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

BACKGROUND:38%, Many studies on the health effects of the glycemic index (GI) are confounded by differences in the intakes of other 37+/-10 macronutrients and fibre. Little data exist about the within- and between-subject variability of the GI. OBJECTIVE: Our objectives were therefore the (i) to calculate the GI of eight commonly used food products with similar macronutrient and fibre composition, but with different (CHO). sources of carbohydrates (ii) to examine the inter- and intra-individual variability of the incremental area under the curve (iAUC) after and consuming the reference solution (iii) to compare the effect of three different methods on 2-h postprandial blood glucose responses. DESIGN:and Four groups of 10 healthy subjects consumed in random order the increased (iGI) and decreased GI (dGI) variants and twice (mean+/-standard a glucose solution. All products consisted of 25g available carbohydrates (CHO). For the fruit drink, glucose values were simultaneously analyzed 80%. using venous and capillary blood samples, and by using a continuous glucose monitoring system (CGMS). RESULTS: The GIs for increased RESULTS: and decreased variants were (mean+/-standard error of the mean (SEM)) 69+/-15 and 40+/-4 for bread, 86+/-14 and 48+/-8 for fruit three drink, 51+/-12 and 20+/-4 for cake, and 63+/-17 and 37+/-10 for cookie. The inter- and intra-individual coefficient of variation (CV)increased of the iAUCs of the reference solution was large and varied respectively between 13 and 38%, and between 33 and respectively 80%. CONCLUSIONS: These data suggest that the GI is difficult to use at the individual level.

AbstractSkeletal and muscle triglyceride accumulation is associated with insulin resistance in obesity. Recently, it has been suggested that alpha lipoic acid (ALA)increased improves insulin sensitivity by lowering triglyceride accumulation in non-adipose tissues via activation of skeletal muscle AMP-activated protein kinase (AMPK). We if examined whether chronic ALA supplementation prevents muscular lipid accumulation that is associated with high-fat diets via activation of AMPK. In p< .001). addition, we tested if ALA supplementation was able to improve insulin sensitivity in rats fed low- and high-fat diets.Supplementing male or Wistar rats with .5% ALA for eight weeks significantly reduced body weight, both on low- and high-fat diets (-24% LFD+ALA These vs. LFD, p< .01, and -29% HFD+ALA vs. HFD, p< .001). Oil red O lipid staining revealed a three-fold higher lipid content glucose in skeletal muscle after HFD compared to LFD and ALA-supplemented groups (p< .05). ALA improved whole body glucose tolerance ( approximately glucose 20% lower total AUC in ALA supplemented groups vs. controls, p< .05). These effects were not mediated by increased muscular AMPK and activation or ALA-induced improvement of muscular insulin sensitivity. To conclude, the prevention of high-fat diet-induced muscular lipid accumulation and the low- improved whole body glucose tolerance are likely secondary effects due to the anorexic nature of ALA.

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

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

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

The to metabolic syndrome is an important risk factor for type 2 diabetes mellitus and CVD. Epidemiological studies have now suggested protective provided effects of dairy product consumption on the development of this syndrome. Here we review the physiological effects and possible mechanisms evidence involved of three main dairy constituents (Ca, protein, fat) on important components of the metabolic syndrome. Ca supplements improve the reduced serum lipoprotein profile, particularly by decreasing serum total and LDL-cholesterol concentrations. They also lower systolic and diastolic blood pressure. Insufficient reduce evidence exists for a significant role of Ca supplements or dairy in body-weight management. Effects of Ca may be related such to intestinal binding to fatty acids or bile acids, or to changes in intracellular Ca metabolism by suppressing calciotropic hormones.inconsistently Dietary proteins may increase satiety in both the short and longer term, which may result in a reduced energy intake.effects They have also been reported to improve the serum lipoprotein profile as compared with carbohydrates. Dairy proteins are precursors of peptides, angiotensin-I-converting enzyme-inhibitory peptides, which may lower blood pressure. Such effects, however, have inconsistently been reported in human studies. Finally, conjugated of linoleic acid, which effectively lowers body weight in animals, has no such effect in humans in the quantities provided by blood dairy products. To reduce the intake of SFA, the consumption of low-fat instead of high-fat dairy products is recommended. In more conclusion, more research is warranted to better understand the physiological effects and the mechanisms involved of dairy products in the exists prevention and treatment of the metabolic syndrome.

Beneficial Keijer, effects of low glycemic index (GI) diets in rodents have been studied using healthy low-fat diets, while the effects might the be different on high-fat diets inducing progression of insulin resistance. We fed C57BL/6J male mice high-fat low/high-GI (LGI/HGI) diets for insulin 13 wk. Glucose and insulin tolerance and serum substrates, including adipokines, were measured longitudinally. The LGI group showed a significantly tissue higher glucose tolerance from wk 2 onwards, which was supported by lower serum insulin and free fatty acids levels at carbohydrate, 8 wk, and a tendency for lower leptin levels, while resistin levels remained similar. At 11 wk, when differences in modulation serum resistin started to increase, differences in serum insulin were diminished. Although food intake was similar throughout the study, body higher. weights and epididymal adipose tissue mass became significantly lower in the LGI group at necropsy. Several serum substrates and adipose high-fat, tissue leptin mRNA levels, as analyzed by Q-PCR, were, again, significantly lower, whereas adiponectin mRNA levels were higher. Taken together,Q-PCR, an LGI high-fat diet maintains higher glucose tolerance and insulin sensitivity via adipose tissue modulation solely because of a difference lower in the type of carbohydrate, supporting a nutritional approach in the fight against insulin resistance.-Van Schothorst, E. M., Bunschoten, A.,lower, Schrauwen, P., Mensink, R. P., Keijer, J. Effects of a high-fat, low versus high glycemic index diet: retardation of insulin P., resistance involves adipose tissue modulation.

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