The aim of this study was to determine the association between omentin Val109Asp and FTOrs9939609 polymorphisms and insulin resistance in newly-diagnosed T2D patients.
From the recently identified T2D risk variants only the risk variant of the FTO gene (rs8050136) showed statistically significant association with BMI, FMI, and WC.
FTOrs8050136 being associated with type 2 diabetes through its effect on obesity); differential linkage disequilibrium across studies of the identified genetic markers with the respective culprit polymorphisms (e.g., possibly the case for CDKAL1 polymorphisms or for rs9300039 and markers in linkage disequilibrium, as shown by additional studies); and potential bias.
This was a cross-sectional study of 236 patients with type 2 diabetes (age 60.0 ± 10.3 years; diabetes duration 12.7 ± 8.2 years; 53.4% females) who were genotyped for FTOrs9939609.
In this case-control study, the associations of rs2241766 T/G of ADIPOQ, rs9289231 T/G of KALRN, and rs9939609 A/T of FTO polymorphisms with genetic susceptibility to CAD in type 2 diabetic (T2D) patients were investigated.
Implications of critical PPARγ2, ADIPOQ and FTO gene polymorphisms in type 2 diabetes and obesity-mediated susceptibility to type 2 diabetes in an Indian population.
Using MGA, some common gene variants were found to have little (<5%) but significant impact on the heritability of T2D related QTs [KCNJ11 (rs5219), p=0.004]; [IGF2BP2 (rs4402960), p=0.02]; [SLC30A8 (rs13266634), p=0.05]; [CAPN10 (rs2975760), p=0.031]; [FTO (rs8050136), p=0.023]; [FTO (rs9939609), p=0.018] and [SLC30A8 (rs13266634), p=0.05].
In the "obese-type 2 diabetes" scan, FTO variants had the strongest type 2 diabetes effect (rs8050136: relative risk [RR] 1.49 [95% CI 1.34-1.66], P = 1.3 x 10(-13)), with only weak evidence for TCF7L2 (rs7901695 RR 1.21 [1.09-1.35], P = 0.001).
The protein intake-increasing allele C of FTO was significant associated with higher risk of T2DM (Beta ± SE = 0.104 ± 0.014, P = 4.40 × 10<sup>- 11</sup>), higher level of HOMA-IR (Beta ± SE = 0.016 ± 0.004, P = 9.55 × 10<sup>- 5</sup>), HOMA-B (Beta ± SE = 0.008 ± 0.003, P = 0.020).
Through comparison of various statistical methods, seven metabolites were identified that are significantly altered in obesity and T2D based on the FTO risk allele (adjusted p < 0.05).
Because genetic variants within the fat mass and obesity-associated (FTO) gene have been associated with both pathologies, our aim was to evaluate the association of single nucleotide polymorphisms (SNPs) within the FTO, previously related to obesity or T2DM, with FLD in HIV-infected patients.
Variant rs8050136 lies within intron 1 of the FTO gene on chromosome 16 and marks a locus strongly associated with type 2 diabetes and obesity and widely replicated across many populations.
T2D was associated with TCF7L2 and FTO but not HLA, and the risk conferred by sweetened beverages appeared modified by FTO (OR 1.45, 95% CI 1.21-1.73 in non-carriers).
Given that the phenotype of polycystic ovary syndrome (PCOS) overlaps with obesity and type 2 diabetes, we hypothesize that the common rs9939609 variant of FTO gene is related to PCOS susceptibility.
Polymorphisms in the FTO (fat-mass and obesity-associated) gene have been associated with the body mass index, cancer, type 2 diabetes and hypertension.
The methods are illustrated through meta-analysis of interaction between Single Nucleotide Polymorphisms in FTO gene and body mass index on high-density lipoprotein cholesterol data from a set of eight studies of type 2 diabetes.
For the rs9939609 variant (FTO), the dominant model AA/(AT+TT) revealed significant association with T2D [odds ratio (OR)=2.03, P=0.021], but was non-significant post correction for multiple testing (P=0.002).
These results demonstrated that miR-495 could promote the transformation of macrophages into M1-type pro-inflammatory macrophages by inhibiting the expression of its target gene FTO, and aggravate the insulin resistance and adipose tissue inflammation in T2D mice, which provided a certain theoretical basis for the targeted treatment of T2D.