Red wine intake but not other alcoholic beverages increases total antioxidant capacity and improves pro-inflammatory profile after an oral fat diet in healthy volunteers.

INTRODUCTION: Different alcoholic beverages exert different effects on inflammation and oxidative stress but these results are controversial and scanty in some aspects. We analyze the effect of different alcoholic beverages after a fat-enriched diet on lipid profile, inflammatory factors and oxidative stress in healthy people in a controlled environment. METHODS: We have performed a cross-over design in five different weeks. Sixteen healthy volunteers have received the same oral fat-enriched diet (1486kcal/m(2)) and a daily total amount of 16g/m(2) of alcohol, of different beverages (red wine, vodka, brandy or rum) and equivalent caloric intakes as sugar with water in the control group. We have measured the levels of serum lipids, high sensitivity C-reactive protein (hsCRP), tumor necrosis factor α (TNFα), interleukin 6 (IL-6), soluble phospholipase A2 (sPLA2), lipid peroxidation (LPO) and total antioxidant capacity (TAC). RESULTS: Red wine intake was associated with decreased of mean concentrations of hsCRP, TNFα and IL-6 induced by fat-enriched diet (p<0.05); nevertheless, sPLA2 concentrations were not significantly modified. After a fat-enriched diet added with red wine, TAC increased as compared to the same diet supplemented with rum, brandy, vodka or the control (water with sugar) (p<0.05). CONCLUSIONS: Moderate red wine intake, but not other alcoholic beverages, decreased pro-inflammatory factors and increased total antioxidant capacity despite a fat-enriched diet intake in healthy young volunteers.

Identification of seven novel SMPD1 mutations causing Niemann-Pick disease types A and B.

Niemann-Pick disease (NPD) types A and B are autosomal, recessively inherited, lysosomal storage disorders caused by deficient activity of acid sphingomyelinase (E.C. 3.1.4.12) because of mutations in the sphingomyelin phosphodiesterase-1 (SMPD1) gene. Here, we present the molecular analysis and clinical characteristics of 15 NPD type A and B patients. Sequencing the SMDP1 gene revealed eight previously described mutations and seven novel mutations including four missense [c.682T>C (p.Cys228Arg), c.1159T>C (p.Cys387Arg), c.1474G>A (p.Gly492Ser), and c.1795C>T (p.Leu599Phe)], one frameshift [c.169delG (p.Ala57Leufs*20)] and two splicing (c.316+1G>T and c.1341delG). The most frequent mutations were p.Arg610del (21%) and p.Gly247Ser (12%). Two patients homozygous for p.Arg610del and initially classified as phenotype B showed different clinical manifestations. Patients homozygous for p.Leu599Phe had phenotype B, and those homozygous for c.1341delG or c.316+1G>T presented phenotype A. The present results provide new insight into genotype/phenotype correlations in NPD and emphasize the difficulty of classifying patients into types A and B, supporting the idea of a continuum between these two classic phenotypes.

Retención urinaria como primeramanifestación de rombencefalitispor Listeria monocytogenes / Urinary retention as the first sign of thromboencephalitis due to Listeria monocytogenes

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Red wine intake prevents nuclear factor-kappaB activation in peripheral blood mononuclear cells of healthy volunteers during postprandial lipemia.

BACKGROUND: Several epidemiological studies have demonstrated the beneficial effect of red wine intake in reducing total and cardiovascular mortality. This effect has been attributed in part to its antioxidant properties. Because the monocytes/macrophages and the nuclear transcription factor kappaB (NF-kappaB) are implicated in the pathogenesis of atherosclerotic lesions, we examined the effect of red wine intake on the activation of NF-kappaB in peripheral blood mononuclear cells. METHODS AND RESULTS: Sixteen healthy volunteers were studied 3 times each: after a moderate dose, a low dose, and no wine with a fat-enriched breakfast. Lipid profile and NF-kappaB activation (electrophoretic mobility shift assay) were examined in blood samples taken before and 3, 6, and 9 hours after wine intake. In addition, mononuclear cells were incubated with VLDL in the presence of some antioxidants (quercetin and alpha-tocopherol succinate) contained in red wine to study their effects on NF-kappaB activation. Subjects receiving a fat-enriched breakfast had increased NF-kappaB activation in peripheral blood mononuclear cells coinciding with the augmentation in total triglycerides and chylomicrons. Red wine intake prevented NF-kappaB activity even though it induced a certain increase in serum lipids, particularly VLDL, that did not increase after the fat ingestion alone. However, another form of alcohol intake (vodka) did not modify the NF-kappaB activation provided by postprandial lipemia. In cultured mononuclear cells, isolated human VLDL caused NF-kappaB activation in a time-dependent manner that did not occur in the presence of the red wine antioxidants quercetin and alpha-tocopherol. CONCLUSIONS: Our results provide a new potential mechanism to explain the beneficial effects of red wine intake in the reduction of cardiovascular mortality.

[Pravastatin increases the activity pf the LDL receptors in lymphocytes of individuals with heterozygous familial hypercholesterolemia]. / La pravastatina aumenta la actividad de receptores de LDL en linfocitos de individuos con hipercolesterolemia familiar heterocigota.

An investigation was conducted on the effects of pravastatin, an inhibitor of the HMG CoA reductase, on lipoproteins concentrations and degradation of LDL (low density lipoproteins) in 14 patients with familial hypercholesterolemia (FH). Therapy with pravastatin for twelve weeks, 20 mg every 12 hours, and a low fat (30% calories) and cholesterol (less than 300 mg/daily) diet decreased serum concentrations of LDL cholesterol and apolipoprotein B by 35.5% and 24%, respectively (p < 0.001 for both parameters). On the other hand, apolipoprotein A-1 concentrations increased by 15.1% (p < 0.05) and HDL cholesterol (high density lipoproteins) by 6.8%; concentrations of apolipoprotein A-II did not change. LDL degradation in peripheral lymphocytes increased by 41.3% (p < 0.05) and a correlation was observed (p < 0.05) between percentage of LDL degradation and percentage in the LDL cholesterol decrease. Likewise, a positive trend (p = 0.057) was observed between increases in LDL degradation and aging. These findings indicate that pravastatin favorably influences the lipoprotein profile and that this effect is mediated, at least partly, by an increase in cellular capacity of LDL degradation.

Levels of lipoprotein(a) and plasma lipids in Spanish children aged from 4 to 18 years.

Increased plasma lipoprotein(a)-Lp(a)-levels are linked to a high risk of cardiovascular disease unrelated to other lipoproteins. It seems that Lp(a) values in childhood remain unaltered up to adulthood. In a randomly chosen population of 1970 children, aged from 4 to 18 years and living in a Spanish community, the following serum parameters were studied: total cholesterol, total triglycerides, Lp(a), high-density lipoprotein cholesterol and low-density lipoprotein cholesterol. Mean Lp(a) serum values were 15.0 +/- 14.7 mg dl-1. No differences were seen between either sex in the first years of childhood. Of the studied children, 15.1% presented Lp(a) concentrations above 30 mg dl-1. A correlation between Lp(a) and total cholesterol concentrations, which disappeared when low-density lipoprotein cholesterol concentrations were corrected according to cholesterol present in Lp(a), was observed.

Effect of dietary monounsaturated fatty acids on plasma lipoproteins and apolipoproteins in women.

To determine the effects of dietary fat saturation on plasma lipoproteins, we studied 21 free-living normolipidemic women (13 pre- and 8 postmenopausal) on three consecutive diet periods. During the first 4 wk they consumed a saturated diet rich in palm oil and butter [19% saturated fatty acids (S), 14% monounsaturated fatty acids (M), and 3.5% polyunsaturated fatty acids (P)], followed by 6 wk of a monounsaturated diet rich in olive oil (11% S, 22% M, and 3.6% P), and 6 wk of a polyunsaturated diet rich in sunflower oil (10.7% S, 12.5% M, and 12.8% P). Compared with the diet rich in saturated fatty acids, both diets rich in unsaturated fatty acids had similar lowering effects on total and low-density-lipoprotein cholesterol. High-density lipoprotein cholesterol and apolipoprotein A-I were higher in the monounsaturated-rich period than in the polyunsaturated-rich (10.5% and 12.7% respectively, P less than 0.001) and the saturated-rich period (5.3%, and 7.9%, respectively, P less than 0.05). These effects were independent of menopause status. Our data show that at this level of fat intake (36% as calories), a monounsaturated-rich diet results in a less atherogenic lipid profile than either polyunsaturated- or saturated-rich diets.

Effects of long-term monounsaturated- vs polyunsaturated-enriched diets on lipoproteins in healthy men and women.

The effect of dietary-fat saturation on plasma lipoprotein concentrations was assessed in 46 men and 32 women placed on a diet enriched in polyunsaturated fatty acids (sunflower oil) for 12 wk and, under isocaloric conditions, on a diet enriched in monounsaturated fatty acids (olive oil) for the next 16 wk in men and 28 wk in women. Fat comprised 37% of the total energy intake in men and 36% in women. At the end of the monounsaturated fatty acid diet no change occurred in total cholesterol (TC) in men but it increased by 9% in women. High-density-lipoprotein (HDL) cholesterol increased by 17% in men and by 30% in women. The atherogenic index (TC:HDL cholesterol) fell significantly in both sexes. No significant changes occurred in plasma low-density-lipoprotein cholesterol or in total triglycerides values. These data show that when compared with polyunsaturates, monounsaturates increased HDL cholesterol and reduced the atherogenic risk profile in both sexes.