Adiponectin, IGFBP-1 and -2 are independent predictors in forecasting prediabetes and type 2 diabetes

ObjectiveAdiponectin and insulin-like growth factor (IGF) binding proteins IGFBP-1 and IGFBP-2 are biomarkers of insulin sensitivity. IGFBP-1 reflects insulin sensitivity in the liver, adiponectin in adipose tissue and IGFBP-2 in both tissues. Here, we study the power of the biomarkers adiponectin, IGFBP-1, IGFBP-2, and also included IGF-I and IGF-II, in predicting prediabetes and type 2 diabetes (T2D) in men and women with normal oral glucose tolerance (NGT).DesignSubjects with NGT (35-56 years) recruited during 1992-1998 were re-investigated 8-10 years later. In a nested case control study, subjects progressing to prediabetes (133 women, 164 men) or to T2D (55 women, 98 men) were compared with age and sex matched NGT controls (200 women and 277 men).MethodsThe evaluation included questionnaires, health status, anthropometry, biochemistry and oral glucose tolerance test.ResultsAfter adjustment, the lowest quartile of adiponectin, IGFBP-1 and IGFBP-2 associated independently with future abnormal glucose tolerance (AGT) in both genders in multivariate analyses. High IGFs predicted weakly AGT in women. In women, low IGFBP-2 was the strongest predictor for prediabetes (OR:7.5), and low adiponectin for T2D (OR:29.4). In men, low IGFBP-1 was the strongest predictor for both prediabetes (OR:13.4) and T2D (OR:14.9). When adiponectin, IGFBP-1 and IGFBP-2 were combined, the ROC-AUC reached 0.87 for women and 0.79 for men, higher than for BMI alone.ConclusionDifferences were observed comparing adipocyte- and hepatocyte-derived biomarkers in forecasting AGT in NGT subjects. In women the strongest predictor for T2D was adiponectin and in men IGFBP-1, and for prediabetes IGFBP-2 in women and IGFBP-1 in men

Soluble CD93 Is Involved in Metabolic Dysregulation but Does Not Influence Carotid Intima-Media Thickness

Type 2 diabetes and cardiovascular disease are complex disorders involving metabolic and inflammatory mechanisms. Here we investigated whether sCD93, a group XIV c-type lectin of the endosialin family, plays a role in metabolic dysregulation or carotid intima-media thickness (IMT). Although no association was observed between sCD93 and IMT, sCD93 levels were significantly lower in subjects with type 2 diabetes (n = 901, mean ± SD 156.6 ± 40.0 ng/mL) compared with subjects without diabetes (n = 2,470, 164.1 ± 44.8 ng/mL, P < 0.0001). Genetic variants associated with diabetes risk (DIAGRAM Consortium) did not influence sCD93 levels (individually or combined in a single nucleotide polymorphism score). In a prospective cohort, lower sCD93 levels preceded the development of diabetes. Consistent with this, a cd93-deficient mouse model (in addition to apoe deficiency) demonstrated no difference in atherosclerotic lesion development compared with apoe(-/-) cd93-sufficient littermates. However, cd93-deficient mice showed impaired glucose clearance and insulin sensitivity (compared with littermate controls) after eating a high-fat diet. The expression of cd93 was observed in pancreatic islets, and leaky vessels were apparent in cd93-deficient pancreases. We further demonstrated that stress-induced release of sCD93 is impaired by hyperglycemia. Therefore, we propose CD93 as an important component in glucometabolic regulation

Long-term exposure to ambient air pollution and traffic noise and incident hypertension in seven cohorts of the European study of cohorts for air pollution effects (ESCAPE)

We investigated whether traffic-related air pollution and noise are associated with incident hypertension in European cohorts.; We included seven cohorts of the European study of cohorts for air pollution effects (ESCAPE). We modelled concentrations of particulate matter with aerodynamic diameter ≤2.5 µm (PM2.5), ≤10 µm (PM10), &gt;2.5, and ≤10 µm (PMcoarse), soot (PM2.5 absorbance), and nitrogen oxides at the addresses of participants with land use regression. Residential exposure to traffic noise was modelled at the facade according to the EU Directive 2002/49/EC. We assessed hypertension as (i) self-reported and (ii) measured (systolic BP ≥ 140 mmHg or diastolic BP ≥ 90 mmHg or intake of BP lowering medication (BPLM). We used Poisson regression with robust variance estimation to analyse associations of traffic-related exposures with incidence of hypertension, controlling for relevant confounders, and combined the results from individual studies with random-effects meta-analysis. Among 41 072 participants free of self-reported hypertension at baseline, 6207 (15.1%) incident cases occurred within 5-9 years of follow-up. Incidence of self-reported hypertension was positively associated with PM2.5 (relative risk (RR) 1.22 [95%-confidence interval (CI):1.08; 1.37] per 5 µg/m³) and PM2.5 absorbance (RR 1.13 [95% CI:1.02; 1.24] per 10 - 5m - 1). These estimates decreased slightly upon adjustment for road traffic noise. Road traffic noise was weakly positively associated with the incidence of self-reported hypertension. Among 10 896 participants at risk, 3549 new cases of measured hypertension occurred. We found no clear associations with measured hypertension.; Long-term residential exposures to air pollution and noise are associated with increased incidence of self-reported hypertension

Distribution of BMI in analyzed children and adults.

<p>A) Distribution of BMI SDS (BMI Z-Score) adjusted for age and gender according to Rolland-Cachera et al, 1982 <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0041652#pone.0041652-RollandCachera1" target="_blank">[24]</a> among lean (BMI SDS: −1.4−1.8) and overweight/obese (BMI SDS: 2.2–10.5) children; B) Distribution of BMI in the lean (BMI<25 kg/m²), overweight and mildly obese (282), and severely obese (BMI≥35 kg/m²) adults studied; C) BMI-SDS distribution of those children positive for Adv36 in ELISA; D) BMI-distribution of those adults positive for Adv36 in ELISA.</p

Study groups and the studies they were used for.

<p>f: females, m: males.</p><p>Study 1: Comparison between ELISA and serum neutralization assay.</p><p>Study 2: Adv36 prevalence in Sweden.</p><p>Study 3: Association analyses between Adv36 and metabolic parameters in a) children and b) adults.</p

Association between Adv36 and obesity.

<p>A) Higher proportion of children with positive Adv36 serology among pediatric obesity patients (BMI SDS: 2.2–10.5) than lean (BMI SDS: −1.4−1.8) children from high schools in Stockholm. B) Higher prevalence of positive Adv36 serology among severely obese (BMI≥35 kg/m²) females compared to lean (BMI<25 kg/m²) and overweight/mildly obese (O.w./mild obese) (282) females in Stockholm and Uppsala. Error bars indicate standard error of proportion. Due to a low number of severely obese males (n = 11), Adv36 association to severe obesity in males could not be analyzed. However, no difference in Adv36 positivity was found between females and males in lean and overweight/mildly obese groups, and no difference in prevalence of Adv36 positivity was detected among males between lean and overweight/mildly obese.</p