Clinical characteristics of study population.

<p>Data are given as percentages, mean (SD) or median (interquartile range). CHD: Coronary heart disease. T2DM: type 2 diabetes. T1DM: type 1 diabetes. BMI: body mass index. WHR: waist-to-hip ratio. eGFR: estimation of glomerular filtration rate. ACR: Urinary albumin to creatinine ratio. PTH: parathyroid hormone. 25(OH)D: 25-hydroxy-vitamin D. FGF-23: Fibroblast growth factor 23. hsCRP: high-sensitivity C-reactive protein. IL-6: interleukin 6. sTNFαR1: soluble fraction of tumor necrosis factor α receptor 1. sTNFαR2: soluble fraction of tumor necrosis factor α receptor 2. ICAM-1: soluble intercellular adhesion molecule-1. VCAM-1: soluble vascular cell adhesion molecule-1. aPWV: aortic pulse wave velocity.</p><p>Clinical characteristics of study population.</p

Association of FGF-23 with aPWV in the patients with T1DM.

<p>Model 1 adjusted for age, sex, eGFR, current smoking (No/Yes), arterial hypertension (No/Yes), dyslipidaemia (No/Yes), BMI and FGF-23. Model 2 adjusted for covariates in model 1 and variables reflecting mineral metabolism (calcium, phosphate, PTH and 25(OH)D). Model 3 adjusted for covariates in model 2 and duration of diabetes (years) and the presence of microvascular complications (diabetic retinopathy, nephropathy and peripheral polyneuropathy) and low-grade inflammation general score and endothelial dysfunction score. 25(OH)D were additionally adjusted for seasonality.</p><p>Association of FGF-23 with aPWV in the patients with T1DM.</p

Association of FGF-23 with aPWV in the control group.

<p>Model 1 adjusted for age, sex (male/female), eGFR, current smoking (No/Yes), arterial hypertension (No/Yes), dyslipidaemia (No/Yes), BMI and FGF-23. Model 2 adjusted for covariates in model 1 and reflecting mineral metabolism (calcium, phosphate, PTH and 25(OH)D). Model 3 adjusted for covariates in model 2 and low-grade inflammation general score and ED score. 25(OH)D were additionally adjusted for seasonality.</p><p>Association of FGF-23 with aPWV in the control group.</p

Association of FGF-23 with aPWV in the whole population.

<p>Model 1 adjusted for age, sex (male/female), eGFR, current smoking (No/Yes), arterial hypertension (No/Yes), dyslipidaemia (No/Yes), BMI, TD1M (No/Yes) and FGF-23. Model 2 adjusted for covariates in model 1 and reflecting mineral metabolism (calcium, phosphate, PTH and 25(OH)D). Model 3 adjusted for covariates in model 2 and low-grade inflammation general score and ED score. 25(OH)D were additionally adjusted for seasonality.</p><p>Association of FGF-23 with aPWV in the whole population.</p

Lack of Postprandial Peak in Brain-Derived Neurotrophic Factor in Adults with Prader-Willi Syndrome - Fig 3

<p><b>Postprandial BDNF (Brain-derived neurotrophic factor) (A) and leptin (B) levels in subjects with Prader-Willi syndrome (PWS), in obese controls, and in lean controls.</b> A peak in BDNF at 60 min was observed only in lean subjects (p<0.05 baseline vs 60 min in lean controls). Subjects with PWS had lower BDNF levels at 60 and 120 min than lean controls (p<0.05). Leptin levels within groups did not change between baseline and postprandial measurements. PWS subjects had higher leptin levels than the other groups at all time points (p<0.001).</p

Baseline characteristics of all groups.

<p>Baseline characteristics of all groups.</p

Plasma Brain-derived neurotrophic factor (BDNF) levels in subjects with Prader-Willi syndrome (PWS) and in obese and lean control subjects.

<p>PWS subjects vs. obese and lean controls, P = 0.05.</p

Lack of Postprandial Peak in Brain-Derived Neurotrophic Factor in Adults with Prader-Willi Syndrome - Fig 4

<p><b>Fasting and postprandial plasma Brain-derived neurotrophic factor (BDNF) (A) and leptin (B) levels (circles) in the three groups, overlaid with hunger score (stars) over time.</b> Note that postprandial BDNF peak in lean controls coincides with the lowest hunger score. PWS = Prader Willi Syndrome. Hunger was quantified on a visual analogue scale ranging from 0 to 100.</p

Hunger score at fasting (circles) versus 60’ after the meal (stars) in the different genetic subtypes of Prader-Willi syndrome subjects.

<p>P = 0.034 for uniparental disomy, nonsignificant for the rest. Hunger was quantified on a visual analogue scale from 0 to 100.</p