Our hypothesis was that variants in CCK, GLP-1, and TCF7L2 (transcription factor 7-like 2 locus), which is associated with greatest genetic risk for development of type 2 diabetes mellitus, are associated with GE and independently with glucose tolerance.
The purpose of this study was to determine if TCF7L2 variants and body mass index/waist circumference (BMI/WC) act synergistically to influence the incidence of type 2 diabetes in a Chinese population.
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).
Puerto Ricans with the TCF7L2-rs7903146 and rs12255372T2D risk genotypes, although still high, had better anthropometric profiles when adhering to a MedDiet, suggesting that this diet may offset unfavorable genetic predisposition.
Multivariate model analysis, including T2D status, age, and body mass index (BMI), displayed significant covariance in PPARGC-1α rs8192678; SIRT1 rs7896005; TCF7L2rs7903146 and rs122243326; UCP3 rs3781907; and HHEX rs1111875 with a P < 0.05.
The aim of this study was to investigate the association between the transcription factor 7-like 2 gene (<i>TCF7L2</i>) rs7903146 polymorphism and peripheral arterial disease in type 2 diabetes.
The study aimed to evaluate the impact of the single nucleotide polymorphism (SNP) rs7903146 on the transcription factor 7-like 2 (TCF7L2) gene in stress-related hyperglycaemia (SRH), defined as blood glucose≥11mmol/L in at least two blood samples during the first 3 days in the intensive care unit (ICU), and on 28-day and 1-year mortality, and incidence of type 2 diabetes (T2D) at 6 months and 1 year in patients hospitalized in the ICU.
Computational analysis reveal that out of 99 identified key hub gene candidates from 348 DEGs, only four genes (CCL2, ELMO1, VEGFA and TCF7L2) along with FOS playing key role in causing T2D and its associated disorders, like nephropathy, neuropathy, rheumatoid arthritis and cancer via p53 or Wnt signaling pathways.
This Perspectives in Care article highlights the role of type 2 diabetes-associated genetic factors (e.g., gene variants at transcription factor 7-like 2 [<i>TCF7L2</i>]) and obesity (via insulin resistance, inflammation, β-cell stress, or all three) in the pathogenesis of type 1 diabetes and their impacts on age at diagnosis.
Clinical Impact of the TCF7L2 Gene rs7903146Type 2 Diabetes Mellitus Risk Polymorphism in Women with Gestational Diabetes Mellitus: Impaired Glycemic Control and Increased Need of Insulin Therapy.
Several genetic variants in proximity to TCF7L2 have been linked to type 2 diabetes through genome-wide association studies in various human populations.
The aim of this study was to investigate the associations between the TCF7L2rs7903146 polymorphism, adiponectin levels, age at onset of obesity and the occurrence of type 2 diabetes (T2D) in a sample of obese Polish adults.
Given the role of peripheral serotonin in metabolic homeostasis and type 2 diabetes, this finding provides a first hint that the well-known impact of the TCF7L2 polymorphism on type 2 diabetes risk may involve a serotonin-dependent pathway.
For instance, transcription factor 7-like 2 (TCF7L2) and proteasome 26S subunit, non-ATPase 9 (PSMD9) are two genes independently reported as contributing to T2D and SCZ, and PSMD9 to MDD as well.
The transcription factor 7-like 2 (TCF7L2) gene confers one of the strongest genetic predispositions to type 2 diabetes, but diabetes development can be modified by diet.