Subclinical inflammation is a risk factor for cardiovascular disease. The mechanisms underlying increased levels of inflammatory markers and their changes in response to weight loss are not fully understood yet. It has been proposed that elevated concentrations of C-reactive protein (CRP) are mediated by cytokines produced in adipose tissue. We investigated the changes in circulating CRP after weight reduction, in relation to parameters relevant to the metabolic syndrome. Forty 25- to 35-year-old obese female volunteers participated in an intervention program of dietary education and supervised physical activity for a period of 9 weeks. Anthropological parameters and biochemical measurements (high-sensitivity CRP [hsCRP], plasma lipoproteins, interleukin 6 [IL-6], adiponectin) were analyzed before and after the intervention. Body mass index decreased by more than 7% from 31.5 +/- 4.1 to 29.1 +/- 3.9. Plasma free fatty acid (FFA) concentrations decreased by 30%, high-density lipoprotein cholesterol increased by 8%, and fasting insulin concentrations decreased by 15%. There were no significant changes in either low-density lipoprotein cholesterol or triacylglycerol concentrations. Subcutaneous and visceral adipose tissue mass decreased by 12% and 18%. High-sensitivity CRP concentrations decreased by 30%; however, mean plasma IL-6 and adiponectin concentrations remained unchanged. In linear regression analysis, the changes in plasma hsCRP concentrations were associated with baseline hsCRP concentration, change in triacylglycerols and FFA concentrations, and in waist circumference. The decrease in hsCRP concentration after weight reduction does not appear to be mediated by decreases in circulating IL-6 or adiponectin concentrations; however, change in hsCRP concentration is related to changes in waist circumference and lipid metabolism, reflected by plasma triacylglycerol and FFA levels.
Redoxpotentiale organischer Verbindungen stellen sich hlufig sehr langsam ein und lassen sich mit den ublichen Titrationsautomaten nicht exakt bestimmen, da diese die Titrationslosung meist relativ schnell oder nach fest vorwahlbaren, aber fur die Gleichgewichtseinstellung oft nicht ausreichenden Zeitintervallen zugeben. Unser Redoxtitrations-Automat jedoch gibt neue Titrationsfliissigkeit immer erst dann zu, wenn sich das Gleichgewicht eingestellt hat. Dies wird dadurch erreicht, daB der jeweilige Potentialwert gemessen, verstarkt und auf einem Kondensator des Steuergerats gespeichert wird. Nach einer beliebig einstellbaren Zeit (Vergleichszeit) wird das Potential nochmals gemessen und auf einem zweiten Kondensator gespeichert. Darauf werden vom Steuergerat die beiden gespeicherten Potentialwerte verglichen. Sind die Werte verschieden, so ist das Gleichgewicht noch nicht erreicht und die Zugabe weiterer Titrationslijsung wird gesperrt. Sind jedoch die Spannungen an den beiden Kondensatoren gleich, so ist das Gleichgewicht erreicht. In diesem Fall veranlaBt das Steuergerat einen Titrationsschreiber zur Aufzeichnung eines Kurvenpunktes und die Kolbenburette zur Abgabe einer bestimmten Menge Titrationsfliissigkeit. Dieser Abfrage-und Regelvorgang wiederholt sich periodisch, bis die gesamte Titrationskurve aufgezeichnet ist. Dabei konnen die Einstellungszeiten fur die einzelnen Gleichgewichtspotentiale sehr verschieden sein. Da sich auBerdem die Empfindlichkeit des Steuergerats verandern IaBt, kann man auch die Normalpotentiale von Substanzen, deren Gleichgewichtspotentiale sich sehr langsam einstellen, automatisch bestimmen. So fanden wir zum Beispiel fur das Redox-Normalpotential des 7 -Hydroxyactinomycins C1 [2]interessant im Zusammenhang mit der Bindung der Actinomycine an DNS [3] -+204 mV. 438 433 435 [bl 360 356 357 Ibl 45 1 452 452 [b] 155 [c] 154.1 154.8 [d] Tabelle 1. Redoxpotentiale einiger Verbindungen Substanz Ea gemesscn [a] Eo Literatur [+ mV1 [+ m v l Urn die Reproduzierbarkeit zu bestimmen, haben wir einige Redoxpotentiale mehrmals gemessen (vgl. Tabelle 1). Die Fehlerbreite der Einzelmessung betragt etwa & 2 mV (ermittelt aus 10 Titrationen einer Verbindung). Der Zeitaufwand fur eine Titration liegt zwischen 6 und 8 Stdn. Durch Umsetzung aquimolekularer Mengen SC(SH)2 [I] und Oxalylchlorid konnte erstmals das in schonen weinroten Nadeln kristallisierende 1.3-Dithiolan-2-thion-4.5-dion (I) quantitativ erhalten werden.s Die verdiinnte Losung von (COC1)z in CHC13 wird bei 0 "C unter FeuchtigkeitsausschluB langsam zu einer Losung von SC(SH)z in CHCIJ getropft. (I) entsteht in glatter Reaktion unter sofortiger HCI-Entwicklung. Zur Beendigung der Reaktion wird 10 min auf 50°C erhitzt. Nach Abdampfen des CHCI, wird (I) (Fp 66 "C, Kp2 90 "C, d? 1,890) aus n-Hexan umkristallisiert. Beim Erhitzen unter Atmospharendruck (N2) zersetzt sich (I) oberhalb 100°C in C, C02, CO, COS und CS2. In CHCI3, CCI4, Benzol, Ather u. a. ist (I) leicht, in Paraffinen maBig loslich. Polare Losungsmittel wie Methanol und Athanol ...
Dietary intervention is the first and usually successful approach in the treatment of high LDL cholesterol (LDL-C) concentration, but it is frequently accompanied by a decrease in HDL concentration. We studied 14 male volunteers on two different diets, high saturated fatty acid (SFA) and high PUFA, in a crossover design to test whether a decrease in HDL can affect reverse cholesterol transport from relabeled macrophages. A significant decrease of LDL-C (in mmol/l) after a PUFA diet compared with an SFA diet from 3.15 6 0.65 to 2.80 6 0.56 (P , 0.01) was accompanied by a significant decrease of HDL cholesterol (HDL-C) (in mmol/l) from 1.21 6 0.30 to 1.10 6 0.32 (P , 0.05). These changes did not affect cholesterol efflux (CHE) from macrophages (9.74 6 1.46% vs. 9.53 6 1.41%). There was no correlation between individual changes of HDL-C and changes of CHE. It is concluded that the decrease of HDL-C after successful dietary intervention of LDL-C is not accompanied by a decrease of CHE.-Kralova Lesna, I., P. Coronary heart disease (CHD) due to atherosclerosis of the coronary arteries is the main cause of mortality in the Western world (1). One of the typical phenotypes associated with increased risk of CHD includes increased LDL cholesterol (LDL-C) and reduced concentrations of HDL. Several epidemiological and physiological data indicate that a change in lifestyle (diet, physical training) can significantly improve lipoprotein profile and prognosis of CHD (2, 3). Meta-analysis of 60 controlled trials (4), focused on the effects of dietary FAs, clearly demonstrated a significant decrease in LDL concentration when saturated fatty acids (SFAs) in a diet were replaced with unsaturated FAs, and this decrease was accompanied by a significant decrease in HDL concentration. It is not clear whether such a decrease of HDL cholesterol (HDL-C) concentration compromises the otherwise atheroprotective effect of such a diet change.The importance of low concentrations of HDL as risk factor for cardiovascular diseases was initially demonstrated in Miller et al. (5), and this finding has been repeatedly confirmed (6, 7).HDL represents a large family of particles differing in size, shape, and composition. Among several protective actions of HDL [protection of endothelial function, and anti-oxidative, anti-inflamatory, and anti-aggregative effects (8-10)], the capacity of HDL to accept cellular lipids and reverse cholesterol transport (RCT) are thought to be the most important. RCT is the key pathway for efflux of cholesterol molecules to extracellular acceptors and their transport to the liver to be metabolized to bile acids. Despite the fact that RCT from macrophages contributes only a little to the whole centripetal transport of cholesterol, this pathway is crucial (11), inasmuch as accumulation of esterified cholesterol in these cells is one of the first features of atherosclerosis.RCT is a complex process involving several steps. First, unesterified cholesterol is carried out to the plasma membrane and then is taken up int...
Background: Apolipoprotein A5 (APOA5) is a determinant of plasma lipids, and its role in body mass index (BMI) determination is discussed. This study was aimed at the investigation of the relationship between common APOA5 gene variants and body weight/plasma lipid decrease in overweight females. Methods: We analyzed 98 unrelated overweight and obese nondiabetic Czech females (BMI >27.5). APOA5 T-1131→C and Ser19→Trp variants were genotyped. Before and after 9 weeks of lifestyle modification, biochemical and anthropometrical measurements and assessment of nutritional intake were performed. The lifestyle modification program consisted of a reduction in energy intake and an exercise program (aerobic exercise 4 times per week, 60 min each). Results: The mean age of the participants was 30.7 ± 3.7 years, the mean BMI before the intervention was 31.4 ± 3.8 and the weight loss was 5.9 ± 2.5 kg (7 ± 3%). There were 86 T-1131T homozygotes and 12 carriers of the C-1131 allele and 82 Ser19Ser homozygotes and 16 carriers of the Trp19 allele, respectively; 72 females had the commonest T-1131T/Ser19Ser haplotype. No significant association between BMI decrease and APOA5 variants was found, but T-1131T carriers have a significantly higher body weight both before and after the intervention (p < 0.05; p = not significant for BMI). The fasting glycemia was significantly higher in Trp19 carriers both before and after the intervention (p < 0.01). Further, plasma triglyceride levels decreased in Ser19Ser homozygotes but increased in Trp19 carriers (1.42 ± 0.62 to 1.28 ± 0.48 vs. 1.15 ± 0.47 to 1.41 ± 0.80 mmol/l; p < 0.05 for differences between the groups). Similarly, in carriers of at least 1 less common APOA5 allele (n = 26), plasma low-density lipoprotein cholesterol levels did not decrease as they did in T-1131T/Ser19Ser carriers (3.11 ± 0.70 to 3.27 ± 0.81 vs. 3.39 ± 0.81 to 3.16 ± 0.86 mmol/l; p < 0.05 for differences between the groups). Conclusions: APOA5 gene variants have effects on the decrease in plasma triglyceride and low-density lipoprotein cholesterol level in females in a model combining their dietary habits and physical activity changes.
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