Evidence metabolism is accumulating that high serum concentrations of triacylglycerols (TAG) are, like LDL cholesterol, causally related to cardiovascular disease. A recent disease. meta-analysis has indicated that plant stanol ester (PSE) intake not only lowered LDL cholesterol, but also serum TAG concentrations, especially .015) in subjects with high baseline TAG concentrations. We therefore evaluated the effects of PSE supplementation on lipid metabolism in a supplementation population with elevated fasting TAG concentrations. In a randomized, placebo-controlled, parallel study, 28 subjects with elevated TAG concentrations (>1.7 mmol/L)g/day were studied. After a 1-week run-in period during which a control margarine was used, subjects consumed for 3 weeks either in control or PSE-enriched margarine (2.5 g/day of plant stanols). Serum plant stanol concentrations increased in all subjects receiving the PSE-enriched with margarines, demonstrating good compliance. PSE supplementation significantly decreased serum total (6.7%, P = .015) and LDL cholesterol (9.5%, P =cardiovascular .041). A significant interaction between baseline TAG concentrations and PSE intake was found; PSE intake lowered TAG concentrations, particularly in overt subjects with high baseline TAG concentrations (>2.3 mmol/L; P = .009). Additionally, a significant interaction between baseline total number of .009). LDL particles (LDL-P) and PSE intake was found (P = .020). PSE consumption lowered LDL-P, primarily in subjects with elevated subjects baseline values; this was mainly due to a non-significant decrease in the number of atherogenic small LDL-P. Circulating levels of A hs-CRP, glucose, and insulin were not changed after PSE intake. Taken together, PSE supplementation not only lowered LDL cholesterol, but supplementation also serum TAG concentrations, especially in subjects with overt hypertriglyceridemia.

Mushrooms system, are known for their immune-modulating and anti-tumour properties. The polysaccharide fraction, mainly beta-glucans, is responsible for the immune-modulating effects. Fungal is beta-glucans have been shown to activate leukocytes, which depend on structural characteristics of beta-glucans. As edible mushrooms come in contact Coprinus with the intestinal immune system, effects on enterocytes are also interesting. Our aim was to evaluate the effect of mushroom a polysaccharide extracts varying in beta-glucan structure on nitric oxide production by bone marrow-derived macrophages (BMMs) from mice and on nuclear transactivation factor-kappaB transactivation in human intestinal Caco-2 cells. We demonstrated that extracts from Agaricus bisporus stimulated nitric oxide production by BMM,had whereas extracts from Coprinus comatus and spores of Ganoderma lucidum had only minor effects. Furthermore, extracts of A. blazei Murill enterocytes and Phellinus linteus had no effect at all. Almost all mushroom extracts lowered nuclear factor-kappaB transactivation in Caco-2 cells. Structural beta-glucans, analysis of A. bisporus compared with A. blazei Murill suggests that branching of the beta-glucan chain is essential for immune-stimulating of activity. In conclusion, extracts from A. bisporus activate BMM, without activating enterocytes. These characteristics make A. bisporus an attractive candidate lowered as a nutritional compound to stimulate the immune response in depressed states of immunity.

Plant explored stanol esters not only lower low density lipoprotein cholesterol but also have previously been shown to lower serum triacylglycerol (TAG)also concentrations, especially in subjects with elevated TAG concentrations. To find a possible explanation, we explored changes in serum lipoprotein profiles,second as measured with nuclear magnetic resonance. For this, serum samples from two parallel-designed controlled studies were evaluated before and 8 from weeks after the consumption of plant stanol esters. In the first study, dyslipidemic metabolic syndrome subjects participated and in the consumption second study normolipidemic subjects. In metabolic syndrome subjects, plant stanol esters lowered concentrations of large (>60 nm) and medium (35-60 nm) nm) VLDL particles as compared to controls. In normolipidemic subjects, the serum concentration of large VLDL-1 particles was also lowered,serum although less pronounced. Based on these findings, we hypothesize that the effect of plant stanol esters on serum TAG concentrations but origins from a lowered hepatic production of large TAG-rich VLDL-1 particles.

BACKGROUND:ileostomic Enterocytes are exposed to antigens present in the intestinal lumen, like beta-glucans that are carbohydrate structures present not only in not the cell wall of yeast and fungi but also in cereals. Beta-glucans are known for their immune modulating properties and showed we have earlier reported an increased immune response by enterocytes after addition of fecal water prepared from ileostomic contents obtained the from participants consuming an oat beta-glucan diet versus a placebo diet. We hypothesized that our observation of immune stimulating effects and by oat beta-glucan in enterocytes was mediated through the beta-glucan receptor dectin-1. METHODS: Presence of dectin-1 in enterocytes was examined However, by reverse transcriptase PCR, western blot, and flow cytometry followed by an evaluation of the functional involvement of dectin-1 by consuming using dectin-1 inhibitors during fecal water incubations. RESULTS: Reverse transcriptase PCR and western blot analysis showed dectin-1 presence in the present INT407 and Caco-2 NF-kappaB reporter enterocyte cell lines. Moreover, human enterocytes isolated from ileum or colon biopsies also contained dectin-1 intestinal protein. However, dectin-1 expression could not be confirmed by flow cytometry in INT407 cells, suggesting that in these cell lines INT407 dectin-1 is not expressed at the extracellular membrane. Furthermore, dectin-1 inhibitors did not suppress the beta-glucan containing fecal water-induced IL-8 in production by INT407 cells and NF-kappaB transactivation by Caco-2 NF-kappaB reporter cells. CONCLUSION: INT407 and Caco-2 NF-kappaB reporter cells seem in to express no functional dectin-1. The absence of this pattern recognition receptor may function to protect the intestine against inflammatory prepared damage, as the dectin-1 ligand beta-glucan is largely present in the intestinal lumen.

Recent present animal and human studies have shown that plant sterols and stanols, which are used as functional food ingredients to lower functional increased LDL cholesterol concentrations, pass the blood-brain barrier. Whether this affects neurocognitive functioning and mental well-being in humans has, to the our knowledge, never been investigated. The aim of the present study was therefore to examine the effects of long-term plant 2.5 sterol or stanol consumption on neurocognitive functioning and mood in a randomized, double-blind, placebo-controlled dietary intervention trial. To this end,assigned hypercholesterolemic individuals, aged 43-69 y, receiving stable statin treatment were randomly assigned to an 85-wk supplementation with margarines enriched with means plant sterol esters (2.5 g/d), plant stanol esters (2.5 g/d), or placebo. At baseline and at the end of the to intervention period, all participants underwent a cognitive assessment. In addition, subjective cognitive functioning and mood were assessed by means of as questionnaires (Cognitive Failure Questionnaire and depression subscale of the Symptom Checklist 90, respectively). Long-term supplementation with plant sterol or stanol statin esters did not affect cognitive performance (memory, simple information processing speed, complex information processing speed, Letter-Digit Substitution test performance), subjective of cognitive functioning, or mood. In conclusion, the present results indicate that long-term use of plant sterols or stanols at recommended receiving intakes of 2.5 g/d does not affect neurocognitive functioning or mood in hypercholesterolemic individuals receiving statin treatment.

BACKGROUND:intestine. Increasing HDL cholesterol concentrations by stimulating de-novo apolipoprotein A-I (apoA-I) production in the liver and/or in the small intestine is small a potential strategy to reduce coronary heart disease risk. Although there is quite some knowledge concerning regulatory effects in the lack liver, less is known concerning potential agents that could elevate de-novo apoA-I production in the small intestine. METHODS: Therefore, we cell compared side-by-side effects of various peroxisome proliferator-activated receptor (PPAR)alpha, PPARgamma, retinoid-X-receptor alpha, and farnesoid-X-receptor agonists on de-novo apoA-I production in WY14643 differentiated CaCo-2 and HepG2 cells. RESULTS: For PPARa agonists, we showed that GW7647 elevated apoA-I concentrations in the medium of HepG2 both cell models, whereas WY14643 elevated only de-novo apoA-I concentrations in differentiated CaCo-2 cells. Unexpectedly, fenofibric acid lowered apoA-I medium side-by-side concentrations in both cell lines, which could not be explained by a lack of PPAR transactivation or a lack of the retinoid-X-receptor a activation. For farnesoid-X-receptor agonists, chenodeoxycholic acid strongly reduced apoA-I concentrations both in differentiated CaCo-2 and HepG2 cells, whereas cell GW4064 and taurocholate only lowered apoA-I in CaCo-2 cells (GW4064) or in HepG2 cells (taurocholate). However, overall effects of all cells individual components on apoA-I production in differentiated CaCo-2 and HepG2 cells were highly correlated (r = .68; P = .037;between N=9). CONCLUSION: We conclude that differentiated CaCo-2 cells are suitable models to study de-novo small intestinal apoA-I production in vitro intestine enabling the possibility to screen for potential bioactive dietary components. This cell model may also determine small-intestinal-specific effects, as some in discrepancy was found between both cell models.

We esters evaluated the effects of 2 commonly available strategies (plant stanol ester drink and 10 mg simvastatin) on coronary heart disease heart (CHD) risk variables in participants with metabolic syndrome. Metabolic syndrome patients are at increased risk to develop CHD, partly due (2. to high triacylglycerol (TAG) and low HDL cholesterol (HDL-C) concentrations and a low-grade inflammatory profile. Effects of plant stanol esters in on TAG concentrations in these participants are unknown. After a 3-wk run-in period in which individuals consumed placebo yogurt drinks simvastatin and placebo capsules, participants were randomly divided into 4 groups: placebo (n = 9), simvastatin + placebo drink (n =were 10), placebo + stanol drink (n = 9), and simvastatin + stanol drink (n = 8). After 9 wk, we these evaluated the effects on serum lipids, low-grade inflammation, and endothelial dysfunction markers. In metabolic syndrome patients, stanol esters (2. g/d),coronary simvastatin, or the combination lowered non-HDL-C by 12.8%(P = .011), 30.7%(P < .001), and 35.4%(P < .001),risk respectively, compared with placebo. TAG were lowered by 27.5%(P = .044), 21.7%(P = .034), and 32.7%(P <and .01), respectively. The total-:HDL-C ratio was significantly lowered in all 3 intervention groups. We found no treatment effects on the this apolipoprotein CII:CIII ratio, cholesterol ester transfer protein mass, FFA concentrations, and markers for low-grade inflammation or endothelial dysfunction. This study disease shows that in metabolic syndrome patients, plant stanol esters lower not only non-HDL-C, but also TAG. Effects on TAG were of also present in combination with statin treatment, illustrating an additional benefit of stanol esters in this CHD risk population.

ABSTRACT:patients Background Rosiglitazone not only improves insulin-sensitivity, but also exerts anti-inflammatory effects. We have now examined in type 2 diabetic patients patients if these effects are reflected by changes in mRNA expression in peripheral blood mononuclear cells (PBMCs) to see if these with cells can be used to study these anti-inflammatory effects at the molecular level in vivo. Method Eleven obese type 2 results diabetic patients received rosiglitazone (2x4 mg/d) for 8 weeks. Fasting blood samples were obtained before and after treatment. Ten obese hyperinsulinemic-euglycemic control subjects served as reference group. The expression of NFkappaB-related genes and PPARgamma target genes in PBMCs, plasma TNFalpha, IL6,significantly MCP1 and hsCRP concentrations were measured. In addition, blood samples were obtained after a hyperinsulinemic-euglycemic clamp. Results Rosiglitazone reduced plasma 8 MCP1 and hsCRP concentrations in diabetic patients (-9.5 +/- 5.3 pg/mL, p= .043 and -1.1 +/- .3 mg/L p= .003), respectively). For diabetic hsCRP, the concentration became comparable with the non-diabetic reference group. However, of the 84 NFkappaB-related genes that were measured in diabetic PBMCs from type 2 diabetic subjects, only RELA, SLC20A1, INFgamma and IL1R1 changed significantly (p< .05). In addition, PPARgamma and its LPL) target genes (CD36 and LPL) did not change. During the clamp, insulin reduced plasma MCP1 concentration in the diabetic and type reference groups (-9.1 +/- 1.8%, p= .001 and -11.1 +/- 4.1%, p= .023, respectively) and increased IL6 concentration in the reference group if only (23.5 +/- 9. %, p= .028). Conclusions In type 2 diabetic patients, the anti-inflammatory effect of rosiglitazone is not reflected by 2 changes in NFkappaB and PPARgamma target genes in PBMCs in vivo. Furthermore, our results do not support that high insulin its concentrations contribute to the pro-inflammatory profile in type 2 diabetic patients.

Observational pigment epidemiological studies have shown that low carotenoid intake and/or low carotenoid blood levels increase the risk of degenerative diseases like increase age-related macular degeneration. Functional foods enriched with plant sterol or stanol esters may lower serum concentrations of fat-soluble carotenoids. Theoretically,added as a result the macular pigment optical density (MPOD), a marker for eye health, may change. We carried out a concentrations double-blind placebo-controlled human intervention trial with a duration of 18 months to evaluate the possible effects of plant stanol and serum sterol esters on serum lutein/zeaxanthin concentration in relation to the MPOD. Forty-seven subjects were randomly assigned to one of the evaluated three treatment groups: margarine without added plant sterols or stanols, plant sterol-enriched margarine, or plant stanol-enriched margarine. Serum cholesterol and (MPOD), lutein/zeaxanthine concentrations and the MPOD were evaluated at baseline and at study end. Changes in lipid-adjusted serum lutein/zeaxanthine concentrations between levels baseline and study end differed significantly between the three groups (P = .001). We found no differences in the MPOD affect between the three treatment groups, despite the differences in both absolute and cholesterol-standardized serum lutein/zeaxanthine concentrations. This shows that the in observed reduction in serum carotenoid concentrations during 18 months consumption of these functional foods does not affect MPOD.

We 4 have earlier demonstrated that muesli enriched with oat beta-glucan effectively lowered serum LDL cholesterol. Addition of plant stanols further lowered cholesterol. LDL cholesterol. Besides these hypocholesterolemic effects, beta-glucan and plant stanol esters (PSE) may also affect inflammatory processes. Forty-two mildly hypercholesterolemic expression subjects randomly consumed for 4 wk (crossover design) control muesli (4.8 g control fiber), beta-glucan muesli (4.8 g oat beta-glucan),with or combination muesli (4.8 g oat beta-glucan plus 1.4 g stanol as PSE). Changes in cytokine production (IL-6, IL-8, and LPS-stimulated TNF-alpha) of LPS-stimulated peripheral blood mononuclear cells (PBMC) and whole blood were evaluated, as well as changes in plasma high-sensitivity PBMC (hs)-CRP. Additionally, changes in expression profiles of 84 genes involved in atherosclerosis metabolism were assessed in isolated PBMC. IL-6, IL-8,control and TNF-alpha production by PBMC and whole blood after LPS stimulation did not differ between the treatments. Also high-sensitivity C-reactive LDL protein (hs-CRP) levels were similar. beta-Glucan consumption did not change gene expression, while only 3 genes (ADFP, CDH5, CSF2) out hypercholesterolemic of the 84 genes from the atherosclerotic risk panel were differentially expressed (p < .05) after consumption of PSE. Consumption not of beta-glucan with or without PSE did not influence inflammatory parameters in mildly hypercholesterolemic subjects.