A co-twin-control study that allows full control of genetic influence showed that only obesity was significantly associated with higher CRP levels: Odds ratios (95% confidence intervals) were 1.23 (1.04,1.46) for 1 kg/m(2) increase in body mass index and 1.12 (1.03,1.22) for 1% increased in total body fat, respectively.
In this cohort, mean (SD) habitual sleep duration based on self-report was 7.6 (1.6) h and mean sleep duration by polysomnography (PSG) on the night prior to blood sampling was 6.2 (1.3) h. After adjusting for obesity and apnea severity, each additional hour of habitual sleep duration was associated with an 8% increase in C-reactive protein (CRP) levels (P=0.004) and 7% increase in interleukin-6 (IL-6) levels (P=0.0003).
The association of the CRP SNPs with endometrial cancer risk and their modification on the association between obesity and endometrial cancer risk were evaluated.
The aim of the study was to verify whether IFI30, CD163, CXCL9 and TSLP gene polymorphisms contribute to explain the inter-individual variability of the inflammatory profile of obesity assessed by plasma high-sensitivity CRP concentrations.
Interactions between two previously studied VDR polymorphisms (rs7968585 and rs2239179) and 25OHD concentrations on metabolic and cardiovascular disease-related outcomes such as obesity- (body mass index, waist circumference, waist-hip ratio (WHR)), cardiovascular- (systolic and diastolic blood pressure), lipid- (high- and low-density lipoprotein, triglycerides, total cholesterol), inflammatory- (C-reactive protein, fibrinogen, insulin growth factor-1, tissue plasminogen activator) and diabetes- (glycated haemoglobin) related markers were examined in the 1958 British Birth cohort (n up to 5160).
The objective of the study was to explore in a population-based sample whether the relation between leptin and CRP is independent of obesity level and whether genetic causes of CRP elevation contribute to leptin levels.
The urinary CRP and 8-isoprostane significantly correlated with the obesity measures (body mass index, waist circumference, and waist-to- height ratio) and ET-1, inflammatory, and oxidative markers.
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 studied how CRP, ferritin and albumin change following LSG surgery in relation to obesity, metabolic syndrome (MetS) ATPIII risk components and diabetes mellitus (DM).
Obesity and COC use were associated with alterations in lipid and inflammatory cardiometabolic parameters, particularly increased CRP levels and decreased HDL-c, which are considered markers of cardiovascular disease (CVD) risk.
PWS presented similar percentage of body fat (%), lower body mass index (BMI) z-scores, insulin resistance, triglycerides, MetS severity, C-reactive protein (CRP), tumor necrosis factor-α (TNF-α) and MVPA and higher high-density lipoprotein (HDL) and adiponectin (ADP) than OB.
Since the role of adipokine retinol-binding protein-4 (RBP4) in obesity remains uncertain and its relationship with other adipokines and inflammatory markers has not been examined in detail, we investigated the relationships of RBP4 mRNA expression and circulating protein levels with obesity, anthropometric and metabolic variables, as well as with obesity-related inflammatory markers adiponectin and C-reactive protein.
Secondarily, cortisol stimulation will contribute to the development of central obesity which is known to facilitate the development of metabolic syndrome, including slightly increased levels of inflammatory biomarkers such as C-reactive protein and fibrinogen.
We examined both WBC count and CRP level, independently and in combination, as predictive markers for type 2 diabetes and also considered the influence of obesity and other individual characteristics on the relationship.
The association between AHEI and high-risk CRP was stronger for those with diabetes (p-interaction < 0.0001), obesity (p-interaction = 0.005), or ages 45-74 y (p-interaction = 0.011).
Maternal obesity is associated with alteration of immunological factors concentrations in the human milk, such as C-reactive protein (CRP), leptin, IL-6, insulin, TNF-Alpha, ghrelin, adiponectin, and obestatin.
Since markers of inflammation are supposed to predict type 2 diabetes, interleukin-6 (IL-6) and C-reactive protein (CRP) in combination with parameters of obesity, insulin resistance and hyperandrogenism were determined in 57 PCOS women and in 20 age-matched healthy controls.
The presence of obesity at ≥ 2 follow-ups showed the highest mean values (SE) for IL-6 [2.45 (1.05)] and CRP [3.74 (1.11)] and the lowest mean value for adiponectin [8.60 (0.37)] (adjusted analyses, females) compared with other exposures; the highest mean of IL-6 [1.65 (1.05)] and CRP [1.78 (1.11)] and the lowest mean of adiponectin [9.98 (0.38)] were for the number of follow-ups with ≥2 exposures compared to those with no exposures at any follow-up (adjusted analyses, females).