Chronic intake of high-dose of blueberry leaf extract does not augment the harmful effects of ethanol in rats.

Excessive alcohol consumption is a risk factor for liver diseases. Enhancement of alcohol metabolism could be an effective strategy to prevent these adverse effects since it promotes the clearance of ethanol and acetaldehyde from the serum. Polyphenol-rich products have shown to protect against alcohol-related liver damage. Blueberry leaves have attracted attention as they are rich polyphenols such as proantocyanidins and chlorogenic acid. In this study, we investigated the effects of a high dose of blueberry leaf extract (BLEx) on alcohol metabolism during chronic intake of ethanol. Seven-week old Sprague-Dawley (SD) rats were divided into four groups: normal liquid diet group (NLD), normal liquid diet + BLEx group (NLD + BLEx), alcohol liquid diet group (ALD), and alcohol liquid diet + BLEx (ALD + BLEx). Then, rats were fed experimental diet for 5 weeks and at the end of feeding period, body weight, food intake, liver weight, indices of liver injury, expression and activity of alcohol metabolism-related and anti-oxidative enzymes, and levels of carbonyl protein, triglyceride (TG), and total cholesterol (T-Chol) were measured. Body weight and food intake decreased, whereas liver aldehyde dehydrogenase (ALDH) activity, liver microsomal cytochrome P450 2E1 (CYP2E1) protein and mRNA expression, and heme oxygenase 1 (HO-1) mRNA expression were upregulated by ethanol intake. Dietary BLEx, however, did not affect any of these ethanol-related changes. Indices of liver injury, expression and activity of other alcohol metabolism-related enzymes, liver carbonyl protein, TG, and T-Chol levels were not altered by ethanol and BLEx. Thus, chronic BLEx intake does not ameliorate the harmful effects of ethanol.

Blueberry Leaf Polyphenols Prevent Body Fat Accumulation in Mice Fed High-fat, High-sucrose Diet.

Blueberry leaf is currently a popular dietary supplement. Effects of dietary blueberry leaf and its active components on body fat accumulation were examined. C57BL/6J mice were fed high-fat, high-sucrose diet with or without 3% blueberry leaf extract (BLEx) or 3% concentrated-polyphenolic BLEx (CP BLEx) for 8 weeks. Compared to mice fed a high-fat, high-sucrose diet without blueberry leaf, BLEx and CP BLEx significantly reduced body weight and adipose tissue weight gain. Adipocytes were also smaller and and liver lipid accumulatioin was significantly inhibited in mice fed either BLEx or CP BLEx. These effects tended to be more pronounced in mice fed CP BLEx compared to in mice fed BLEx. Together, results suggest that blueberry leaf inhibits body fat accumulation typically observed in mice fed a high-fat, high-sucrose diet, and that inhibition is attributable to polyphenolic components in leaf extracts.

Vaccinium ashei leaves extract alleviates insulin resistance via AMPK independent pathway in C2C12 myotube model.

Blueberry (Vaccinium ashei) leaf has recently attracted attention as an anti-obesity food component. In this study, we examined the effects of blueberry leaf extract (BLEx) on insulin signaling in C2C12 differentiated myoblasts. The results showed that BLEx promotes the intracellular uptake of 2-[N-(7-Nitrobenz-2-oxa-1,3-diazol-4-yl)amino]-2-deoxy-D-glucose (2-NBDG) and phosphorylation of Akt under insulin stimulation. In addition, pretreatment with BLEx ameliorated TNF-α-nduced insulin resistance with regard to 2-NBDG uptake and Akt phosphorylation. Moreover, BLEx prevented the TNF-α-induced activation of JNK and NF-kB pathways and phosphorylation of IRS-1 at serine residue. BLEx failed to induce phosphorylation of AMPK as well as did not prevent the restoration of 2-NBDG uptake under TNF-α-induced insulin resistance. Overall, skeletal muscle is a putative target for the anti-diabetic effect of BLEx by amelioration of insulin resistance.

Supplemental psyllium fibre regulates the intestinal barrier and inflammation in normal and colitic mice.

Our previous study demonstrated that supplemental psyllium fibre increased cytoprotective heat-shock protein (Hsp) 25 levels in the intestinal cells of mice. Here, we examined the effect of psyllium fibre on colonic gene and protein expression and faecal microbiota in normal and colitic mice to improve the understanding of the preventive role of the supplement. DNA microarray analysis revealed that a 10 % psyllium fibre diet administered for 5 d up-regulated eleven extracellular matrix (ECM)-associated genes, including collagens and fibronectins, in normal mice. Acute colitis was induced using dextran sodium sulphate (DSS) in mice that were administered a pre-feeding 5 to 10 % psyllium fibre diet for 5 d. Psyllium fibre partially ameliorated or resolved the DSS-induced colon damage and inflammation characterised by body weight loss, colon shortening, increased levels of pro-inflammatory cytokines and decreased tight junction protein expression in the colon. Analysis of faecal microbiota using denaturing gradient gel electrophoresis of the PCR-amplified 16S rRNA gene demonstrated that psyllium fibre affected the colonic microbiota. Intestinal permeability was evaluated by growing intestinal Caco-2 cell monolayers on membrane filter supports coated with or without fibronectin and collagen. Cells grown on collagen and fibronectin coating showed higher transepithelial electrical resistance, indicating a strengthening of barrier integrity. Therefore, increased Hsp25 levels and modification of colonic ECM contribute to the observed psyllium-mediated protection against DSS-induced colitis. Furthermore, ECM modification appears to play a role in the strengthening of the colon barrier. In conclusion, psyllium fibre may be useful in the prevention of intestinal inflammatory diseases.

Dietary psyllium fiber increases intestinal heat shock protein 25 expression in mice.

Heat shock proteins (HSPs) protect intestinal epithelial cell function, integrity and viability against many forms of stress. We hypothesized that dietary fibers (DFs) in the diet may increase HSP expression, since DFs are known to exhibit beneficial effects on intestinal health. The present study investigated the regulation of intestinal HSP expression by DFs, particularly psyllium fiber. Feeding psyllium fiber for 5 d increased HSP25 expression, but not HSP32 and HSP70 expression in the jejunum, ileum, and colon of mice at both the protein and mRNA levels. The increases in HSP25 expression did not correlate with cecal organic acid production by microbial fermentation. The water-insoluble fraction of psyllium fiber largely contributed to the induction of HSP25 expression, but feeding with other water-insoluble DFs from beet, wheat, and oats failed to induce intestinal HSP25 expression. Although the water-holding capacity of psyllium fiber was much higher than those of the other water-insoluble DFs examined, the increase in HSP25 expression induced by feeding polycarbophil, which possesses a high water-holding capacity similar to that of psyllium fiber, was much lower than that induced by psyllium fiber. Finally, induction of malondialdehyde production by hydrogen peroxide, an oxidant, in the colon of mice fed psyllium fiber was lower than that in mice fed with the control diets. Taken together, feeding psyllium fiber, especially the water-insoluble fraction, increases intestinal HSP25 expression and suppresses oxidant-induced malondialdehyde production.