Apigenin Alleviates Obesity-Associated Metabolic Syndrome by Regulating the Composition of the Gut Microbiome

The gut microbiota, often viewed as a “digestive organ,” can influence the development of obesity and related metabolic disorders. Diet is significantly important in shaping the structure and modulating the function of the gut microbiota. Apigenin (Api) widely exists in fruits and vegetables as a naturally occurring flavonoid and has anti-obesogenic, anti-inflammatory, and anti-carcinogenic properties. Its low bioavailability means it has enough time to interact with the intestine thus becomes a potential substrate for the gut intestine; thus, contributing to gut health. Here, we show that Api reduces whole-body weight, low-grade inflammation, and insulin resistance in high-fat diet (HFD)-induced obese mice. Our results reflect that Api supplementation can substantially improve intestinal dysbiosis triggered by HFD and restores gut barrier damage by alleviating metabolic endotoxemia. Augmentation of Akkermansia and Incertae_Sedis along with reduction of Faecalibaculum and Dubosiella at the genus level potentially mediated the protective effects of Api on metabolic syndrome. Furthermore, we show that the impact of Api on the reduction of body weight and the modification of gut microbiota could be transferred from Api-administered mice to HFD-feeding mice via horizontal fecal microbiota transplantation. Taken together, our data highlight the prebiotic role of Api and show its contribution to the restraint of gut dysbiosis and metabolic deterioration associated with obesity in mice.

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Age and Giardia intestinalis Infection Impact Canine Gut Microbiota

Microorganisms ◽

10.3390/microorganisms9091862 ◽

2021 ◽

Vol 9 (9) ◽

pp. 1862

Author(s):

Anne-Sophie Boucard ◽

Myriam Thomas ◽

Wilfried Lebon ◽

Bruno Polack ◽

Isabelle Florent ◽

...

Keyword(s):

Gut Microbiota ◽

Structural Changes ◽

Parasitic Infection ◽

Giardia Intestinalis ◽

Host Susceptibility ◽

Low Grade ◽

Giardia Cyst ◽

Gut Health ◽

Time Points ◽

The Impact

Giardia intestinalis is a flagellated protozoan responsible for giardiosis (also called giardiasis in humans), the most prevalent and widespread parasitic infection in humans and mammals worldwide. The intestinal microbiota is highly diverse and any alteration in its composition may impact on the health of the host. While studies on the mouse model of giardiosis described the role of the gut microbiota in host susceptibility to infection by the parasite, little is known about the gut microbiota during natural infections in dogs and particularly in puppies. In this study, we monitored naturally G. intestinalis-infected puppies for 3 months and quantified cyst excretion every 2 weeks. All puppies remained subclinically infected during the sampling period as confirmed by fecal examination. In parallel, we performed 16S Illumina sequencing of fecal samples from the different time points to assess the impact of G. intestinalis infection on gut microbiota development of the puppies, as well as gut health markers of immunity such as fecal IgA and calprotectin. Sequencing results revealed that the canine fecal microbiota of Giardia-infected puppies becomes more complex and less diverse with increasing age. In addition, significant differences in the structure of the microbiota were observed between puppies with high and low Giardia cyst excretion. Chronic subclinical G. intestinalis infection appears to be associated with some detrimental structural changes in the gut microbiota. G. intestinalis-associated dysbiosis is characterized by an enrichment of facultative anaerobic, mucus-degrading, pro-inflammatory species and opportunistic pathogens, as well as a reduction of Lactobacillus johnsonii at specific time points. Calprotectin levels increased with age, suggesting the establishment of chronic low-grade inflammation in puppies. Further work is needed to demonstrate whether these alterations in the canine gut microbiota could lead to a dysbiosis-related disease, such as irritable bowel syndrome (IBS) or inflammatory bowel disease (IBD).

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

Journal of Animal Science and Biotechnology ◽

10.1186/s40104-021-00596-w ◽

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.

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Insights into the Impact of Microbiota in the Treatment of NAFLD/NASH and Its Potential as a Biomarker for Prognosis and Diagnosis

Biomedicines ◽

10.3390/biomedicines9020145 ◽

2021 ◽

Vol 9 (2) ◽

pp. 145

Author(s):

Julio Plaza-Díaz ◽

Patricio Solis-Urra ◽

Jerónimo Aragón-Vela ◽

Fernando Rodríguez-Rodríguez ◽

Jorge Olivares-Arancibia ◽

...

Keyword(s):

Gut Microbiota ◽

Fecal Microbiota Transplantation ◽

Liver Steatosis ◽

Intestinal Barrier ◽

Fecal Microbiota ◽

Current Treatment ◽

Immune Defense ◽

Alcoholic Fatty Liver ◽

The Impact

Non-alcoholic fatty liver disease (NAFLD) is an increasing cause of chronic liver illness associated with obesity and metabolic disorders, such as hypertension, dyslipidemia, or type 2 diabetes mellitus. A more severe type of NAFLD, non-alcoholic steatohepatitis (NASH), is considered an ongoing global health threat and dramatically increases the risks of cirrhosis, liver failure, and hepatocellular carcinoma. Several reports have demonstrated that liver steatosis is associated with the elevation of certain clinical and biochemical markers but with low predictive potential. In addition, current imaging methods are inaccurate and inadequate for quantification of liver steatosis and do not distinguish clearly between the microvesicular and the macrovesicular types. On the other hand, an unhealthy status usually presents an altered gut microbiota, associated with the loss of its functions. Indeed, NAFLD pathophysiology has been linked to lower microbial diversity and a weakened intestinal barrier, exposing the host to bacterial components and stimulating pathways of immune defense and inflammation via toll-like receptor signaling. Moreover, this activation of inflammation in hepatocytes induces progression from simple steatosis to NASH. In the present review, we aim to: (a) summarize studies on both human and animals addressed to determine the impact of alterations in gut microbiota in NASH; (b) evaluate the potential role of such alterations as biomarkers for prognosis and diagnosis of this disorder; and (c) discuss the involvement of microbiota in the current treatment for NAFLD/NASH (i.e., bariatric surgery, physical exercise and lifestyle, diet, probiotics and prebiotics, and fecal microbiota transplantation).

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Melatonin and diet-induced metabolic syndrome in rats: impact on the hypophysial-testicular axis

Hormone Molecular Biology and Clinical Investigation ◽

10.1515/hmbci-2013-0005 ◽

2013 ◽

Vol 16 (2) ◽

Cited By ~ 1

Author(s):

Pablo A. Scacchi Bernasconi ◽

Nancy P. Cardoso ◽

Roxana Reynoso ◽

Pablo Scacchi ◽

Daniel P. Cardinali

Keyword(s):

Metabolic Syndrome ◽

Body Weight ◽

Uric Acid ◽

Plasma Levels ◽

Density Lipoprotein ◽

The Body ◽

High Fat ◽

Testosterone Secretion ◽

Diet Manipulation ◽

The Impact

AbstractCombinations of fructose- and fat-rich diets in experimental animals can model the human metabolic syndrome (MS). In rats, the increase in blood pressure (BP) after diet manipulation is sex related and highly dependent on testosterone secretion. However, the extent of the impact of diet on rodent hypophysial-testicular axis remains undefined. In the present study, rats drinking a 10% fructose solution or fed a high-fat (35%) diet for 10 weeks had higher plasma levels of luteinizing hormone (LH) and lower plasma levels of testosterone, without significant changes in circulating follicle-stimulating hormone or the weight of most reproductive organs. Diet manipulation brought about a significant increase in body weight, systolic BP, area under the curve (AUC) of glycemia after an intraperitoneal glucose tolerance test (IPGTT), and plasma low-density lipoprotein cholesterol, cholesterol, triglycerides, and uric acid levels. The concomitant administration of melatonin (25 μg/mL of drinking water) normalized the abnormally high LH levels but did not affect the inhibited testosterone secretion found in fructose- or high-fat-fed rats. Rather, melatonin per se inhibited testosterone secretion. Melatonin significantly blunted the body weight and systolic BP increase, the increase in the AUC of glycemia after an IPGTT, and the changes in circulating lipid profile and uric acid found in both MS models. The results are compatible with a primary inhibition of testicular function in diet-induced MS in rats and with the partial effectiveness of melatonin to counteract the metabolic but not the testicular sequelae of rodent MS.

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Contributions of Lactobacillus plantarum PC170 administration on the recovery of gut microbiota after short-term ceftriaxone exposure in mice

Beneficial Microbes ◽

10.3920/bm2019.0191 ◽

2020 ◽

Vol 11 (5) ◽

pp. 489-509

Author(s):

R. Cheng ◽

H. Liang ◽

Y. Zhang ◽

J. Guo ◽

Z. Miao ◽

...

Keyword(s):

Body Weight ◽

Gut Microbiota ◽

Lactobacillus Plantarum ◽

Antibiotic Treatment ◽

Recovery Phase ◽

The Body ◽

Faecal Microbiota ◽

Short Term ◽

Host Animal ◽

The Impact

This study aimed to determine the impact of Lactobacillus plantarum PC170 concurrent with antibiotic treatment and/or during the recovery phase after antibiotic treatment on the body weight, faecal bacterial composition, short-chain fatty acids (SCFAs) concentration, and splenic cytokine mRNA expression of mice. Orally administrated ceftriaxone quantitatively and significantly decreased body weight, faecal total bacteria, Akkermansia muciniphila, and Lactobacillus plantarum, and faecal SCFAs concentration. Ceftriaxone treatment also dramatically altered the faecal microbiota with an increased Chao1 index, decreased species diversities and Bacteroidetes, and more Firmicutes and Proteobacteria. After ceftriaxone intervention, these changes all gradually started to recover. However, faecal microbiota diversities were still totally different from control by significantly increased α- and β-diversities. Bacteroidetes all flourished and became dominant during the recovery process. However, mice treated with PC170 both in parallel with and after ceftriaxone treatment encouraged more Bacteroidetes, Verrucomicrobia, and Actinobacteria, and the diversity by which to make faecal microbiota was very much closer to control. Furthermore, the expression of splenic pro-inflammatory cytokine tumour necrosis factor-α mRNA in mice supplemented with PC170 during the recovery phase was significantly lower than natural recovery. These results indicated that antibiotics, such as ceftriaxone, even with short-term intervention, could dramatically damage the structure of gut microbiota and their abilities to produce SCFAs with loss of body weight. Although such damages could be partly recovered with the cessation of antibiotics, the implication of antibiotics to gut microbiota might remain even after antibiotic treatment. The selected strain PC170 might be a potential probiotic because of its contributions in helping the host animal to remodel or stabilise its gut microbiome and enhancing the anti-inflammatory response as protection from the side effects of antibiotic therapy when it was administered in parallel with and after antibiotic treatment.

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Citrus polymethoxyflavones attenuate metabolic syndrome by regulating gut microbiome and amino acid metabolism

Science Advances ◽

10.1126/sciadv.aax6208 ◽

2020 ◽

Vol 6 (1) ◽

pp. eaax6208 ◽

Cited By ~ 16

Author(s):

Su-Ling Zeng ◽

Shang-Zhen Li ◽

Ping-Ting Xiao ◽

Yuan-Yuan Cai ◽

Chu Chu ◽

...

Keyword(s):

Metabolic Syndrome ◽

Amino Acid ◽

Gut Microbiota ◽

Metabolic Diseases ◽

Amplicon Sequencing ◽

Therapeutic Interventions ◽

Protective Effects ◽

Fecal Microbiome ◽

Metabolomic Profiling ◽

Branched Chain

Metabolic syndrome (MetS) is intricately linked to dysregulation of gut microbiota and host metabolomes. Here, we first find that a purified citrus polymethoxyflavone-rich extract (PMFE) potently ameliorates high-fat diet (HFD)–induced MetS, alleviates gut dysbiosis, and regulates branched-chain amino acid (BCAA) metabolism using 16S rDNA amplicon sequencing and metabolomic profiling. The metabolic protective effects of PMFE are gut microbiota dependent, as demonstrated by antibiotic treatment and fecal microbiome transplantation (FMT). The modulation of gut microbiota altered BCAA levels in the host serum and feces, which were significantly associated with metabolic features and actively responsive to therapeutic interventions with PMFE. Notably, PMFE greatly enriched the commensal bacterium Bacteroides ovatus, and gavage with B. ovatus reduced BCAA concentrations and alleviated MetS in HFD mice. PMFE may be used as a prebiotic agent to attenuate MetS, and target-specific microbial species may have unique therapeutic promise for metabolic diseases.

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Longitudinal Analyses Reveal That Aging-related Alterations in the Intestinal Environment Lead to Gut Dysbiosis With the Potential to Induce Obesity

10.21203/rs.3.rs-119480/v1 ◽

2020 ◽

Author(s):

Yumiko Nakanishi ◽

Ryouko Nozu ◽

Masami Ueno ◽

Kyoji Hioki ◽

Chiharu Ishii ◽

...

Keyword(s):

Gut Microbiota ◽

Middle Age ◽

Fecal Microbiota Transplantation ◽

Fold Increase ◽

Fecal Microbiota ◽

Whole Body ◽

Cellular Functions ◽

Intestinal Environment ◽

Gut Dysbiosis ◽

Specific Pathogen

Abstract Background: Aging is a progressive decline of cellular functions that ultimately affects whole-body homeostasis. Alterations in the gut microbiota associated with aging have been reported, however the molecular basis of the relationships between host aging and the gut microbiota is poorly understood.Result: By using longitudinal microbiome and metabolome characterization, we show that the aging-related alterations in the intestinal environment lead to gut dysbiosis with a potential to induce obesity in mice. In middle-age mice, we observed more than a 2-fold increase in fecal carbohydrates derived from dietary polysaccharides and a significant reduction of gut microbial diversity resembling the microbiota characteristic of obese mice. Consistently, fecal microbiota transplantation from middle-age specific pathogen-free (SPF) mice into young germ-free (GF) mice resulted in increased weight gain and impaired glucose tolerance.Conclusion: Our findings provide new insights into the relationships between host aging and gut dysbiosis and may contribute to the development of a possible solution to aging-related obesity.

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Abstract P116: The Impact of Diet Low in Fruits and Vegetables on Cardiovascular Disease Burden Across 195 Countries in 2015

Circulation ◽

10.1161/circ.135.suppl_1.p116 ◽

2017 ◽

Vol 135 (suppl_1) ◽

Author(s):

Patrick J Sur ◽

Ashkan Afshin

Keyword(s):

Cardiovascular Disease ◽

Fruits And Vegetables ◽

Population Level ◽

Optimal Level ◽

Protective Effects ◽

Disability Adjusted Life Years ◽

Country Level ◽

Disability Adjusted Life ◽

Life Years ◽

The Impact

Introduction: While cardio-protective effects of fruits and vegetables are well-established, the impact of their suboptimal intake on the CVD burden across nations and levels of development has not been evaluated. Objective: To systematically quantify the burden of CVD attributable to low intake of fruits and low intake of vegetables in 195 countries by age, sex, country, and development status in 2015. Methods: We obtained data on consumption of fruits and vegetables from nationally or subnationally representative nutrition surveys and data on their national availability from the UN FAO. Etiologic effect sizes of fruits and vegetables on CVD endpoints were obtained from meta- analyses of prospective cohort studies. The optimal level of intakes for each was determined based on the levels associated with lowest risk of mortality in prospective observational studies. A comparative risk assessment analysis was conducted to quantify the proportion of disability- adjusted life years (DALYs) attributable to low intake of each. The variation of this burden was further evaluated across different levels of our newly developed socio-demographic index (SDI). Results: In 2015, low intake of fruits accounted for 57.3 (95% UI: 37.1- 78.4) million DALYs due to CVD globally (41.5% from IHD and 58.5% from stroke). Low intake of vegetable caused 44.6 (23.6- 68.8) million CVD DALYs (67.3% IHD and 32.7% stroke). The highest burden of CVD attributable to low intake of fruits and vegetables was seen in the middle and low-middle SDI quintiles (17.2 and 14.3% of total DALYs), while the lowest burden for each was seen in high and high-middle SDI quintiles (12.7 and 11.2%). At the country level, the attributable CVD burden ranged from 5.1% of total DALYs (Rwanda) to 23.2% (Bangladesh) for low intake of fruit and from 5.9% (North Korea) to 19.4% (Mongolia) for low intake of vegetable. Conclusion: Our findings suggest that population inventions to increase consumption of fruits and vegetables at population level could save millions of life years globally. Figure. Age-standardized proportion of disability-adjusted life years attributable to low intake of fruits (A) and vegetables (B) from cardiovascular disease among adults (> 25y) in 2015.

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Abstract P247: Gut Microbiota From A Rat Model Of Metabolic Syndrome Lowers Fitness Of High Exercise Capacity Rats (HCR/ Tol ) By Impairing Energy Homeostasis And Increasing Blood Pressure

Hypertension ◽

10.1161/hyp.76.suppl_1.p247 ◽

2020 ◽

Vol 76 (Suppl_1) ◽

Author(s):

Guannan Zhou ◽

Tao Yang ◽

Sivarajan Kumarasamy ◽

Bina Joe ◽

Lauren G Koch

Keyword(s):

Blood Pressure ◽

Metabolic Syndrome ◽

Energy Metabolism ◽

Gut Microbiota ◽

Exercise Capacity ◽

Energy Homeostasis ◽

Current Knowledge ◽

Strong Predictor ◽

Whole Body ◽

Acid Oxidation

Introduction: Low exercise capacity is a strong predictor of cardiovascular disease and overall mortality. Previously we have shown that rats artificially selected for low intrinsic exercise capacity (LCR) have reduced longevity and develop features consistent with metabolic syndrome (MetS) compared to high intrinsic exercise capacity rats (HCR). Current knowledge suggests that gut microbiota is an important contributor for host fitness. Thus, we hypothesized that transferring gut microbiota from LCR rats into inbred high capacity runner (HCR /Tol ) rats would increase risk factors for MetS, including high blood pressure (BP), gain in body weight (BW), and altered resting energy metabolism. Methods: Gut microbiota was depleted in male HCR/ Tol rats (4 mo.) by an antibiotic cocktail given orally (50mg/kg of BW/day) for 5 days, followed by weekly fecal microbiota transfer (FMT) from male LCR or HCR rats (13 mo.) to generate HCR/ Tol -LCR FMT (n = 5) or HCR/ Tol -HCR FMT (n = 6) groups. BW was measured every 4 weeks. At week 11, whole body metabolism was measured by indirect calorimetry (Oxymax, Columbus Instruments). Respiratory Exchange Ratio (RER), Energy Expenditure (EE), glucose and fat oxidation were calculated from oxygen consumption and carbon dioxide release (VO 2 and VCO 2 ). At week 12, BP was measured by tail-cuff method (Kent Scientific) and treadmill exercise test was done at week 13. Results: Compared to HCR/ Tol -HCR FMT , HCR/ Tol -LCR FMT showed a significant gain in BW (7.2% vs 1.9%, P<0.05), elevated systolic BP (147 vs 120 mmHg, P<0.0001), diastolic BP (112 vs 91 mmHg, P<0.01), and mean BP (123 vs 100 mmHg, P<0.001). BP changes in HCR/ Tol -LCR FMT associated with 1) increased VO 2 (355 vs 320 ml/hr, P<0.05), 2) elevated VCO 2 (350 vs 298 ml/hr, P<0.01), 3) increased EE (1.8 vs 1.6 kcal/hr, P<0.01), 4) higher RER (0.96 vs 0.91, P<0.001), 5) higher glucose oxidation (1.36 vs 1.12 g/kg/hr, P<0.001) and 6) reduced fatty acid oxidation (0.09 vs 0.15 g/kg/hr, P<0.01) and a 23% lower exercise capacity. Conclusions: Gut microbiota from LCR rats strongly associated with poor health outcomes, notably elevated BP and impaired energy metabolism. These findings suggest that altered energy homeostasis by microbiota is mechanistically linked to host BP regulation within MetS.

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In Vitro Fecal Fermentation Patterns of Arabinoxylan from Rice Bran on Gut Microbiota in Normal Weight and Overweight/Obese Subjects

Current Developments in Nutrition ◽

10.1093/cdn/nzaa062_017 ◽

2020 ◽

Vol 4 (Supplement_2) ◽

pp. 1560-1560

Author(s):

Inah Gu ◽

Wing Shun Lam ◽

Daya Marasini ◽

Cindi Brownmiller ◽

Brett Savary ◽

...

Keyword(s):

Gut Microbiota ◽

Rice Bran ◽

Block Design ◽

16S Rrna Gene Sequencing ◽

Short Chain Fatty Acids ◽

Normal Weight ◽

Rrna Gene ◽

Gut Health ◽

The Impact

Abstract Objectives Arabinoxylan is a non-starch polysaccharide and rich in wheat, rice and many other cereal grains. Diets high in fiber help promoting gut health in obesity. The objective of this study was to investigate the impact of arabinoxylan from rice bran on the gut microbiota and short chain fatty acids (SCFA) in normal weight (NW) and overweight/obese (OO) subjects through in vitro fecal fermentation. Methods Arabinoxylan was extracted from rice bran fiber. For in vitro fecal fermentation, each fecal sample from NW (n = 6, 3 males and 3 females) and OO (n = 7, 3 males and 4 females) was diluted into anaerobic medium with three treatments: control (no substrates), fructooligosaccharides (FOS, a well-known prebiotic), and arabinoxylan. Samples were incubated at 37˚C and aliquots were taken at 0, 4, 8, 12 and 24 h. SCFA content from samples at all timepoints was analyzed using HPLC. Samples at 0 and 24 h were used for gut microbiota analysis through 16S rRNA gene sequencing. Statistical analyses were performed for the randomized complete block design, where the weight classes are confounded with blocks (subjects). Friedman test was used to determine the difference at 5% level of significance. Results As a result, arabinoxylan treatment significantly increased total SCFA concentration in both NW and OO subjects than control (P < 0.05), comparable to FOS treatment. Between weight classes under arabinoxylan treatment, OO group showed a significantly higher total SCFA content than NW group (P < 0.05). Arabinoxylan changed gut microbial population at the genus level, stimulating Bifidobacterium, Collinsella and Blautia and decreasing Clostridium XIVa and b, Dorea and Oscillibacter (P < 0.05). In addition, different microbiome population was shown in weight classes with three treatments, showing higher Bacteroides in NW and higher Prevotella in OO. Conclusions These results showed that arabinoxylan from rice bran modified gut microbiota in both weight classes, increasing total SCFA content. This study suggests that arabinoxylan from rice bran may have a potential impact on microbial gut health in obesity with prebiotic activities. Funding Sources University of Arkansas.

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