Circulating cardiovascular risk markers in adult CAH patients and healthy, matched controls.

<p>Mean values±1 SD are given.</p><p>*As hsCRP values were not distributed normally, we have calculated log(CRP) values.</p

Lipid profile in adult CAH patients and healthy, matched controls.

<p>Mean values±1 SD are given.</p

Mean 24-hour ambulatory blood pressure measurements (±1 SD) in CAH patients (open squares) and matched controls (closed squares).

<p>Mean 24-hour ambulatory blood pressure measurements (±1 SD) in CAH patients (open squares) and matched controls (closed squares).</p

TLR-3 is functionally active in adipocytes.

<p>(a) Differentiated SGBS adipocytes were stimulated with either a TLR-3 (poly:IC 12.5μg/ml) or TLR-4 (LPS 50ng/ml) agonist. mRNA levels were measured for IL-8, MCP-1, IL-1 β, adiponectin and PPAR-γ. (b-f) SGBS adipocytes were treated with SiRNA against TLR-3 or scr SiRNA and stimulated with poly:IC. mRNA levels of (b) IL-8, (c) MCP-1, (d) IL-1β, (e) adiponectin, (f) PPAR- γ were subsequently measured. * p<0.05, ** p<0.01, *** p<0.001. Data are shown as means ± SEM.</p

TLR-3 is functionally active in adipocytes.

<p>(a) Differentiated SGBS adipocytes were stimulated with either a TLR-3 (poly:IC 12.5μg/ml) or TLR-4 (LPS 50ng/ml) agonist. mRNA levels were measured for IL-8, MCP-1, IL-1 β, adiponectin and PPAR-γ. (b-f) SGBS adipocytes were treated with SiRNA against TLR-3 or scr SiRNA and stimulated with poly:IC. mRNA levels of (b) IL-8, (c) MCP-1, (d) IL-1β, (e) adiponectin, (f) PPAR- γ were subsequently measured. * p<0.05, ** p<0.01, *** p<0.001. Data are shown as means ± SEM.</p

TLR-3 deficiency does not protect mice against metabolic abnormalities.

<p>Wild-type (WT) and TLR-3-/- mice were subjected to 16 weeks of low fat diet (LFD) or high fat diet (HFD). (a) development of the bodyweight, (b) liver weight, (c) epididymal adipose tissue weight, (d) plasma leptin levels, (e) fasting glucose levels, (f) insulin tolerance test (ITT), (g) area under the curve for ITT. * p<0.05, *** p<0.001. Number of mice per group: WT-LFD n = 10; WT-HFD n = 10; TLR-3-/-LFD n = 7; TLR-3-/-HFD n = 9. Data are shown as means ± SEM.</p

TLR-3 deficiency does not ameliorate adipose tissue inflammation.

<p>After 16 weeks of low fat diet (LFD) or high fat diet (HFD) intervention, adipose tissue of wild-type (WT) and TLR-3-/- mice was investigated for inflammatory parameters. (a) Adipose tissue of mice stained for F4/80, magnification 20x, (b) number of crown-like structures in adipose tissue. Inflammatory markers were measured (c) F480, (d) CD68, (e) MCP-1, (f) TNFα, (g) CXCL1. (h) mRNA levels of TLR-3 in WT mice fed a LFD or HFD for 16 weeks. * p<0.05, ** p<0.01. Number of mice per group: WT-LFD n = 10; WT-HFD n = 10; TLR-3-/-LFD n = 7; TLR-3-/-HFD n = 9. Data are shown as means ± SEM.</p

TLR-3 is predominantly expressed in adipocytes.

<p>(a) Biopsies from visceral- (VAT) and subcutaneous adipose tissue (SAT) were obtained from 4 healthy subjects and TLR expression was determined in stromal vascular fraction (SVF) and mature adipocytes (MA). mRNA levels of (b) TLR-3 and (c) PPAR-γ were measured during differentiation of human SGBS adipocytes. * p<0.05, ** p<0.01. Data are shown as means ± SEM.</p

TLR-3 in human adipose tissue.

<p>Subcutaneous adipose tissue samples of 80 healthy individuals were obtained. TLR-3 mRNA levels were associated with (a) BMI, (b) HOMA-IR, (c) plasma CRP-levels, (d) number of crown-like structures in adipose tissue. Association of MAP3K8 mRNA expression in human subcutaneous adipose tissue with mRNA expression of (e) IL-8, (f) MCP-1, (g) FABP4 and (h) adipocytes cell size. * p<0.05. Data are shown as means ± SEM. HOMA-IR = Homeostatic Model Assessment for insulin resistance.</p

Baseline characteristics.

<p>Baseline characteristics.</p