We observed that the frequency of the T allele of the ABCA1C69T gene was significantly higher in healthy subjects compared to T2DMpatients (0.28 vs 0.45; p less than 0.0001; OR (95 percent CI) = 0.4624 (0.3732-0.5729), and therefore the T allele may be a protective factor against T2DM in the Saudi population.
We propose that exendin-4 increases ABCA1 expression in glomerular endothelial cells, which plays an important role in alleviating renal lipid accumulation, inflammation, and proteinuria in mice with type 2 diabetes.
In case of CYP46A1 gene, CC (p < 0.001) and CT (p = 0.001) genotypes and C allele (p < 0.001) were found to be a positive risk factor and TT genotype (p < 0.001) and T allele (p < 0.001) as negative risk factor for T2DM whereas, no association of MDR1 gene was found with T2DM (P values of all genotypes and alleles were greater than 0.001).
To determine the effect of adding cilostazol (100 mg b.i.d.) to standard-dose clopidogrel (75 mg/d) (TRIPLE) compared with double-dose clopidogrel (150 mg/d) (DOUBLE) and the influence of the cytochrome P450 (CYP2C19*2/*3, CYP3A5*3)and ATP-binding cassette subfamily B1(ABCB1C3435T) genetic polymorphisms in type 2 diabetes (T2DM) patients.
To characterize effects of type 2 diabetes (T2D) on mRNA expression levels for 10 Cytochromes P450 (CYP450s), two carboxylesterases, and three drug transporters (ABCB1, ABCG2, SLCO2B1) in human duodenal biopsies.
The genes involved in ABC transporters and Type II diabetes mellitus pathway, KLF12 and CXCL12 may play an important role in the progression of pancreatic neuroendocrine tumors.
The POP-ABC study has an enrollment target of 400 participants (200 African American, 200 Caucasian), aged 18-65 years, with at least 1 parent with type 2 diabetes.
A four-year prospective follow-up study among outpatients with type 2 diabetes mellitus: We analyzed outpatients of 31 primary health centers (Madrid, Spain), with at least two A1C values (at baseline and at the end of the study) who did not meet their ABC goals at baseline.
By contrast, we observed strong evidence of T2D association with ABCC5 (intron 26) for European and African American samples (P = 3E-07) and with ABCC5 adipose expression in Europeans [odds ratio (OR) = 3.8, P = 2E-04].
A previous genome-wide association study linked overexpression of an ATP-binding cassette transporter, ABCC5, in humans with a susceptibility to developing type 2 diabetes with age.
Meta-analysis of all case-control data showed that the E23K allele was associated with type 2 diabetes (K allele OR 1.23 [1.12-1.36], P = 0.000015; KK genotype 1.65 [1.34-2.02], P = 0.000002); but the ABCC8 variants were not associated.
We conclude that the polymorphisms of the SUR1 gene predicted the conversion from impaired glucose tolerance to type 2 diabetes and that the effect of these polymorphisms on diabetes risk was additive with the E23K polymorphism of the Kir6.2 gene.
Type 2 diabetes-associated missense polymorphisms KCNJ11 E23K and ABCC8A1369S influence progression to diabetes and response to interventions in the Diabetes Prevention Program.
The C49620TABCC8 polymorphism is associated with anthropometric risk factors for type 2 diabetes among ADPKD patients, with a protective effect of the TT genotype, but without influence on pancreatic β-cell secretory function or insulin sensitivity.
It has been hypothesized that the p.E23K (KCNJ11) mutation in the 11p15.1 region may play an important role in the development of T2DM.In 2009, Hamming et al. found that the p.1369A (ABCC8) variant may be a causal factor in the disease; therefore, in this study we performed a meta-analysis to evaluate the association between these single nucleotide polymorphisms (SNPs), including our original data on the Siberian population (1384 T2DM and 414 controls).