F M van Dielen

Publications (3)13.12 Total impact

• Article: Increased leptin concentrations correlate with increased concentrations of inflammatory markers in morbidly obese individuals.

  F M van Dielen, C van't Veer, A M Schols, P B Soeters, W A Buurman, J W Greve
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  ABSTRACT: To study whether an increase of plasma leptin concentrations, as observed in the case of increased body weight, is associated with an inflammatory state. Sixty-three healthy subjects with body mass index (BMI) ranging from 20 to 61 kg/m2. Plasma concentrations of leptin, the inflammatory parameter soluble TNF-alpha receptors (TNFR55 and TNFR75), the acute phase proteins lipopolysaccharide binding protein (LBP), serum amyloid A (SAA), alpha-acid glycoprotein (AGP), C-reactive protein (CRP), plasminogen activator inhibitor-1 (PAI-1) and the anti-inflammatory soluble Interleukin-1 decoy receptor (sIL-1RII) were measured. As expected, BMI correlated significantly with leptin (r=0.823, P<0.001), but also with all acute phase proteins, both soluble TNF receptors and PAI concentrations. After correction for BMI and sex, no significant correlation between leptin and the acute phase proteins was seen. Interestingly, however, leptin strongly correlated with both TNF receptors (r=0.523, P<0.001 for TNFR55 and r=0.438, P<0.001 for TNFR75). This study shows the development of a pro-inflammatory state with increasing body weight. The BMI independent relationship between leptin and both soluble TNF-receptors is consistent with a regulatory role for leptin in the inflammatory state in morbidly obese subjects.
  International Journal of Obesity 12/2001; 25(12):1759-66. · 4.69 Impact Factor
• Article: Effects of surgical sympathectomy on skin blood flow in a rat model of chronic limb ischemia.

  F M van Dielen, H A Kurvers, R Dammers, M G oude Egbrink, D W Slaaf, J H Tordoir, P J Kitslaar
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  ABSTRACT: The role of lumbar sympathectomy in the treatment of limb ischemia secondary to arteriosclerosis obliterans has been controversial. Increased temperature and rubor of the skin, which usually follow sympathectomy, have generally been interpreted as indicative of improved nutritive skin blood flow. However, the existence of a (nonnutritive) thermoregulatory level of skin microcirculation makes such an extrapolation questionable. We investigated the total (mainly thermoregulatory) skin blood flow (TSBF) in the hindlimb of 15 male Lewis rats by means of laser Doppler flowmetry and the nutritive skin blood flow (NSBF) by means of capillary microscopy (red blood cell velocity). Transcutaneous oximetry was used to assess skin oxygenation (SO). Measurements were performed before and 2 and 28 days after ligation of the common iliac and iliolumbar artery. Subsequently, either a surgical resection of the sympathetic chain (L2-L6) was performed or a sham operation. Measurements were repeated 2 and 28 days later. For the group of 15 rats as a whole, TSBF (p < 0.05), NSBF (p < 0.05), and SO (p < 0.05) were found to be drastically reduced at day 2 after litigation compared to preligation values. This reduction partially recovered during the following weeks. TSBF (p < 0.05) and NSBF (p < 0.05), however were still reduced at day 28 after ligation compared to preligation values, whereas the SO at this time tended to be lower (p = 0.11). In the sympathectomy group the TSBF was found to be increased at day 2 (p < 0.05) and day 28 (p < 0.05) after sympathectomy, both compared to values obtained at day 28 after ligation. Sympathectomy did not have an effect on NSFB and SO. The sham procedure had no effect on the TSBF, NSBF, or SO. These results indicate that in case of lower limb ischemia, sympathectomy improves skin blood flow at the thermoregulatory but not the nutritive level of skin microcirculation. This may be related to the fact that the thermoregulatory vessels are mainly sympathetically controlled, whereas the nutritive capillaries are mainly controlled by local (nonneural) factors.
  World Journal of Surgery 08/1998; 22(8):807-11. · 2.36 Impact Factor
• Article: Peripheral blood flow and noradrenaline responsiveness: the effect of physiological hyperinsulinemia.

  C H de Haan, F M van Dielen, A J Houben, P W de Leeuw, F C Huvers, J G De Mey, B H Wolffenbuttel, N C Schaper
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  ABSTRACT: Insulin seems to have vasodilator properties, but it is unclear if insulin in postprandial concentrations is a specific vasodilator of skeletal muscle resistance arterioles only or that various types of vessels are affected. The aim of the present study was to determine the direct effects and the time course of regional/local physiological hyperinsulinemia on skeletal muscle arterioles, skin blood flow and peripheral venous tone and the responsiveness of these different vascular beds to noradrenaline. In protocol I (n = 12) we infused insulin into the brachial artery for 180 min (3.5 mU/min) and evaluated the effects on forearm (muscle) blood flow (FBF) and skin blood flow (SBF). Furthermore, noradrenaline (0.025, 0.01 and 0.4 microgram/min) was infused (i.a.) at baseline, at 90 and 180 min after the start of insulin. In protocol 2 (n = 10) the same regional forearm hyperinsulinemia was achieved, but now the local venous responsiveness to noradrenaline (1.7-55 ng/min, at baseline and at 90 and 180 min) was measured in a dorsal hand vein. In protocol 3 we evaluated the local effects of different doses of insulin (1-100 mU/min) infused directly into hand veins preconstricted with phenylephrine. Forearm hyperinsulinemia (approximately 50 mU/l) led to a significant increase in FBF after 180 min (median 26%, interq ranges 5-50, P < 0.05), while SBF was not altered. Forearm hyperinsulinemia did not affect the noradrenergic responsiveness in skeletal muscle or skin. Infused locally into hand veins only the highest dose of insulin (100 mU/min) caused a minor venodilation (7% [2.4-12.5], P < 0.05). Regional forearm physiological hyperinsulinemia has a vasodilator effect on resistance vessels in skeletal muscle, but is slow in onset (180 min). However, skin vasculature and peripheral veins are not affected by this hyperinsulinemia.
  Cardiovascular Research 05/1997; 34(1):192-8. · 6.06 Impact Factor