealthy weight gain based on genetic risk Background Dopamine receptors are involved in midbrain reward circuit activation . Polymorphisms in two dopamine receptor genes , DRD2 and DRD4 , have been associated with altered perception of food reward and weight gain . The objective of this study was to determine whether the same risk alleles were associated with overweight/obesity and with lower reduction of overweight after a 1-year lifestyle intervention . Methods In a longitudinal study the association of polymorphisms in DRD2 ( rs18000497 , risk allele : T , formerly A1 allele at the TaqI A1 polymorphism ) and DRD4 ( variable number of t and em repeats ( VNTR ) ; 48 bp repeat in exon III ; risk alleles : 7 repeats or longer : 7R+ ) was tested on weight loss success following a 1-year lifestyle childhood obesity intervention ( OBELDICKS ) . An additional exploratory cross-sectional case-control study was performed to compare the same DRD polymorphisms in these overweight/obese children and adolescents versus lean adult controls . Subjects were 423 obese and 28 overweight children participating in lifestyle intervention ( 203 males ) , age median 12.0 ( interquartile range 10.0–13.7 ) years , body mass index - st and ard deviation score ( BMI -SDS ) 2.4 ± 0.5 ; 583 lean adults ( 232 males ) ; age median 25.3 ( interquartile range 22.5–26.8 ) years , BMI 19.1 ± 1.9 kg/m2  . BMI , BMI -SDS and skinfold thickness measures were assessed at baseline and after 1 year ; genotyping was performed for DRD2 risk variant rs1800497 and DRD4 exon III VNTR . Results The DRD2 genotype had a nominal effect on success in the weight loss intervention . The weakest BMI -SDS reduction was in children homozygous for two rs1800497 T-alleles ( n = 11 ) compared to the combined group with zero ( n = 308 ) or one ( n = 132 ) rs1800497 T-allele ( -0.08 ± 0.36 vs. -0.28 ± 0.34 ; p < 0.05 ) . There was no association between the DRD4 VNTR alleles and genotypes and success in the weight loss intervention . No associations of the risk alleles of the DRD2 and DRD4 polymorphisms and obesity were observed in the cross-sectional part of the study . Conclusions We did not find association between polymorphisms in DRD2 and DRD4 genes and weight status . However , obese carriers of two DRD2 rs1800497 T-alleles may be at risk for weak responses to lifestyle interventions aim ed at weight reduction . Trial registration Obesity intervention program “ Obeldicks ” is registered at clinical trials.gov ( NCT00435734 ) BACKGROUND Positron emission tomography ( PET ) imaging studies have shown that addiction to a number of substances of abuse is associated with a decrease in dopamine D(2/3 ) receptor binding and decreased presynaptic dopamine release in the striatum . Some studies have also shown that these reductions are associated with the severity of addiction . For example , in cocaine dependence , low dopamine release is associated with the choice to self-administer cocaine . The goal of the present study was to investigate these parameters of striatal dopamine transmission in heroin dependence and their association with drug seeking behavior . METHODS Heroin-dependent and healthy control subjects were scanned with [(11)C]raclopride before and after stimulant administration ( methylpheni date ) to measure striatal D(2/3 ) receptor binding and presynaptic dopamine release . After the PET scans , the heroin-dependent subjects performed heroin self-administration sessions . RESULTS Both striatal D(2/3 ) receptor binding and dopamine release were reduced in the heroin-dependent subjects compared with healthy control subjects . However , neither PET measure of dopamine transmission predicted the choice to self-administer heroin . CONCLUSIONS These findings show that heroin addiction , like addiction to other drugs of abuse , is associated with low D(2/3 ) receptor binding and low presynaptic dopamine . However , neither of these outcome measures was associated with the choice to self-administer heroin 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 prospect i ve 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 Objectives Cigarette smoking is the leading cause 
    Output:
    
It was concluded that there was no support for a reward deficiency theory of food addiction .
In contrast , there are several reports that those with the A1 allele are less able to benefit from an intervention that aim ed to reduce weight , possibly a reflection of increased impulsivity