rs9939609

This is a Turkish-language personalized nutrigenetics and epigenetics coaching report for individual Mehmet Efe Yildirim (Report No. 1332, dated 2023-11-21). The report analyzes the individual's genetic polymorphisms related to nutritional metabolism, food sensitivities, detoxification pathways, and other health-related traits, providing personalized dietary and lifestyle recommendations based on cited scientific literature. This is a direct-to-consumer genetic test report, not a peer-reviewed research study.

This neuroimaging study examined differences in brain structure and function in 93 children (ages 5-10) without obesity, stratified by FTO rs1421085 genotype. Homozygous C allele carriers (CC, n=15) showed significantly greater grey matter volume in the cerebellum and temporal fusiform gyrus (p=0.017-0.050), increased bilateral cerebellar white matter fibre density and cross-section (peak t=6.34, p FWE=0.037), and increased resting-state functional connectivity between the cerebellum and frontotemporal cortices compared to homozygous T allele carriers (TT, n=47). This is the first study to examine FTO-related brain differences in young children before obesity onset, suggesting the cerebellum may be a key structure in FTO-mediated obesity risk mechanisms.

This association study examined 43 diabetes-related SNPs in relation to diastolic dysfunction and cardiovascular disease across two Swedish cohorts. HNF1B rs757210 (T-allele) was the main finding, associated with prevalent diastolic dysfunction in both the discovery cohort (MPP-RES; OR 1.21, P=0.024) and replication cohort (VARA; OR 1.38, P=0.042), and with increased risk of incident CVD (HR 1.05, P=0.042) but not CHF over 30+ years of follow-up.

This observational study examined the association between FTO rs9939609 genotype and food intake in 122 non-obese children (5-10 years old). Each A allele of rs9939609 was significantly associated with approximately 64 additional calories consumed daily (p=0.04), explaining 3% of variance in total caloric intake. The association was stronger in non-African American children (p=0.02) and showed no significant relationships with macronutrient preferences or diet variety.

A literature review of 70 studies examining single nucleotide polymorphisms (SNPs) associated with obesity in Mexican populations published 2011-2021. The authors identified SNPs with differential behavior in Mexican compared to Caucasian populations, including rs17782313 (MC4R), rs6548238 (TMEM18), rs6265 (BDNF), rs7498665 (SH2B1), and notably rs6232 (PCSK1) associated with early-onset obesity in Mexican youth. The review emphasizes ethnicity-dependent genetic effects on BMI heritability (40-70%) and highlights genes involved in cholesterol metabolism and adipokine signaling pathways.

Mendelian Randomization study examining the causal relationship between obesity (BMI) and venous thromboembolism using 95 BMI-associated SNPs in 7,507 VTE cases and 52,632 European ancestry controls. FTO rs1558902 showed the strongest individual association with VTE (OR 1.07, P = 0.005), and genetically predicted high BMI was significantly associated with increased VTE risk (OR 1.59 per SD increase in BMI, P = 5.8 × 10^-6), providing evidence for a causal relationship between obesity and VTE.

This comprehensive review synthesizes literature on gestational diabetes mellitus (GDM), demonstrating its complex multifactorial etiology involving genetic factors (SNPs in GCKR, KCNQ1, MTNR1B, TCF7L2), epigenetic modifications (DNA methylation and microRNA expression), and alterations in microbial composition across multiple body sites. While certain SNP variants are associated with GDM phenotypes globally, genetic predisposition alone does not explain disease development; lifestyle factors can modify epigenetic signatures and microbiota composition to modulate risk. Evidence indicates genes, epigenetic alterations, and microbiota can transfer from mother to offspring with long-term health consequences.

This cross-sectional study of 792 Latin American subjects examined associations between FTO and IRX3 gene variants with obesity and metabolic disorders. While FTO and IRX3 SNPs were not in linkage disequilibrium, the TT genotype of rs9939609 (FTO) was associated with increased waist circumference (adj-p=0.01), and rs3751723 (IRX3) was associated with body weight excess (OR=1.06, adj-p=0.03). A FTO-IRX3 haplotype (G-A-A-T) was also associated with body weight excess (OR=0.67, p=0.04), suggesting gene-gene interaction effects independent of genetic ancestry.

This doctoral thesis examines the role of physical activity, physical fitness, and exercise on immunometabolism during pregnancy across six studies in overweight/obese pregnant women. In the genetic analysis (n=81), neonatal birth weight was significantly greater in mothers carrying the CC genotype at rs6567160 and rs17782313 in the MC4R gene, though gestational weight gain was not influenced by maternal FTO or MC4R genotypes.

This cross-sectional study of 420 Brazilian children and adolescents (7-17 years) examined the relationship between the rs9939609 FTO polymorphism and obesity outcomes, including cardiorespiratory fitness (CRF) interactions. The AA genotype of rs9939609 was associated with increased obesity risk (OR: 3.21 for BMI, 2.59 for waist circumference), with a significant gene-by-environment interaction: students with low CRF and the AA genotype had substantially higher obesity risk (OR: 4.40 for BMI, 3.54 for waist circumference), while this association was absent in individuals with high CRF.

Case-control study of 518 type 2 diabetes cases and 518 controls in a Karnataka (Indian) population examined the association of three SNPs with T2D susceptibility and obesity. PPAR-γ2 rs1801282 and FTO rs9939609 were significantly associated with T2D in the overall sample (OR=1.42, P=0.02 and OR=1.19, P=0.01 respectively), with effects primarily observed in the obese diabetic subgroup. ADIPOQ rs16861194 showed no significant association (OR=1.08, P=0.39). A meta-analysis of 22 studies on PPAR-γ2 and FTO variants in Asian populations confirmed FTO's significant risk association with T2D.

This methods paper describes the development and optimization of a biomicrofluidic platform coupled with gold nanoprobe colorimetric assays for detecting the FTO rs9939609 SNP associated with obesity risk. The optimized platform achieved 160% improvement in colorimetric discrimination through planar air microlenses and advanced optoelectronic acquisition, enabling SNP genotyping with DNA concentrations as low as 5 ng/mL and 10-fold lower solution volumes than conventional methods.

This study used BAC transgenic zebrafish to characterize enhancer activity in the FTO gene region containing obesity-associated SNP rs9939609. The authors created transgenic zebrafish lines with a GFP reporter cassette 1.3 kb upstream of rs9939609 and found hypothalamic and anterior brainstem expression patterns similar to the IRX3 gene, not FTO. This demonstrates that enhancers in FTO intron 1 near rs9939609 regulate IRX3 expression in the developing hypothalamus, not FTO itself.

Association study of 35 GWAS-identified body mass SNPs in 949 elderly Swedish participants (mean age 70-75 years). Significant association found between rs10968576 (LINGO2, intron 4) and BMI with a larger effect size (β = 0.69 kg/m²) than reported in younger populations, suggesting age-specific genetic effects on body mass in the elderly.

This scoping review examined 18 observational studies (n=26,684) from low- and middle-income countries investigating gene-environment interactions affecting obesity risk. The review found statistically significant associations for 12 individual SNPs including FTO rs1421085, rs9939609, rs10163409, rs3751812, MC4R rs17782313, rs12970134, TMEM18 rs7561317, NEGR1 rs2815752, CARTPT rs2239670, UCP2 rs659366, CLOCK rs1801260, and FLJ33544 rs140133294, though most associations were not replicated across different populations and environmental exposures.

This literature review examines the influence of genetic polymorphisms on obesity development and adaptive responses to physical activity, focusing on five candidate genes: COMT (rs4680, Val158Met), DRD2 (rs1800497 Taq1A and rs1799732), FABP2 (rs1799883, Ala54Thr), FTO (rs9939609, A/T), and UCP1 (rs1800592, A-3826G). The review synthesizes molecular mechanisms, phenotypic associations, and implications for human health and training adaptations, noting that physical activity reduces the FTO genetic effect on obesity risk by 30-80% and that various polymorphisms show differential impacts on body composition and metabolic responses to exercise.

Case-control study of 673 preterm birth (PTB) cases vs 1,119 controls across four maternal cohorts testing 35 SNPs in cardiovascular, inflammatory, and metabolic disease genes. Found 13 statistically significant associations with PTB (P<0.05), more than expected by chance (binomial P=0.02). Most significant was HLA-DQA1 rs9272346 G allele protective effect in US White mothers (P=0.02, OR=0.65, 95% CI 0.46-0.94), which nominally replicated in Danish cohort (P=0.02, OR=0.85, 95% CI 0.75-0.97) but lost significance after correction for multiple testing.

Of 40 SNPs previously associated with type 2 diabetes, 19 (48%) introduce or remove CpG sites. In 84 human pancreatic islet donors, all 16 analyzed CpG-SNPs showed statistically significant differential DNA methylation (p≤2.3×10⁻⁵). Several CpG-SNPs including rs391300 (SRR), rs5945326 (DUSP9), rs11708067 (ADCY5), rs5015480 (HHEX), rs13266634 (SLC30A8), rs1801214 (WFS1), rs564398 (CDKN2A), and rs2237895 (KCNQ1) were associated with differential gene expression, alternative splicing, or hormone secretion, suggesting DNA methylation-mediated mechanisms linking genetic variants to type 2 diabetes pathogenesis.

This study examined 8 adult obesity-susceptibility loci in 7,225 children aged 2-18 years using quantile regression to assess whether genetic effects on BMI are uniform across the BMI distribution. The authors found that obesity risk alleles (FTO rs3751812, MC4R rs12970134, TMEM18 rs2867125, BDNF rs6265, SEC16B rs10913469, GNPDA2 rs13130484, NRXN3 rs10146997, and TNNI3K rs1514175) were more strongly associated with BMI increases at the upper tail of the distribution (85th-95th percentiles, β=0.06-0.11, p<10^-6) compared to the lower tail, suggesting that standard linear regression approaches may underestimate genetic effects on childhood obesity.

This study tested seven SNPs from European lipid-associated loci in 3,503 Chinese school-age children and found that six SNPs (rs2144300, rs1260333, rs1260326, rs10105606, rs1748195, rs964184) showed significant associations with triglyceride levels (p < 0.05 FDR-corrected), while three SNPs were associated with total cholesterol and four with LDL-cholesterol. Three SNPs (rs1260333 OR=0.82, rs1260326 OR=0.82, rs964184 OR=1.36) showed strong associations with dyslipidemia risk, demonstrating that lipid-susceptibility variants identified in European populations have similar effects in Chinese children.

A cross-sectional study of 150 Brazilian obese subjects examined associations between three polymorphisms (INSIG2 rs7566605, PCSK9 rs505151, FTO rs9939609) and metabolic syndrome. The INSIG2 rs7566605 G allele showed significant associations with higher systolic blood pressure, diastolic blood pressure, and triglyceride levels (p < 0.05), while no direct associations were found between any polymorphisms and metabolic syndrome prevalence.

This case-control study investigated the association between the FTO rs9939609 polymorphism and obesity-related measures in 136 obese children (aged 12-18) and 24 healthy controls. FTO rs9939609 was genotyped by allele-specific RT-PCR. AA homozygotes had significantly higher BMI (30.4 vs 28.1, p<0.05) and body fat content (39.0% vs 32.9%, p<0.05) compared to TT carriers. The study confirms the association of the FTO risk allele with increased BMI and adiposity in children, though limited sample size prevented full analysis of metabolic parameters.

This meta-analysis of eight PCOS cohorts (2,548 women) found that FTO rs9939609 and rs1421085 polymorphisms have significantly greater effects on BMI and body weight in PCOS patients than in the general population. Each additional effect allele increased BMI by 0.19 z-score units (p=2.26×10⁻¹¹) and body weight by 0.20 z-score units (p=1.02×10⁻¹⁰), demonstrating effects more than two times greater than previously reported.

Association analysis of 31 GWAS-confirmed type 2 diabetes SNPs in 3,089 Indian sib pairs (2,528 for quantitative traits, 561 for diabetes) identified significant associations with intermediate traits: CDKAL1 rs7756992, TCF7L2 rs7903146 and rs12255372 with fasting glucose (β=0.009-0.01, p≤0.01); ADAM30 rs2641348, NOTCH2 rs10923931, TCF-2/HNF1B rs757210, and CDKN2A/B rs10811661 with fasting insulin and HOMA-IR (β=±0.05-0.09, p≤0.05); and THADA rs7578597 with type 2 diabetes (OR 1.5, p=0.03).

This study examines the association of FTO rs9939609 SNP with obesity in a Roma/Gypsy population of 312 individuals from Slovakia. The minor A-allele was significantly associated with increased BMI (OR=1.55, 95% CI: 1.129-2.128, p=0.007), waist circumference, and waist-to-hip ratio, replicating previous findings from European populations despite the Roma population's Asian origins.

This longitudinal study examined 658 white participants from the Bogalusa Heart Study to investigate FTO gene effects on the onset age of overweight in adults. Using survival analysis on 30 FTO tag SNPs, rs9939609 showed the strongest association with overweight onset age (p=0.004), with genotype AA associated with significantly earlier onset (mean 22.82 years at 50% prevalence) compared to AT (28.96 years) and TT (27.76 years), with odds ratios of 0.52 (AA vs AT) and 0.58 (AA vs TT) for survival beyond age 18.

This is a letter to the editor critiquing methodological errors in a meta-analysis on low-carbohydrate versus balanced diets for weight loss and cardiovascular risk. The authors document multiple protocol violations and data extraction errors in the Naude et al. meta-analysis, including inclusion of studies failing their own fat intake criteria, use of end weight instead of weight change, inconsistent handling of intention-to-treat data, and data transcription discrepancies. The letter argues these errors materially affected the meta-analysis conclusions.

This case-control study of 2,033 colorectal cancer cases and 9,640 controls investigated whether BMI and waist size susceptibility variants are associated with colorectal cancer risk. Two obesity SNPs showed significant associations: KCTD15 rs29941 (OR = 0.90, p = 0.01) was protective, while MC4R rs17782313 (OR = 1.12, p = 0.02) increased risk. However, neither association remained significant after multiple comparisons correction, and overall obesity variants showed minimal effects on colorectal cancer.

Meta-analysis of 19 studies (34,195 cases, 89,178 controls) confirmed that the rs17782313 polymorphism near the MC4R gene is associated with type 2 diabetes risk in Europeans and Asians (OR 1.10, 95% CI 1.07-1.13, p=2.83×10⁻¹²). The association remained significant after BMI adjustment (OR 1.06, 95% CI 1.03-1.09, p=2.14×10⁻⁵), suggesting an effect independent of obesity.

Meta-analysis of 32 populations (96,551 East and South Asians) examining FTO-rs9939609 association with obesity and type 2 diabetes. The minor allele increased obesity risk 1.25-fold/allele (p=9.0×10⁻¹⁹), overweight 1.13-fold/allele (p=1.0×10⁻¹¹), and type 2 diabetes 1.15-fold/allele (p=5.5×10⁻⁸), with similar effect sizes across East and South Asian populations as previously observed in Europeans.

This comprehensive review examines the genomics of schizophrenia and pharmacogenomics of antipsychotic drugs, synthesizing evidence on over 200 genes associated with psychotic disorders. The authors discuss five categories of genes relevant to antipsychotic response: disease-associated genes, mechanism-of-action genes, drug metabolism genes (particularly CYP2D6, CYP2C19, CYP2C9, CYP3A4), drug transporter genes, and pleiotropic genes. The review details pharmacogenomic profiles of 20+ antipsychotic drugs and demonstrates significant ethnic and interindividual variation in drug metabolism phenotypes, with examples including CYP2D6 extensive metabolizers (55.71% of population), intermediate metabolizers (34.7%), poor metabolizers (2.28%), and ultra-rapid metabolizers (7.31%).

This study examined the association between the FTO polymorphism rs9939609 and body composition in 6-month-old infants from the Generation R prospective birth cohort study. No significant associations were found between FTO genotype and weight, height, BMI, subcutaneous fat mass (measured by skinfold thickness in 695 children), or body composition measures assessed by DXA (n=216 children). The authors conclude that the lack of association at 6 months suggests the effect of FTO on adiposity increases during childhood rather than manifesting in infancy.

Replication study of 14 obesity-associated SNPs from 13 loci in 18,264 Japanese participants, confirming associations at 11 loci including TMEM18 (rs4854344, p=7.1×10⁻⁷ for BMI), FTO, MC4R, BDNF, and others. Six obesity variants also associated with type 2 diabetes after BMI adjustment (OR 1.05-1.17), with FTO showing strong meta-analyzed association in East Asians (OR 1.13, p=7.8×10⁻¹⁰).

A comprehensive review of nutrigenetics and nutrigenomics examining how genetic variants influence individual responses to nutrients and dietary interventions. The paper discusses associations between numerous SNPs (rs9939609 in FTO, rs2287019 in GIPR, rs7903146 in TCF7L2, rs5219 in KCNJ11, and many others) and metabolic traits including obesity, type 2 diabetes, and other chronic diseases, along with epigenetic mechanisms by which phytochemicals (curcumin, resveratrol, lycopene) modulate gene expression. The review synthesizes current evidence for precision nutrition approaches tailored to individual genetic profiles.

This longitudinal study examined FTO gene SNPs in 658 white subjects from childhood to adulthood. While FTO SNPs showed no significant association with birth weight or longitudinal BMI during childhood, three SNPs (rs9939609, rs17820875, and rs860713) were significantly associated with longitudinal BMI in adulthood (P = 5.3×10⁻⁵, 2.0×10⁻⁴, and 0.001, respectively). The study also identified interactions between birth weight and FTO variants, showing that lower birth weight predisposes to higher adult BMI depending on FTO risk genotypes.

This study examined the association of FTO rs9939609 variant with obesity and metabolic traits in 670 Chinese children (aged 8-11 years). The rs9939609 A allele was significantly associated with obesity risk (OR = 1.79, 95% CI 1.20-2.67, P = 0.004) and higher BMI, weight, waist-to-hip ratio, and body fat compared to TT genotype carriers.

This cross-sectional study in 752 European adolescents (HELENA Study) examined the FTO rs9939609 polymorphism's association with obesity-related traits and its interaction with physical activity. The A allele was associated with increased BMI (+0.42, p=0.01), body fat percentage (+1.03%, p=0.02), and waist circumference (+0.85 cm, p=0.04). Notably, adolescents meeting physical activity recommendations (≥60 min/day moderate-to-vigorous activity) showed significantly attenuated genetic effects, suggesting physical activity can offset FTO-associated obesity risk.

This study tests the thrifty genotype hypothesis by examining 17 confirmed type 2 diabetes susceptibility loci and 13 obesity-susceptibility loci for signatures of positive selection. Using ancestral/derived allele analysis, integrated haplotype scores (iHS), and population differentiation (FST), the authors found limited evidence supporting the thrifty genotype hypothesis. Only rs7901695 at TCF7L2 showed notably elevated FST values (0.579 between JPT+CHB and YRI populations), and FTO showed the strongest selection signal among obesity loci (iHS=1.991).

This comprehensive review synthesizes genomic and pharmacogenomic research in schizophrenia, discussing over 200 candidate genes associated with psychotic disorders, genetic mechanisms including copy number variants and microRNA alterations, and pharmacogenomic factors affecting antipsychotic efficacy and safety. Key genes covered include dopamine receptors (DRD1-5), dysbindin (DTNBP1), DISC1, neurotrophic factors, and metabolic enzymes such as CYP2D6, CYP3A4, and COMT, with emphasis on genotype-phenotype correlations in antipsychotic response and side effects.

This prospective study examined the combined effects of FTO rs1421085 and MC4R rs17782313 obesity risk alleles in two large European cohorts (4,762 Finnish adolescents and 3,167 French adults). Subjects carrying 3-4 risk alleles had a 3-fold increased obesity susceptibility in childhood and 1.8-fold increased risk in adults (OR=1.21, p=0.02), with each additional risk allele increasing fat mass by 0.48% (p=0.001). The effects on type 2 diabetes were mediated through BMI. MC4R showed stronger male-specific effects and FTO effects were accentuated by low physical activity.

This study examined the interaction between the FTO rs9939609 variant and physical activity on BMI in 15,925 Swedish and 2,511 Finnish non-diabetic adults. The A allele was associated with increased BMI (0.13 kg/m² in Sweden, 0.43 kg/m² in Finland, p<0.0001), but contrary to previous reports, no significant gene-by-physical activity interaction was observed (p=0.71 in Sweden, p=0.18 in Finland), suggesting physical activity does not substantially modify FTO variant effects on obesity risk.

This case-control and family-based association study tested whether 18 type 2 diabetes susceptibility loci are associated with type 1 diabetes in 7,606 type 1 diabetic cases and 8,218 controls. Only PPARG (rs1801282/Pro12Ala, OR=0.91, p=0.004) and HHEX-IDE (rs1111875, OR=0.94, p=0.003) showed evidence of association with type 1 diabetes. The authors conclude that type 1 and type 2 diabetes do not share a common genetic background, supporting the view that type 1 diabetes is primarily an autoimmune disease.

This is a summary of Group 14 analyses from the Genetic Analysis Workshop 16 (GAW16) demonstrating the use of longitudinal data from the Framingham Heart Study in genome-wide association studies. Multiple analytical approaches were compared for identifying genetic associations with metabolic and cardiovascular traits including BMI, type 2 diabetes, blood pressure, lipid levels, and coronary heart disease, using various statistical methods such as linear mixed models, growth mixture modeling, and generalized estimating equations.

Analysis of 27 FTO gene variants in 1,424 Hispanic Americans and 604 African Americans from the Insulin Resistance Atherosclerosis Family Study (IRASFS) found multiple SNPs associated with BMI, waist circumference, and subcutaneous adipose tissue (p-values 0.001-0.05 in Hispanics), confirming FTO's role in overall fat mass rather than visceral fat distribution. Key variants rs9939609, rs8050136, rs1121980, rs1421085, rs17817449, and rs3751812 showed consistent associations with adiposity measures, with effect sizes of 0.3-2.4 kg/m² per allele for BMI in Hispanic Americans.

This case-control study of 1453 type 2 diabetes patients and 1361 controls from South Asian Indians found that FTO gene variants rs9939609 and rs7193144 were strongly associated with type 2 diabetes (OR=1.26, 95% CI 1.13-1.40, p=3×10⁻⁵ for rs9939609; OR=1.31 for rs7193144), but showed only weak association with BMI and obesity measures. Unlike in European populations, the T2D association remained significant after adjusting for BMI, suggesting FTO variants influence diabetes risk through mechanisms beyond body mass index in South Asian populations.

In the Diabetes Prevention Program (n=3,548), the FTO rs9939609 minor A allele was associated with higher baseline BMI (p=0.003) but not with changes in obesity traits. The INSIG2 rs7566605 minor C allele was associated with more subcutaneous adiposity at baseline (p=0.04), and CC homozygotes lost 1.7 kg more weight with lifestyle intervention (p=0.02) and showed greater reductions in subcutaneous and visceral adipose areas (p=0.01-0.03) compared to G allele carriers.

This study examined 704 Old Order Amish individuals and identified 26 FTO gene variants associated with BMI (P=.04 to <.001), with rs1861868 (0.75 BMI increase per A allele, P<.001) and rs1477196 (0.84 BMI increase per C allele, P<.001) showing the strongest associations. Notably, the study found a significant gene-by-environment interaction where increased physical activity substantially blunted the effects of FTO variants on body weight, suggesting that genetic predisposition to obesity can be mitigated through adequate physical activity.

This prospective study of 16,143 individuals from the Malmö Preventive Project (mean follow-up 23 years) investigated whether genetic variants in 26 genes previously associated with type 2 diabetes or metabolic syndrome components could predict future development of metabolic syndrome. Polymorphisms in TCF7L2 (rs7903146, OR 1.10, p=0.00097), FTO (rs9939609, OR 1.08, p=0.0065), WFS1 (rs10010131, OR 1.07, p=0.0078), and IGF2BP2 (rs4402960, OR 1.07, p=0.021) predicted metabolic syndrome development, with TCF7L2, WFS1, and IGF2BP2 acting through hyperglycemia and FTO through obesity. A composite genotype score of 17 polymorphisms predicted metabolic syndrome risk (OR 1.04, p<0.00001), with carriers of ≥19 risk alleles having 51% increased risk compared to carriers of ≤12 alleles.

This case-control study of 463 UK PCOS patients and 1,336 controls demonstrates that FTO variant rs9939609 is significantly associated with polycystic ovary syndrome (PCOS), with an odds ratio of 1.30 per minor allele (p=7.2×10−4). The association was attenuated but remained significant after adjustment for BMI (p=2.9×10−3), suggesting that while obesity mediates much of the FTO effect on PCOS risk, additional genetic mechanisms may be involved. No association was detected between FTO genotype and testosterone or free androgen index levels in either UK PCOS patients or Finnish controls.

This replication study tested newly identified type 2 diabetes susceptibility loci in a Norwegian population-based cohort of 1,638 type 2 diabetes patients and 1,858 controls. The authors confirmed associations for rs10811661 near CDKN2B (OR 1.20, p=0.004), rs9939609 in FTO (OR 1.14, p=0.006), and rs13266634 in SLC30A8 (OR 1.20, p=3.9×10⁻⁴). They found borderline association for rs4402960 in IGFBP2 (OR 1.10, p=0.074) but no support for SNPs near FLJ39370 and PKN2.