Impact of black raspberries on the normal and malignant Apc deficient murine gut microbiome

Abstract Objectives Approximately 1.4 million people suffer from inflammatory bowel disease, which is a major risk factor for developing colitis associated colorectal cancer (CAC). Dietary interventions with the goal to reduce colon inflammation and encourage gut microbiome homeostasis may be a strategy to reduce the risk of CAC. The antioxidants and anti-inflammatory compounds present in black raspberries (BRB) have demonstrated protective effects in the colon epithelium and may alter the composition of the gut microbiome. Previously, we showed that dietary supplementation with black raspberries significantly suppressed colitis and colon tumorigenesis promoted by the consumption of a Western type diet in mice. The goal of this study was to compare the efficacy of dietary intervention with whole, freeze-dried black raspberries on colitis and colon tumorigenesis in mice consuming either a standard diet or a Western type diet that emulates typical U.S. nutrient intakes. Methods C57BL/6 J male and female mice were fed a standard diet (AIN93G) or the total Western diet (TWD) supplemented with 0 to 10% (w/w) black raspberry powder for a total of 16 weeks. All mice were dosed with axozymethane and provided 1% dextran sodium sulfate in drinking water for 10 days to promote colonic inflammation and tumorigenesis. Results As previously observed, mice fed TWD experienced more pronounced symptoms of colitis with a 40% increase in the disease activity index (DAI) score. Preliminary analyses suggest that dietary supplementation with 10% BRB suppressed the DAI score in mice fed TWD such that the colitis symptoms in these mice were not apparently different compared to the AIN93G-fed controls. However, addition of 10% BRB did not appear to provide a benefit to mice fed the AIN basal diet. Composition of the fecal microbiome over the course of disease development will be determined by standard 16S rRNA sequencing, and assessment of tumor outcome is ongoing. Conclusions Consumption of a Western type diet increased symptoms of colitis, whereas dietary supplementation with 10% BRB appeared to ameliorate TWD-enhanced colitis in mice. Funding Sources USDA NIFA Grant# 2018-67017-27516 and UAES Project UTA-1178.

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Characterization of the Functional Changes in Mouse Gut Microbiome Associated with Increased Akkermansia muciniphila Population Modulated by Dietary Black Raspberries

ACS Omega ◽

10.1021/acsomega.8b00064 ◽

2018 ◽

Vol 3 (9) ◽

pp. 10927-10937 ◽

Cited By ~ 18

Author(s):

Pengcheng Tu ◽

Xiaoming Bian ◽

Liang Chi ◽

Bei Gao ◽

Hongyu Ru ◽

...

Keyword(s):

Gut Microbiome ◽

Functional Changes ◽

Black Raspberries ◽

Akkermansia Muciniphila

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Folate and vitamin B-12 deficiencies additively impaired memory function and disturbed the gut microbiota in amyloid-β infused rats

International Journal for Vitamin and Nutrition Research ◽

10.1024/0300-9831/a000624 ◽

2019 ◽

pp. 1-13 ◽

Cited By ~ 2

Author(s):

Sunmin Park ◽

Sunna Kang ◽

Da Sol Kim

Keyword(s):

Insulin Resistance ◽

Gut Microbiota ◽

Insulin Signaling ◽

Gut Microbiome ◽

Metabolic Diseases ◽

Memory Function ◽

Amyloid Β ◽

Impaired Memory ◽

Ca1 Region ◽

Folate And Vitamin B12

Abstract. Folate and vitamin B12(V-B12) deficiencies are associated with metabolic diseases that may impair memory function. We hypothesized that folate and V-B12 may differently alter mild cognitive impairment, glucose metabolism, and inflammation by modulating the gut microbiome in rats with Alzheimer’s disease (AD)-like dementia. The hypothesis was examined in hippocampal amyloid-β infused rats, and its mechanism was explored. Rats that received an amyloid-β(25–35) infusion into the CA1 region of the hippocampus were fed either control(2.5 mg folate plus 25 μg V-B12/kg diet; AD-CON, n = 10), no folate(0 folate plus 25 μg V-B12/kg diet; AD-FA, n = 10), no V-B12(2.5 mg folate plus 0 μg V-B12/kg diet; AD-V-B12, n = 10), or no folate plus no V-B12(0 mg folate plus 0 μg V-B12/kg diet; AD-FAB12, n = 10) in high-fat diets for 8 weeks. AD-FA and AD-VB12 exacerbated bone mineral loss in the lumbar spine and femur whereas AD-FA lowered lean body mass in the hip compared to AD-CON(P < 0.05). Only AD-FAB12 exacerbated memory impairment by 1.3 and 1.4 folds, respectively, as measured by passive avoidance and water maze tests, compared to AD-CON(P < 0.01). Hippocampal insulin signaling and neuroinflammation were attenuated in AD-CON compared to Non-AD-CON. AD-FAB12 impaired the signaling (pAkt→pGSK-3β) and serum TNF-α and IL-1β levels the most among all groups. AD-CON decreased glucose tolerance by increasing insulin resistance compared to Non-AD-CON. AD-VB12 and AD-FAB12 increased insulin resistance by 1.2 and 1.3 folds, respectively, compared to the AD-CON. AD-CON and Non-AD-CON had a separate communities of gut microbiota. The relative counts of Bacteroidia were lower and those of Clostridia were higher in AD-CON than Non-AD-CON. AD-FA, but not V-B12, separated the gut microbiome community compared to AD-CON and AD-VB12(P = 0.009). In conclusion, folate and B-12 deficiencies impaired memory function by impairing hippocampal insulin signaling and gut microbiota in AD rats.

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