Purpose: Blueberry and cranberry are rich in anthocyanins. The present study was to investigate the effects of anthocyanin extracts from blueberry and cranberry on body weight and gut microbiota.Methods: C57BL/6 J Mice were divided into six groups (n = 9 each) fed one of six diets namely low-fat diet (LFD), high-fat diet (HFD), HFD with the addition of 1% blueberry extract (BL), 2% blueberry extract (BH), 1% cranberry extract (CL), and 2% cranberry extract (CH), respectively.Results: Feeding BL and BH diets significantly decreased body weight gain by 20-23%, total adipose tissue weight by 18-20%, and total liver lipids by 16-18% compared with feeding HFD. Feeding CH diet but not CL diet reduced the body weight by 27%, accompanied by a significant reduction of total plasma cholesterol by 25% and tumor necrosis factor alpha (TNF-a) by 38%. The metagenomic analysis showed that the supplementation of blueberry and cranberry anthocyanin extracts reduced plasma lipopolysaccharide concentration, accompanied by a reduction in the relative abundance of Rikenella and Rikenellaceae. Dietary supplementation of berry anthocyanin extracts promoted the growth of Lachnoclostridium, Roseburia, and Clostridium_innocuum_group in genus level, leading to a greater production of fecal short-chain fatty acids (SCFA).Conclusions: It was concluded that both berry anthocyanins could manage the body weight and favorably modulate the gut microbiota at least in mice..

The high polyphenols content of cranberry accounts for its strong antioxidant activity underlying the beneficial health effects of this fruit. Rotenone (ROT) is a specific inhibitor of mitochondrial complex I in the brain which leads to the generation of oxidative stress. To date, there are few data indicating that toxicity of ROT is not limited to the brain but can also affect other tissues. We aimed to examine whether ROT-induced oxidative stress could be counteracted by cranberry juice not only in the brain but also in the liver and kidney. Wistar rats were given the combined treatment with ROT and cranberry juice (CJ) for 35 days. Parameters of antioxidant status were determined in the organs. ROT enhanced lipid peroxidation solely in the brain. The increase in the DNA damage was noticed in all organs examined and in leukocytes. The beneficial effect of CJ on these parameters appeared only in the brain. Additionally, CJ decreased the activity of serum hepatic enzymes. The effect of CJ on antioxidant enzymes was not consistent, however, in some organs, CJ reversed changes evoked by ROT. Summing up, ROT can cause oxidative damage not only in the brain but also in other organs. CJ demonstrated a protective effect against ROT-induced toxicity

The Vaccinium genus comprises more than 126 genera of perennial flowering plants that are commonly adapted to poor and acidic soils or epiphytic environments. Their molecular and genomic characterization is a result of the recent advent in next-generation sequencing technology. In the current research, extracts were prepared in different media, such as petroleum ether, methanol and ethanol. An extract of Vaccinium macrocarpon (cranberry) was used at a dose of 200-400 mg/kg by weight (B.wt). Levels of oxidative stress markers, i.e., superoxide dismutase (SOD), catalase (CAT), glutathione (GSH), advanced oxidation protein products (AOPPs) and malondialdehyde (MDA), were measured. A histopathological study of six vital organs in rats was also conducted. The results indicated that the antioxidant levels were lower in the group given only ethylene oxide (EtO) but higher in the groups receiving cranberry extract as a treatment. Major improvements were also observed in stress markers such as advanced oxidation protein products (AOPPs) and MDA following cranberry treatment. Histopathological changes induced by EtO were observed in the heart, kidney, liver, lung, stomach and testis and were reversed following cranberry treatment. The major toxic effects of EtO were oxidative stress and organ degeneration, as observed from various stress markers and histopathological changes. Our study showed that this extract contains strong antioxidant properties, which may contribute to the amelioration of the observed toxic effects..

Lead (Pb) has been identified as a hazardous heavy metal and a pollutant in the environment, especially due to its human activity. It poisons several physiological systems, such as the hepatic, renal, reproductive, as well as nervous systems, because of an elevation in oxidative damage caused by the formation of reactive oxygen species (ROS). Cranberry is a powerful antioxidant in addition to being a component of an anti-inflammatory disease treatments. The goal of this study was to see if cranberry extract could protect rats from toxicity caused by lead acetate. Addition of cranberry extract at a dose of 75 and 150 mg/kg to rats allowed to treat with lead acetate at a dose of 50 mg/kg to 6 weeks significantly protected the rats from the lead acetate-induced increase in both serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), lactate dehydrogenases (LDH), total and direct bilirubin, alkaline phosphatase (ALP), creatinine, urea, total cholesterol (TC), triglycerides (TG), LDL-C and VLDL-C in addition against an elevation of serum glucose, tumor necrosis factor-alpha (TNF-α) and malondialdehyde (MDA).Treatment with cranberry extract at a dose of 75 and 150 mg/kg also led to a valuable rise in serum total soluble protein, albumin, globulin, HDL-C, triiodothyronine (T3), total thyroxine (T4) as well as hepatic and renal tissue of reduced glutathione (GSH), superoxide dismutase (SOD), catalase activity (CAT) and total antioxidant capacity (TAC) as compared to lead acetate-treated rats. Cranberry has hepato-renal protective impacts in restoring liver and kidney function, according to histopathological evaluation of hepatic and renal tissues. These findings have shown, in conclusion, that cranberry extract has such a strong protective effect in rats suffering from hepato-renal toxicity caused by lead acetate.

The non-dialyzable material (NDM) of polyphenol-rich cranberry extract (CRE) powder (NDM-CRE) was studied for its effect of inducing body weight (BW) loss in 13 different mouse lines with well-defined genetically diverse backgrounds, named the collaborative cross (CC). From the age of 8 weeks, the mice were maintained on a high-fat diet (HFD) for 18 weeks, to induce obesity, and BW was measured biweekly. From week 12, CRE was injected intraperitoneally (IP) (50 mg kg-1) 3 times a week per mouse for a 6 week period. Statistical analysis results have shown a significant increase in body weight between week 0 and week 12; the increase in BW of 13 lines of mice on HFD was in the range of 10.41% to 68.65% for males and 9.78% to 64.74% for females. After injecting NDM-CRE extract, our analysis has shown an induced change in BW between week 12 and week 18. In males, NDM-CRE caused a significant decrease in BW of 5 out of the 13 lines in the range of -5.68% to -16.69% and a significant increase of 8.31% in BW of one male line, whereas in seven lines there was no significant decrease (-2.14% to -4.09%). In females, NDM-CRE caused a significant decrease in BW of 5 out of the 13 lines in the range of -3.90% to -11.83%, whereas in eight lines there were no significant changes in BW and it ranged between -1.50% and 4.90%. The broad-sense heritability (H2) and genetic coefficient of variation (CVg) were estimated and found to be between 0.71 and 0.81 for H2, and 0.18 and 0.24 for CVg of females and males, respectively, with respect to the efficacy of NDM-CRE on body weight reduction. Our results have shown that hosts with different genetic backgrounds respond differently to body weight increase, as well as to NDM-CRE treatment for body weight reduction. These results provide a platform for assessing more CC lines and mapping genes underlying the efficacy of the NDM-CRE treatment as a way of understanding pharmacogenomics.

Lead poisonousness is a widely recognized type of heavy metal poisoning in humans and animals. So, this study aimed to assess the ameliorative role of cranberry extract use on hematological changes induced by lead acetate in rats. A total number of 40 adult male albino rats weighing approximately 200 +or- 20 g were randomly assigned into four groups; Normal control group, group 2; Positive control, lead acetate at a dose of (50 PPM) for 45 days, group 3; Lead acetate at a dose of (50 PPM) then Cranberry extract (75 mg/kg) for 45 days also group 4; Lead acetate (50 PPM) then Cranberry extract (150 mg/kg) for 45 days. Blood samples were collected in EDTA tubes for hematological examinations. Oral administration of lead acetate (50 PPM) significantly decreased total erythrocyte count, hemoglobin, packed cell volume and mean cell volume levels in comparison with the normal control group (P< 0.0001). Addition of cranberry extract at a dose of 75 and 150 mg/kg significantly increased the total erythrocyte count, hemoglobin, packed cell volume and mean cell volume levels in comparison with the positive control group (P< 0.0001). Oral administration of lead acetate (50 PPM) significantly increased total leukocytes count, lymphocyte, neutrophils, eosinophil and monocytes count in comparison with the normal control group (P< 0.0001). Addition of cranberry extract at a dose of 75 and 150 mg/kg significantly decreased the total leukocytes count, lymphocyte, neutrophils, eosinophil and monocytes count in comparison with the positive control group (P< 0.0001). Our results clearly indicate that cranberry extract ameliorates hematological changes in lead acetate-treated rats

The dramatic rise in the global occurrence of obesity and associated diseases calls for new strategies to promote weight loss. However, while the beneficial effects of weight loss are well known, rapid loss of fat mass can also lead to the endogenous release of liposoluble molecules with potential harmful effects, such as persistent organic pollutants (POP). The aim of this study was to evaluate the impact of a polyphenol-rich cranberry extract (CE) on POP release and their potential deleterious effects during weight loss of obese mice. C57BL/6 J mice were fed an obesogenic diet with or without a mixture of POP for 12 weeks and then changed to a low-fat diet to induce weight loss and endogenous POP release. The POP-exposed mice were then separated in two groups during weight loss, receiving either CE or the vehicle. Unexpectedly, despite the higher fat loss in the CE-treated group, the circulating levels of POP were not enhanced in these mice. Moreover, glucose homeostasis was further improved during CE-induced weight loss, as revealed by lower fasting glycemia and improved glucose tolerance as compared to vehicle-treated mice. Interestingly, the CE extract also induced changes in the gut microbiota after weight loss in POP-exposed mice, including blooming of Parvibacter, a member of the Coriobacteriaceae family which has been predicted to play a role in xenobiotic metabolism. Our data thus suggests that the gut microbiota can be targeted by polyphenol-rich extracts to protect from increased POP exposure and their detrimental metabolic effects during rapid weight loss

Berries are rich in polyphenols and plant cell wall polysaccharides (fibers), including cellulose, hemicellulose, arabinans and arabino-xyloglucans rich pectin. Most of polyphenols and fibers are known to be poorly absorbed in the small intestine and reach the colon where they interact with the gut microbiota, conferring health benefits to the host. This study assessed the contribution of polyphenol-rich whole cranberry and blueberry fruit powders (CP and BP), and that of their fibrous fractions (CF and BF) on modulating the gut microbiota, the microbial functional profile and influencing metabolic disorders induced by high-fat high-sucrose (HFHS) diet for 8 weeks. Lean mice-associated taxa, including Akkermansia muciniphila, Dubosiella newyorkensis, and Angelakisella, were selectively induced by diet supplementation with polyphenol-rich CP and BP. Fiber-rich CF also triggered polyphenols-degrading families Coriobacteriaceae and Eggerthellaceae. Diet supplementation with polyphenol-rich CP, but not with its fiber-rich CF, reduced fat mass depots, body weight and energy efficiency in HFHS-fed mice. However, CF reduced liver triglycerides in HFHS-fed mice. Importantly, polyphenol-rich CP-diet normalized microbial functions to a level comparable to that of Chow-fed controls. Using multivariate association modeling, taxa and predicted functions distinguishing an obese phenotype from healthy controls and berry-treated mice were identified. The enterotype-like clustering analysis underlined the link between a long-term diet intake and the functional stratification of the gut microbiota. The supplementation of a HFHS-diet with polyphenol-rich CP drove mice gut microbiota from Firmicutes/Ruminococcus enterotype into an enterotype linked to healthier host status, which is Prevotella/Akkermansiaceae. This study highlights the prebiotic role of polyphenols, and their contribution to the compositional and functional modulation of the gut microbiota, counteracting obesity..

Background: Although polyphenol-rich cranberry extracts reportedly have an antiobesity effect, the exact reason for this remains unclear. Objectives: In light of the reported health benefits of the polyphenolic compounds in cranberry, we investigated the effects and mechanism of a cranberry polyphenolic extract (CPE) in high-fat diet (HFD)-fed obese mice. Methods: The distributions of individual CPE compounds were characterized by HPLC fingerprinting. Male C57BL/6J mice (4 wk old) were fed for 16 wk normal diet (ND, 10% fat energy) or HFD (60% fat energy) with or without 0.75% CPE in drinking water (HFD + CPE). Body and adipose depot weights, indices of glucose metabolism, energy expenditure (EE), and expression of genes related to brown adipose tissue (BAT) thermogenesis, and inguinal/epididymal white adipose tissue (iWAT/eWAT) browning were measured. Results: After 16 wk, the body weight was 22.5% lower in the CPE-treated mice than in the HFD group but remained 17.9% higher than in the ND group. CPE treatment significantly increased EE compared with that of the ND and HFD groups. The elevated EE was linked with BAT thermogenesis, and iWAT/eWAT browning, shown by the induction of thermogenic genes, especially uncoupling protein 1 (Ucp1), and browning-related genes, including Cd137, a member of the tumor necrosis factor receptor superfamily (Tnfrsf9). The mRNA expression and abundance of uncoupling protein 1 in BAT of CPE-fed mice were 5.78 and 1.47 times higher than in the HFD group, and 0.61 and 1.12 times higher than in the ND group, respectively. Cd137 gene expression in iWAT and eWAT of CPE-fed mice were 2.35 and 3.13 times higher than in the HFD group, and 0.84 and 1.39 times higher than in the ND group, respectively. Conclusions: Dietary CPE reduced but did not normalize HFD-induced body weight gain in male C57BL/6J mice, possibly by affecting energy metabolism..

Increased consumption of fruits may decrease the risk of chronic inflammatory diseases including inflammatory bowel disease (IBD). Gut microbiota dysbiosis plays an important etiological role in IBD. However, the mechanisms of action underlying the anti-inflammatory effects of dietary cranberry (Vaccinium macrocarpon) in the colon and its role on gut microbiota were unclear. In this study, we determined the anti-inflammatory efficacy of whole cranberry in a mouse model of dextran sodium sulfate (DSS)-induced colitis, as well as its effects on the structure of gut microbiota. The results showed that dietary cranberry significantly decreased the severity of colitis in DSS-treated mice, evidenced by increased colon length, and decreased disease activity and histologic score of colitis in DSS-treated mice compared to the positive control group (p<0.05). Moreover, the colonic levels of pro-inflammatory cytokine (IL-1 beta , IL-6 and TNF- alpha ) were significantly reduced by cranberry supplementation (p<0.05). Analysis of the relative abundance of fecal microbiota in phylum and genus levels revealed that DSS treatment significantly altered the microbial structure of fecal microbiota in mice. alpha diversity was significantly decreased in the DSS group, compared to the healthy control group. But, cranberry treatment significantly improved DSS-induced decline in alpha -diversity. Moreover, cranberry treatment partially reversed the change of gut microbiota in colitic mice by increasing the abundance of potential beneficial bacteria, for example, Lactobacillus and Bifidobacterium, and decreasing the abundance of potential harmful bacteria, such as Sutterella and Bilophila. Overall, our results for the first time demonstrated that modification of gut microbiota by dietary whole cranberry might contribute to its inhibitory effects against the development of colitis in DSS-treated mice.