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

Baseline characteristics.

<p>Baseline characteristics.</p

Obesity and macrophage influx in adipose tissue of HFD-fed WT and MAP3K8-ko animals.

<p>MAP3K8-ko and WT mice were fed a LFD or HFD during 16 weeks. (a) Bodyweight development upon LFD or HFD feeding. (b) Epididymal white adipose tissue (eWAT) weight after 16 weeks of LFD or HFD. (c) Liver weight after 16 weeks of LFD or HFD. (d) Plasma CXCL1 levels after 16 weeks of LFD or HFD (e) Macrophage influx into the adipose tissue as determined by immunohistochemistry, F4/80 (serotec) staining: 20× magnification or 40× as indicated: (f) Number of crown-like structures per field. (g–i) qPCR analysis for macrophage infiltration markers, (g) CD68, (h) F4/80, (i) MCP-1 in adipose tissue of MAP3K8-ko and WT animals. * p<0.05, ** p<0.01, *** p<0.001.</p

MAP3K8 in humans is associated with IL-1β, IL-6 and IL-8 cytokine expression.

<p>Biopsies from subcutaneous adipose tissue were obtained from healthy subjects with varying levels of obesity. Association of MAP3K8 mRNA expression in human subcutaneous adipose tissue with mRNA expression of (a) IL-1ß, (b) IL-6, (c) IL-8, (d) TNF-α, (e) serum amyloid A levels (SAA: Q1≤0.7 mg/L, Q4≥1.6 mg/L), (f) C-reactive protein (CRP: Q1≤0.5 mg/L, Q4≥2.0 mg/L). *p<0.05, **p<0.01.</p