***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: Clinical ly relevant weight loss is achievable through lifestyle modification , but unintentional weight regain is common . We investigated whether recently discovered genetic variants affect weight loss and /or weight regain during behavioral intervention .  Participants at high-risk of type 2 diabetes ( Diabetes Prevention Program [ DPP ] ; N = 917/907 intervention/comparison ) or with type 2 diabetes ( Look AHEAD [ Action for Health in Diabetes ] ; N = 2,014/1,892 intervention/comparison ) were from two parallel arm ( lifestyle vs. comparison ) r and omized controlled trials . The associations of 91 established obesity-predisposing loci with weight loss across 4 years and with weight regain across years 2–4 after a minimum of 3 % weight loss were tested . Each copy of the minor G allele of MTIF3 rs1885988 was consistently associated with greater weight loss  following lifestyle intervention over 4 years across the DPP and Look AHEAD . No such effect was observed across comparison arms , leading to a nominally significant single nucleotide polymorphism × treatment interaction ( P = 4.3 × 10−3 ) . However , this effect was not significant at a study -wise significance level ( Bonferroni threshold P < 5.8 × 10−4 ) . Most obesity-predisposing gene variants were not associated with weight loss or regain within the DPP and Look AHEAD trials , directly or via interactions with lifestyle The common single-nucleotide polymorphism in the FTO ( fat mass and obesity associated ) gene is consistently associated with an increased risk of obesity . However , the knowledge of a potential modifying effect of the FTO gene on changes in body weight achieved by lifestyle intervention is limited . We examined whether the FTO gene variant ( rs9939609 , T/A ) is associated with body weight and BMI and long-term weight changes in the Finnish Diabetes Prevention Study ( DPS ) . Altogether , 522 ( aged 40 - 65 years ; BMI > or=25 kg/m(2 ) ) subjects with impaired glucose tolerance ( IGT ) were r and omized to control and lifestyle intervention groups . SNP rs9939609 was genotyped from 502 subjects . At baseline , those with the AA genotype had  higher BMI  than subjects with other genotypes ( P = 0.006 ) . The association was observed in women ( P = 0.016 ) but not in men . During the 4-year follow-up , the subjects with the AA genotype had consistently the highest BMI ( P = 0.009 ) in the entire study population . The magnitude of weight reduction was greater in the intervention group , but the risk allele did not modify weight change in either of the groups . Our results confirm the association between the common FTO variant and BMI in a cross-sectional setting and during the long-term lifestyle intervention . We did not observe association between FTO variant and the magnitude of weight reduction achieved by long-term lifestyle intervention . Based on the results from the DPS , it is unlikely that the common variant of the FTO gene affects the success of lifestyle modification on weight loss BACKGROUND & AIMS Many companies provide genetic tests for obesity-related polymorphisms ( nutrigenetics ) and make dietary recommendations for weight loss that are based on the results . We performed a r and omized controlled trial to determine whether more participants who followed a nutrigenetic-guided diet  lost ≥5 % of their body weight than participants on a st and ard balanced diet for 8 and 24 weeks . METHODS We performed a prospect i ve study of 51 obese or overweight U.S. veterans on an established weight management program at the Veterans Administration San Diego Healthcare System ( the MOVE ! program ) . Participants were r and omly assigned to groups placed on a nutrigenetic-guided diet ( balanced , low-carbohydrate , low-fat , or Mediterranean ; n = 30 ) or a st and ard balanced diet ( n = 21 ) . Nutrigenetic diets were selected on the basis of results from the Pathway FIT test . RESULTS There was no significant difference in the percentage of participants on the balanced diet vs the nutrigenetic-guided diet who lost 5 % of their body weight at 8 weeks ( 35.0 % ± 20.9 % vs 26.9 % ± 17.1 % , respectively ; P = .28 ) or at 24 weeks . Both groups had difficulty adhering to the diets . However , adherence to the nutrigenetic-guided diet correlated with weight loss ( r = 0.74 ; P = 4.0 × 10(-5 ) ) , but not adherence to st and ard therapy ( r = 0.34 ; P = .23 ) . Participants who had low-risk polymorphisms for obesity  lost more weight than all other participants at 8 weeks ( 5.0 % vs 2.9 % , respectively ; P = .02 ) and had significantly greater reductions in body mass index ( 6.4 % vs 3.6 % , respectively ; P = .03 ) and waist circumference ( 6.5 % vs 2.6 % , respectively ; P = .02 ) at 24 weeks . CONCLUSIONS In a prospect i ve study , a nutrigenetic-based diet did not increase weight loss compared with a st and ard balanced diet . However , genetic features can identify individuals most likely to benefit from a balanced diet weight loss strategy ; these findings require further investigation . Clinical Trials.gov number : NCT01859403 BACKGROUND Common polymorphisms of the fat mass and obesity associated gene ( FTO ) have been linked to obesity in some population s. One of these genetic variants ( rs9939609 ) has been related to an increased risk of obesity . OBJECTIVE Our aim was to evaluate weight loss and adipocytokine levels after two hypocaloric diets with different macronutrient distribution in obese subjects with RS9939609 gene variant . DESIGN 305 obese patients were enrolled in a prospect i ve way . In the basal visit , patients were r and omly allocated during 3 months to low carbohydrates and low fat . RESULTS After treatment with both diets and in both genotypes , weight , fat mass , waist circumference and systolic blood pressures decreased . With the diet type I and in TT genotype , insulin ( -6.6 ± 9.8 IU/L ) and homeostasis model assessment ( -2.9 ± 6.1 units ) decreased . With the diet type II and in both genotypes ( wild and mutant type ) , insulin ( -5.2 ± 6.1 vs. -3.8 ± 6.1 IU/L ; p < 0.05 ) and homeostasis model assessment ( -2.4 ± 4.8 vs. -1.1 ± 3.8 kg ; p < 0.05 ) decreased . In the A allele group , a significant decrease was detected in total cholesterol levels ( -11.5 ± 20.1 mg/dL ) , low density lipoprotein cholesterol levels ( -13.2 ± 20.9 mg/dL ) and c-reactive protein levels ( -1.3 ± 3.8 mg/dL ) secondary to weight loss after treatment with diet II . The decrease of leptin levels was higher in mutant type group than wild type group with low fat diet ( -10.3 ± 36.1 vs. -28.6 ± 53.7 ng/mL ; p < 0.05 ) . CONCLUSION Metabolic improvement secondary to weight loss was better in A carriers with a low fat hypocaloric diet Background : Genome-wide association studies have provided new insights into the genetic factors that contribute to the development of obesity . We hypothesized that these genetic markers would also predict magnitude of weight loss and weight regain after initial weight loss . Methods : Established obesity risk alleles available on the Illumina CARe iSelect ( IBC ) chip were characterized in 3899 overweight or obese participants with type 2 diabetes from the Look AHEAD ( Action for Health in Diabetes ) , a r and omized trial to determine the effects of intensive lifestyle intervention ( ILI ) and diabetes support and education ( DSE ) on cardiovascular morbidity and mortality . Primary analyses examined the interaction between 13 obesity risk polymorphisms in eight genes and r and omized treatment arm in predicting weight change at year 1 , and weight regain at year 4 among individuals who lost 3 % or more of their baseline weight by year 1 . Results : No single-nucleotide polymorphisms ( SNPs ) were significantly associated with magnitude of weight loss or interacted with treatment arm at year 1 . However , fat mass and obesity associated gene ( FTO ) rs3751812 predicted weight regain within DSE ( 1.56 kg per risk allele , P=0.005 ) , but not ILI ( P=0.761 ) , result ing in SNP × treatment arm interaction ( P=0.009 ) . In a partial replication of prior research , the obesity risk ( G ) allele at BDNF rs6265 was associated with greater weight regain across treatment arms ( 0.773 kg per risk allele ) , although results were of borderline statistical significance ( P=0.051 ) . Conclusions : Variations in the FTO and BDNF loci may contribute risk of weight regain after weight loss OBJECTIVE We aim ed to investigate the influence of positive family history ( FH+ ) of diabetes and 19 known genetic risk loci on the effectiveness of lifestyle changes and their predictive value on the incidence of type 2 diabetes  in the Finnish Diabetes Prevention Study ( DPS ) . RESEARCH DESIGN AND METHODS A total of 522 subjects with impaired glucose tolerance ( IGT ) were r and omized into the control ( n = 257 ) and intervention ( n = 265 ) groups . The mean follow-up was 6.2 years ( median 7 years ) , and the lifestyle intervention , aim ed at  weight reduction , healthy diet , and increased physical activity  , lasted for 4 years ( range 1–6 years ) . An oral glucose tolerance test ( OGTT ) and assessment of basic clinical variables were performed annually . RESULTS The effect of intervention on the incidence of diabetes was almost similar in subjects with FH+ compared with subjects with a negative family history ( FH− ) of diabetes during the entire follow-up . In the Cox model , including FH , genetic risk SNPs , and r and omization group , and adjusted for the effects of age , sex , BMI , and study center , only lifestyle intervention had a significant effect ( hazard ratio 0.55 , 95 % CI 0.41–0.75 , P < 0.001 ) on the incidence of diabetes . Further analyses showed that in addition to the baseline glucose and insulin values , 1-year changes in 2-h glucose and 2-h insulin achieved by lifestyle intervention had a significant effect on the incidence of diabetes . CONCLUSIONS These results emphasize the effectiveness of  lifestyle intervention  in reducing the risk of diabetes in high-risk individuals independently of genetic or familial risk of type 2 diabetes BACKGROUND Differences in the interindividual response to dietary intervention could be modified by genetic variation in nutrient-sensitive genes . OBJECTIVE This study examined single nucleotide polymorphisms ( SNPs ) in presumed nutrient-sensitive c and i date genes for obesity and obesity-related diseases for main and dietary interaction effects on weight , waist circumference , and fat mass regain over 6 mo . DESIGN In total , 742 participants who had lost ≥ 8 % of their initial body weight were r and omly assigned to follow 1 of 5 different ad libitum diets with different glycemic indexes and contents of dietary protein . The SNP main and SNP-diet interaction effects were analyzed by using linear regression models , corrected for multiple testing by using Bonferroni correction and evaluated by using quantile-quantile ( Q-Q ) plots . RESULTS After correction for multiple testing , none of the SNPs were significantly associated with weight , waist circumference , or fat mass regain . Q-Q plots showed that ALOX5AP rs4769873 showed a higher observed than predicted P value for the association with less waist circumference regain over 6 mo ( -3.1 cm/allele ; 95 % CI : -4.6 , -1.6 ; P/Bonferroni-corrected P = 0.000039/0.076 ) , independently of diet . Additional associations were identified by using Q-Q plots for SNPs in ALOX5AP , TNF , and KCNJ11 for main effects ; in LPL and TUB for glycemic index interaction effects on waist circumference regain ; in GHRL , CCK , MLXIPL , and LEPR on weight ; in PPARC1A , PCK2 , ALOX5AP , PYY , and ADRB3 on waist circumference ; and in PPARD , FABP1 , PLAUR , and LPIN1 on fat mass regain for dietary protein interaction . CONCLUSION The observed effects of SNP-diet interactions on weight , waist , and fat mass regain suggest that genetic variation in nutrient-sensitive genes can modify the response to diet . This trial was registered at clinical trials.gov as NCT00390637 OBJECTIVE To examine whether the effect of FTO loci on obesity-related traits could be modified by  physical activity ( PA ) levels in European adults . METHODS Of 1,607 Food4Me participants r and omized , 1,2 
    Output:
    
Overall , differential changes in body mass index , body weight , and waist circumference in response to weight loss intervention were not significantly different between FTO genotypes .
We have observed that carriage of the FTO minor allele was not associated with differential change in adiposity after weight loss interventions .
These findings show that individuals carrying the minor allele respond equally well to dietary , physical activity , or drug based weight loss interventions and thus genetic predisposition to obesity associated with the FTO minor allele can be at least partly counteracted through such interventions .