After adjusting for traditional risk factors and high-sensitivity C-reactive protein, 10-year new-onset T2DM risk was significantly increased in subjects in the highest tertile of baseline serum ferritin levels [odds ratio (OR)=1.80, 95% confidence interval (CI): 1.17-2.79] and in subjects with high serum ferritin levels in both 2002 and 2007 (OR=1.54, 95% CI: 1.01-2.34).
Finally, most of the well-known (i.e., blood pressure, heart rate, waist to hip, triglycerides, and HDL-C) and novel CVD risk factors [i.e., inflammation markers (C-reactive protein, leukocytes, and chemoattractant protein-1), fibrinogen, and glucose homeostasis (i.e., insulin resistance, and glycated hemoglobin)] are substantially (<i>p</i> < 0.0001) altered in severe-obese-LH: 0-2 vs overweight-LH: 0-2, pointing to the fact that obesity leads to worsen the CVD/T2D risk factor profile.
We confirm previous GWAS findings, namely that the minor rs1183910 A allele is associated with an increased risk of developing type 2 diabetes (p(trend) = 0.003), decreased levels of C-reactive protein (CRP; p(trend) = 6 × 10(-76)) and γ-glutamyltransferase (p(trend) = 4 × 10(-48)), and increased levels of total cholesterol (p(trend) = 3 × 10(-10)) and LDL-cholesterol (p(trend) = 3 × 10(-11)).
High plasma levels of IL-6, CRP and SAA were associated with unstable CAD, as well as established risk factors including type 2 diabetes mellitus, smoking, low glomerular filtration rate, low TGs and low HDL-C. After adjusting for established cardiovascular risk markers and the other two inflammatory markers, SAA was found to be an independent risk factor for cardiovascular mortality after a short-term follow-up (6 months-1 year) with a HR per SD of 1.41.
Correction to: Soluble CD163, adiponectin, C-reactive protein and progression of dysglycaemia in individuals at high risk of type 2 diabetes mellitus: the ADDITION-PRO cohort.
Elevated CRP and IL6 levels were associated with increased risk of developing T2DM [OR (95% CI): 7.51 (2.11, 26.74) and 4.95 (1.28, 19.11)], respectively.
We aimed to investigate whether CRP was mediating the association between HNF1A G319S and type 2 diabetes in an Aboriginal Canadian population with a high prevalence of diabetes.
In this study, familial aggregation was estimated, and we tested for association between serum CRP levels and polymorphisms within the CRP and APOE genes in sib-ships with type 2 diabetes mellitus, a population at increased risk for cardiovascular disease.
In a non-diabetic population (n = 630), the same -948 allele that conferred increased risk of T2D was significantly associated with higher plasma levels of fibrinogen and C-reactive protein (p = 0.0022 and 0.0038, respectively).
We genotyped representative SNPs in approximately 1300 Pima samples and found a single variant in the CRP promoter (SNP 133552) that was associated with T2DM (P=0.014), as well as a common haplotype (CGCG) that was associated with both T2DM (P=0.029) and corrected insulin response, a surrogate measure of insulin secretion in non-diabetic subjects (P=0.050).
We investigated whether a 1-year intensive lifestyle intervention (ILI) for weight loss would avert the unfavorable cardiometabolic effects associated with GCKR Leu446Pro when compared with a diabetes mellitus support and education arm in overweight/obese individuals with type 2 diabetes mellitus with triglyceride (n=3214) and CRP (n=1411) data participating in a randomized lifestyle intervention study for weight loss, Action for Health in Diabetes Mellitus (Look AHEAD).
Multivariate logistic regression analysis revealed that male sex, high blood pressure, hypertriglyceridemia, BMI ≥30kg/m², age ≥50 years, sleep duration <6.5 hours, C-reactive protein ≥4.5mg/L, Beck Depression Inventory >12, and apnea-hypopnea index ≥5/h were significant risk factors of type 2 diabetes in major depression.
The study included 201 patients.Significant factors associated with increased LOS include type 2 diabetes mellitus (P < 0.012), obesity (P < 0.001), raised C-reactive protein (P < 0.0001), raised white cell count (P < 0.0001), raised temperature (P < 0.0001), septic shock (P < 0.003), multiorgan failure (P < 0.01), extended-spectrum beta-lactamases or methicillin-resistant Staphylococcus aureus colonization (P < 0.04) and intensive care unit admission (P < 0.0004).
Three panels of non-smoking individuals were examined between 3/2007 and 12/2008: 1) with type 2 diabetes mellitus (T2D, n=83), 2) with impaired glucose tolerance (IGT, n=104), and 3) with a potential genetic predisposition which could affect detoxifying and inflammatory pathways (n=87) defined by the null polymorphism for glutathione S-transferase M1 (GSTM1) in combination with a certain single nucleotide polymorphism on the C-reactive protein (CRP) or the fibrinogen gene.
The CRP+1444C>T polymorphism was associated with CRP levels in Mexican adolescents and could be used as a genetic marker for the early detection of individuals at risk for developing obesity-related conditions such as cardiovascular disease or type 2 diabetes mellitus in early adulthood.
The major objectives of this study were to examine the association of rs10757278 and rs2383206 SNPs on Chr9p21 with the incidence of CAD in the presence and absence of type 2 diabetes (T2D) in Egyptians and to correlate these genetic variants with several disease biomarkers (TC, CRP, and HbA1c).
In the Bruneck study, there was a 12% higher risk of type-2 diabetes for a one standard deviation lower concentration of log Lp(a) (HR = 1.12 [95% CI 0.95-1.32]; P = 0.171), after adjustment for age, sex, alcohol consumption, body mass index, smoking status, socioeconomic status, physical activity, systolic blood pressure, HDL cholesterol, log high-sensitivity C-reactive protein and waist-hip ratio.
O/MS pigs showed, on average, a 2-fold increase in plasma C-reactive protein (P < .05) and cortisol (P < .09) concentrations compared with controls; DM pigs showed, on average approximately, a 40-fold increase in plasma tumor necrosis factor α levels (P < .05) and a 2-fold increase in cortisol concentrations (P < .05) compared with controls.
This technique has been used to provide evidence of causal associations of serum estradiol concentrations, smoking, body mass index, and type 2 diabetes with bone mineral density and the lack of associations of serum thyroid stimulating hormone, urate, C-reactive protein, and 25‑hydroxyvitamin D concentrations with bone mineral density in generally healthy populations.