42 research outputs found

    Abdominal Adiposity Is Associated With Elevated C-Reactive Protein Independent of BMI in Healthy Nonobese People

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    Objective: There is debate over the most appropriate adiposity markers of obesityassociated health risks. We evaluated the relationship between fat distribution and highsensitivity C-reactive protein (hs-CRP), independent of total adiposity. Research design and methods : We studied 350 people with abdominal adiposity (waist-to-hip ratio (WHR) ≥0.9 in male and ≥0.85 in female subjects) and 199 control subjects (WHR< 0.9 in male and <0.85 in female subjects) matched for BMI and age. We measured hs-CRP and major cardiovascular risk factors. Results Participants with abdominal adiposity had BMI similar to that in control subjects (24.8 ±2.5 vs. 24.7 ±2.2 kg/m2, respectively), but significantly higher waist circumference (96.4 6.±0 vs. 83.3 ±6.7 cm; p < 0.01) and WHR (1.07 ± 0.08 vs. 0.85 ±0.05; p<0.001). Compared with the control subjects, participants with abdominal adiposity had an adverse cardiovascular risk factor profile, significantly higher hs-CRP (1.96 ±2.60 vs. 1.53 ± 1.74 mg/dl; p< 0.01), and a twofold prevalence of elevated CRP values (≥3 mg/dl). Conclusions In non obese people, moderate abdominal adiposity is associated with markers of subclinical inflammation independent of BMI

    Uncoupling protein 2 G(-866)A polymorphism: a new gene polymorphism associated with C-reactive protein in type 2 diabetic patients.

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    BACKGROUND: This study evaluated the relationship between the G(-866)A polymorphism of the uncoupling protein 2 (UCP2) gene and high-sensitivity C reactive protein (hs-CRP) plasma levels in diabetic patients. METHODS: We studied 383 unrelated people with type 2 diabetes aged 40-70 years. Anthropometry, fasting lipids, glucose, HbA1c, and hs-CRP were measured. Participants were genotyped for the G (-866)A polymorphism of the uncoupling protein 2 gene. RESULTS: Hs-CRP (mg/L) increased progressively across the three genotype groups AA, AG, or GG, being respectively 3.0 ± 3.2, 3.6 ± 5.0, and 4.8 ± 5.3 (p for trend = 0.03). Since hs-CRP values were not significantly different between AA and AG genotype, these two groups were pooled for further analyses. Compared to participants with the AA/AG genotypes, homozygotes for the G allele (GG genotype) had significantly higher hs-CRP levels (4.8 ± 5.3 vs 3.5 ± 4.7 mg/L, p = 0.01) and a larger proportion (53.9% vs 46.1%, p = 0.013) of elevated hs-CRP (> 2 mg/L). This was not explained by major confounders such as age, gender, BMI, waist circumference, HbA1c, smoking, or medications use which were comparable in the two genotype groups. CONCLUSIONS: The study shows for the first time, in type 2 diabetic patients, a significant association of hs-CRP levels with the G(-866)A polymorphism of UCP2 beyond the effect of major confounders
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