scholarly journals Dietary Interventions to Prevent High Fructose Diet-associated Worsening of Colitis and Colitis-associated Tumorigenesis in Mice

2021 ◽  
Author(s):  
Ryohei Nishiguchi ◽  
Srijani Basu ◽  
Hannah A Staab ◽  
Naotake Ito ◽  
Xi Kathy Zhou ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
Control Diet ◽  
Experimental Colitis ◽  
Protective Effects ◽  
Diet Change ◽  
Chronic Colitis ◽  
Acute Colitis ◽  
High Fructose Diet ◽  
High Consumption ◽  
High Fructose

Abstract Diet is believed to be an important factor in the pathogenesis of Inflammatory Bowel Disease. High consumption of dietary fructose has been shown to exacerbate experimental colitis, an effect mediated through the gut microbiota. This study evaluated whether dietary alterations could attenuate the detrimental effects of a high fructose diet (HFrD) in experimental colitis. First, we determined whether the pro-colitic effects of a HFrD could be reversed by switching mice from a HFrD to a control diet. This diet change completely prevented HFrD-induced worsening of acute colitis, in association with a rapid normalization of the microbiota. Second, we tested the effects of dietary fiber, which demonstrated that psyllium was the most effective type of fiber for protecting against HFrD-induced worsening of acute colitis, compared to pectin, inulin or cellulose. In fact, supplemental psyllium nearly completely prevented the detrimental effects of the HFrD, an effect associated with a shift in the gut microbiota. We next determined whether the protective effects of these interventions could be extended to chronic colitis and colitis-associated tumorigenesis. Using the azoxymethane/dextran sodium sulfate model, we first demonstrated that HFrD feeding exacerbated chronic colitis and increased colitis-associated tumorigenesis. Using the same dietary changes tested in the acute colitis setting, we also showed that mice were protected from HFrD-mediated enhanced chronic colitis and tumorigenesis, upon either diet switching or psyllium supplementation. Taken together, these findings suggest that high consumption of fructose may enhance colon tumorigenesis associated with long-standing colitis, an effect that could be reduced by dietary alterations.

scholarly journals Dietary resveratrol attenuation of intestinal inflammation and oxidative damage is linked to the alteration of gut microbiota and butyrate in piglets challenged with deoxynivalenol

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Yueqin Qiu ◽  
Jun Yang ◽  
Li Wang ◽  
Xuefen Yang ◽  
Kaiguo Gao ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
Oxidative Damage ◽  
Protein Expression ◽  
Intestinal Inflammation ◽  
Control Diet ◽  
Intestinal Barrier Function ◽  
Protective Effects ◽  
Gut Health ◽  
Antioxidant Genes ◽  
Mrna And Protein Expression

Abstract Background Deoxynivalenol (DON) is a widespread mycotoxin that induces intestinal inflammation and oxidative stress in humans and animals. Resveratrol (RES) effectively exerts anti-inflammatory and antioxidant effects. However, the protective effects of RES on alleviating DON toxicity in piglets and the underlying mechanism remain unclear. Therefore, this study aimed to investigate the effect of RES on growth performance, gut health and the gut microbiota in DON-challenged piglets. A total of 64 weaned piglets [Duroc × (Landrace × Yorkshire), 21-d-old, 6.97 ± 0.10 kg body weight (BW)] were randomly allocated to 4 treatment groups (8 replicate pens per treatment, each pen containing 2 males; n = 16 per treatment) for 28 d. The piglets were fed a control diet (CON) or the CON diet supplemented with 300 mg RES/kg diet (RES group), 3.8 mg DON/kg diet (DON) or both (DON+RES) in a 2 × 2 factorial design. Results DON-challenged piglets fed the RES-supplemented diet had significantly decreased D-lactate concentrations and tumor necrosis factor alpha (TNF-α) and interleukin 1 beta (IL-1β) mRNA and protein expression, and increased zonula occludens-1 (ZO-1) mRNA and protein expression compared with those of DON-challenged piglets fed the unsupplemented diet (P < 0.05). Compared with unsupplemented DON-challenged piglets, infected piglets fed a diet with RES showed significantly decreased malondialdehyde (MDA) levelsand increased mRNA expression of antioxidant enzymes and antioxidant genes (i.e., GCLC, GCLM, HO-1, SOD1 and NQO-1) and glutamate-cysteine-ligase modulatory subunit (GCLM) protein expression (P < 0.05). Moreover, RES supplementation significantly abrogated the increase in the proportion of TUNEL-positive cells and the protein expression of caspase3 in DON-challenged piglets (P < 0.05). Finally, RES supplementation significantly increased the abundance of Roseburia and butyrate concentrations, while decreasing the abundances of Bacteroides and unidentified-Enterobacteriaceae in DON-challenged piglets compared with DON-challenged piglets alone (P < 0.05). Conclusions RES supplementation improved gut health in DON-challenged piglets by strengthening intestinal barrier function, alleviating intestinal inflammation and oxidative damage, and positively modulating the gut microbiota. The protective effects of RES on gut health may be linked to increased Roseburia and butyrate concentrations, and decreased levels of Bacteroides and unidentified-Enterobacteriaceae.

scholarly journals High-Fructose Diet Increases Inflammatory Cytokines and Alters Gut Microbiota Composition in Rats

2020 ◽  
Vol 2020 ◽  
pp. 1-10 ◽  
Author(s):  
Yong Wang ◽  
Wentao Qi ◽  
Ge Song ◽  
Shaojie Pang ◽  
Zhenzhen Peng ◽  
...  
Keyword(s):  
Uric Acid ◽  
Inflammatory Response ◽  
Gut Microbiota ◽  
Inflammatory Cytokines ◽  
Proinflammatory Cytokines ◽  
Lipid Accumulation ◽  
Fasting Blood Glucose ◽  
High Fructose Diet ◽  
Fructose Intake ◽  
High Fructose

High-fructose diet induced changes in gut microbiota structure and function, which have been linked to inflammatory response. However, the effect of small or appropriate doses of fructose on gut microbiota and inflammatory cytokines is not fully understood. Hence, the abundance changes of gut microbiota in fructose-treated Sprague-Dawley rats were analyzed by 16S rRNA sequencing. The effects of fructose diet on metabolic disorders were evaluated by blood biochemical parameter test, histological analysis, short-chain fatty acid (SCFA) analysis, ELISA analysis, and Western blot. Rats were intragastrically administered with pure fructose at the dose of 0 (Con), 2.6 (Fru-L), 5.3 (Fru-M), and 10.5 g/kg/day (Fru-H) for 20 weeks. The results showed that there were 36.5% increase of uric acid level in the Fru-H group when compared with the Con group. The serum proinflammatory cytokines (IL-6, TNF-α, and MIP-2) were significantly increased ( P < 0.05 ), and the anti-inflammatory cytokine IL-10 was significantly decreased ( P < 0.05 ) with fructose treatment. A higher fructose intake induced lipid accumulation in the liver and inflammatory cell infiltration in the pancreas and colon and increased the abundances of Lachnospira, Parasutterella, Marvinbryantia, and Blantia in colonic contents. Fructose intake increased the expressions of lipid accumulation proteins including perilipin-1, ADRP, and Tip-47 in the colon. Moreover, the higher level intake of fructose impaired intestinal barrier function due to the decrease of the expression of tight junction proteins (ZO-1 and occludin). In summary, there were no negative effects on body weight, fasting blood glucose, gut microbiota, and SCFAs in colonic contents of rats when fructose intake is in small or appropriate doses. High intake of fructose can increase uric acid, proinflammatory cytokines, intestinal permeability, and lipid accumulation in the liver and induce inflammatory response in the pancreas and colon.

The Adipokine Metrnl Ameliorates Chronic Colitis in Il-10–/– Mice by Attenuating Mesenteric Adipose Tissue Lesions During Spontaneous Colitis

2019 ◽  
Vol 13 (7) ◽  
pp. 931-941 ◽  
Author(s):  
Lugen Zuo ◽  
Sitang Ge ◽  
Yuanyuan Ge ◽  
Jingjing Li ◽  
Bing Zhu ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Activity Index ◽  
Disease Activity Index ◽  
Experimental Colitis ◽  
Protective Effects ◽  
Systemic Delivery ◽  
Chronic Colitis ◽  
Mesenteric Adipose Tissue ◽  
Proinflammatory Mediators ◽  
Ppar Γ

Abstract Background Crosstalk between mesenteric adipose tissue [MAT] and the intestines affects the progression of Crohn’s disease [CD]. The adipokine metrnl regulates adipocyte function and has anti-inflammatory activity. We aimed to explore metrnl expression in CD MAT, investigate the influence of metrnl on the experimental colitis disease course and determine the mechanism underlying this effect. Methods Metrnl expression in MAT specimens obtained from patients with and without CD was tested by immunohistochemistry. Male Il-10–/– mice with spontaneous enteritis were divided into positive control and metrnl-treated [Metrnl-Fc, 10 mg/kg/d, intraperitoneally, 8 weeks] groups. Age-matched male wild-type [WT] mice were used as negative controls. The effects of metrnl on enteritis and mesenteric lesions and the potential controlling mechanisms were evaluated. Results Metrnl expression was higher in human CD MAT than in control MAT. Systemic delivery of metrnl significantly ameliorated chronic colitis in Il-10–/– mice, as demonstrated by decreases in the disease activity index, inflammatory score and proinflammatory mediators. The protective effects of metrnl on MAT included reduced mesenteric hypertrophy, increased adipocyte size, improved adipocyte intrinsic function and ameliorated inflammation. Metrnl treatment activated STAT5/PPAR-γ signaling and promoted adipocyte differentiation in the MAT. Conclusions Metrnl expression was increased in the MAT of CD patients. Metrnl administration attenuated mesenteric lesions by promoting adipocyte function and differentiation partly through STAT5/PPAR-γ signaling pathway activation, thereby ameliorating CD-like colitis in mice.

scholarly journals Interaction with Gut Microbiota Plays a Causative Role in Grape Powder-Mediated Anti-Colitis Effects in Mice

2020 ◽  
Vol 4 (Supplement_2) ◽  
pp. 499-499
Author(s):  
Yiying Zhao ◽  
Qing Jiang
Keyword(s):  
Gut Microbiota ◽  
Rectal Bleeding ◽  
Tissue Damage ◽  
Control Diet ◽  
Spleen Weight ◽  
Causative Role ◽  
Protective Effects ◽  
Gut Health ◽  
Colonic Tissue ◽  
Microbial Composition

Abstract Objectives Gut microbiota is recognized to play a regulatory role in gut health and diseases. Previously, in a mouse model of colitis-associated colorectal cancer, we found that 10% grape powder (10GP) diet, which contains 0.033% polyphenols, attenuated colitis symptoms and restored colitis-changed gut microbial composition. However, it is not clear whether microbial modulation by 10GP directly contributes to the observed protective effects. To address the question, we compared the effect of 10GP on colitis in the presence and absence of antibiotics in mice. Methods Male Balb/c mice were gavaged with either water or antibiotic cocktail (ABX) daily for 7 days. For both water and ABX-treated mice, we further divided them into three subgroups: 1) healthy control (non-DSS), 2) mice fed with control diet and treated by 1.8% dextran sodium sulfate (DSS) in drinking water, and 3) mice fed with 10GP diet and treated with DSS (DSS-10GP). During the study, we monitored mice’ body weight and evaluated their colitis symptoms including stool consistency and rectal bleeding. All mice were sacrificed 9–10 days after DSS administration. Results Compared with conventional mice, ABX-treated mice had lowered liver and colon weight, increased level of fecal acetate and decreased levels of fecal butyrate and propionate. For both conventional and ABX-treated mice, DSS treatment caused colitis symptoms including rectal bleeding and diarrhea, colonic tissue damage, increased spleen weight and shortened colon length. Importantly, 10GP significantly alleviated DSS-induced colitis symptoms in non-ABX conventional mice, as indicated by attenuated fecal bleeding and diarrhea, reduced colonic tissue damage, and lowered spleen weight and colon weight to length ratio as inflammatory indexes. In contrast, these protective effects of 10GP were not observed in the ABX-treated mice. Conclusions 10GP diet showed protective effects against DSS-induced colitis in conventional mice, but not ABX-treated mice. This observation indicates that interaction between 10GP and gut microbiota plays a causative role in 10GP-mediated protective effects on colitis. Funding Sources California Table Grape Commission.

scholarly journals Kaempferol Alleviates Murine Experimental Colitis by Restoring Gut Microbiota and Inhibiting the LPS-TLR4-NF-κB Axis

2021 ◽  
Vol 12 ◽  
Author(s):  
Yifan Qu ◽  
Xinyi Li ◽  
Fengying Xu ◽  
Shimin Zhao ◽  
Xuemei Wu ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
Fecal Microbiota Transplantation ◽  
Inflammatory Diseases ◽  
Intestinal Barrier ◽  
Fluorescein Isothiocyanate ◽  
Experimental Colitis ◽  
Intestinal Microbiome ◽  
Attractive Alternative ◽  
Protective Effects ◽  
Linear Discriminant

Intestinal microbiota dysbiosis is an established characteristic of ulcerative colitis (UC). Regulating the gut microbiota is an attractive alternative UC treatment strategy, considering the potential adverse effects of synthetic drugs used to treat UC. Kaempferol (Kae) is an anti-inflammatory and antioxidant flavonoid derived from a variety of medicinal plants. In this study, we determined the efficacy and mechanism of action of Kae as an anti-UC agent in dextran sulfate sodium (DSS)-induced colitis mice. DSS challenge in a mouse model of UC led to weight loss, diarrhea accompanied by mucous and blood, histological abnormalities, and shortening of the colon, all of which were significantly alleviated by pretreatment with Kae. In addition, intestinal permeability was shown to improve using fluorescein isothiocyanate (FITC)–dextran administration. DSS-induced destruction of the intestinal barrier was also significantly prevented by Kae administration via increases in the levels of ZO-1, occludin, and claudin-1. Furthermore, Kae pretreatment decreased the levels of IL-1β, IL-6, and TNF-α and downregulated transcription of an array of inflammatory signaling molecules, while it increased IL-10 mRNA expression. Notably, Kae reshaped the intestinal microbiome by elevating the Firmicutes to Bacteroidetes ratio; increasing the linear discriminant analysis scores of beneficial bacteria, such as Prevotellaceae and Ruminococcaceae; and reducing the richness of Proteobacteria in DSS-challenged mice. There was also an evident shift in the profile of fecal metabolites in the Kae treatment group. Serum LPS levels and downstream TLR4-NF-κB signaling were downregulated by Kae supplementation. Moreover, fecal microbiota transplantation from Kae-treated mice to the DSS-induced mice confirmed the effects of Kae on modulating the gut microbiota to alleviate UC. Therefore, Kae may exert protective effects against colitis mice through regulating the gut microbiota and TLR4-related signaling pathways. This study demonstrates the anti-UC effects of Kae and its potential therapeutic mechanisms, and offers novel insights into the prevention of inflammatory diseases using natural products.

scholarly journals High-Fructose Diet Alters Intestinal Microbial Profile and Correlates with Early Tumorigenesis in a Mouse Model of Barrett’s Esophagus

2021 ◽  
Vol 9 (12) ◽  
pp. 2432
Author(s):  
Andrea Proaño-Vasco ◽  
Theresa Baumeister ◽  
Amira Metwaly ◽  
Sandra Reitmeier ◽  
Karin Kleigrewe ◽  
...  
Keyword(s):  
Mouse Model ◽  
Gut Microbiota ◽  
Microbial Communities ◽  
Barrett’S Esophagus ◽  
Barrett's Esophagus ◽  
Industrialized Countries ◽  
High Fructose Diet ◽  
Microbial Profile ◽  
High Fructose ◽  
Colon Cancer Cell Lines

Esophageal adenocarcinoma (EAC) is mostly prevalent in industrialized countries and has been associated with obesity, commonly linked with a diet rich in fat and refined sugars containing high fructose concentrations. In meta-organisms, dietary components are digested and metabolized by the host and its gut microbiota. Fructose has been shown to induce proliferation and cell growth in pancreas and colon cancer cell lines and also alter the gut microbiota. In a previous study with the L2-IL-1B mouse model, we showed that a high-fat diet (HFD) accelerated EAC progression from its precursor lesion Barrett’s esophagus (BE) through changes in the gut microbiota. Aiming to investigate whether a high-fructose diet (HFrD) also alters the gut microbiota and favors EAC carcinogenesis, we assessed the effects of HFrD on the phenotype and intestinal microbial communities of L2-IL1B mice. Results showed a moderate acceleration in histologic disease progression, a mild effect on the systemic inflammatory response, metabolic changes in the host, and a shift in the composition, metabolism, and functionality of intestinal microbial communities. We conclude that HFrD alters the overall balance of the gut microbiota and induces an acceleration in EAC progression in a less pronounced manner than HFD.

scholarly journals High Fat-High Fructose Diet-Induced Changes in the Gut Microbiota Associated with Dyslipidemia in Syrian Hamsters

Nutrients ◽  
2020 ◽  
Vol 12 (11) ◽  
pp. 3557
Author(s):  
Rachael G. Horne ◽  
Yijing Yu ◽  
Rianna Zhang ◽  
Nyan Abdalqadir ◽  
Laura Rossi ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
Dietary Intervention ◽  
High Fat ◽  
Low Fat ◽  
Microbial Composition ◽  
Syrian Hamsters ◽  
High Fructose Diet ◽  
Plasma Triglycerides ◽  
High Fructose ◽  
Induced Changes

Aim: The objective of this study was to characterize the early effects of high fructose diets (with and without high fat) on both the composition of the gut microbiota and lipid metabolism in Syrian hamsters, a reproducible preclinical model of diet-induced dyslipidemia. Methods: Eight-week-old male hamsters were fed diets consisting of high-fat/high-fructose, low-fat/high-fructose or a standard chow diet for 14 days. Stool was collected at baseline (day 0), day 7 and day 14. Fasting levels of plasma triglycerides and cholesterol were monitored on day 0, day 7 and day 14, and nonfasting levels were also assayed on day 15. Then, 16S rRNA sequencing of stool samples was used to determine gut microbial composition, and predictive metagenomics was performed to evaluate dietary-induced shifts in deduced microbial functions. Results: Both high-fructose diets resulted in divergent gut microbiota composition. A high-fat/high-fructose diet induced the largest shift in overall gut microbial composition, with dramatic shifts in the Firmicute/Bacteroidetes ratio, and changes in beta diversity after just seven days of dietary intervention. Significant associations between genus level taxa and dietary intervention were identified, including an association with Ruminococceace NK4A214 group in high-fat/high-fructose fed animals and an association with Butryimonas with the low-fat/high-fructose diet. High-fat/high-fructose feeding induced dyslipidemia with increases in plasma triglycerides and cholesterol, and hepatomegaly. Dietary-induced changes in several genus level taxa significantly correlated with lipid levels over the two-week period. Differences in microbial metabolic pathways between high-fat/high-fructose and low-fat/high-fructose diet fed hamsters were identified, and several of these pathways also correlated with lipid profiles in hamsters. Conclusions: The high-fat/high-fructose diet caused shifts in the host gut microbiota. These dietary-induced alterations in gut microbial composition were linked to changes in the production of secondary metabolites, which contributed to the development of metabolic syndrome in the host.

scholarly journals A high-fructose diet worsens eccentric left ventricular hypertrophy in experimental volume overload

2011 ◽  
Vol 300 (1) ◽  
pp. H125-H134 ◽  
Author(s):  
Andrée-Anne Bouchard-Thomassin ◽  
Dominic Lachance ◽  
Marie-Claude Drolet ◽  
Jacques Couet ◽  
Marie Arsenault
Keyword(s):  
Ejection Fraction ◽  
Ventricular Function ◽  
Aortic Regurgitation ◽  
Control Diet ◽  
Volume Overload ◽  
Left Ventricular ◽  
Amp Kinase ◽  
High Fructose Diet ◽  
High Fructose ◽  
Eccentric Hypertrophy

The development of left ventricular (LV) hypertrophy (LVH) can be affected by diet manipulation. Concentric LVH resulting from pressure overload can be worsened by feeding rats with a high-fructose diet. Eccentric LVH is a different type of hypertrophy and is associated with volume overload (VO) diseases. The impact of an abnormal diet on the development of eccentric LVH and on ventricular function in chronic VO is unknown. This study therefore examined the effects of a fructose-rich diet on LV eccentric hypertrophy, ventricular function, and myocardial metabolic enzymes in rats with chronic VO caused by severe aortic valve regurgitation (AR). Wistar rats were divided in four groups: sham-operated on control diet (SC; n = 13) or fructose-rich diet (SF; n = 13) and severe aortic regurgitation fed with the same diets [aortic regurgitation on control diet (ARC), n = 16, and aortic regurgitation on fructose-rich diet (ARF), n = 13]. Fructose-rich diet was started 1 wk before surgery, and the animals were euthanized 9 wk later. SF and ARF had high circulating triglycerides. ARC and ARF developed significant LV eccentric hypertrophy after 8 wk as expected. However, ARF developed more LVH than ARC. LV ejection fraction was slightly lower in the ARF compared with ARC. The increased LVH and decreased ejection fraction could not be explained by differences in hemodynamic load. SF, ARC, and ARF had lower phosphorylation levels of the AMP kinase compared with SC. A fructose-rich diet worsened LV eccentric hypertrophy and decreased LV function in a model of chronic VO caused by AR in rats. Normal animals fed the same diet did not develop these abnormalities. Hypertriglyceridemia may play a central role in this phenomenon as well as AMP kinase activity.

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