Low Dietary Fiber Intake Links Development of Obesity and Lupus Pathogenesis.

Changed dietary habits in Western countries such as reduced fiber intake represent an important lifestyle factor contributing to the increase in inflammatory immune-mediated diseases. The mode of action of beneficial fiber effects is not fully elucidated, but short-chain fatty acids (SCFA) and gut microbiota have been implicated. The aim of this study was to explore the impact of dietary fiber on lupus pathology and to understand underlying mechanisms. Here, we show that in lupus-prone NZB/WF1 mice low fiber intake deteriorates disease progression reflected in accelerated mortality, autoantibody production and immune dysregulation. In contrast to our original assumption, microbiota suppression by antibiotics or direct SCFA feeding did not influence the course of lupus-like disease. Mechanistically, our data rather indicate that in low fiber-fed mice, an increase in white adipose tissue mass, fat-inflammation and a disrupted intestinal homeostasis go along with systemic, low-grade inflammation driving autoimmunity. The links between obesity, intestinal leakage and low-grade inflammation were confirmed in human samples, while adaptive immune activation predominantly correlated with lupus activity. We further propose that an accelerated gastro-intestinal passage along with energy dilution underlies fiber-mediated weight regulation. Thus, our data highlight the often-overlooked effects of dietary fiber on energy homeostasis and obesity prevention. Further, they provide insight into how intricately the pathologies of inflammatory immune-mediated conditions, such as obesity and autoimmunity, might be interlinked, possibly sharing common pathways.

Dietary fiber deficiency as a component of malnutrition associated with psychological alterations in alcohol use disorder.

BACKGROUND & AIMS: Chronic alcohol consumption can cause malnutrition that may contribute to alcohol-induced organ injury and psychological disorders. We evaluated the link between nutrient intake, especially dietary fibers (DF) and different parameters reflecting mental health and well being, namely anxiety, depression, alcohol craving, sociability, fatigue and intestinal comfort in alcohol use disorder (AUD) patients. METHODS: Cross-sectional data from 50 AUD patients, hospitalized for a 3-week detoxification program were used. Three 24-h recalls allowed to calculate dietary habits and nutrient intakes, that was also assessed in healthy subjects (HS). Diet quality was measured using the NOVA score. Psychological factors and intestinal discomfort were evaluated using validated self-administered questionnaires. RESULTS: Energy intake (excluding alcoholic beverage), total fat, monounsaturated and polyunsaturated fatty acids, protein and DF intakes were lower in AUD subjects compared to HS. Ninety percent of patients had a DF intake below the recommendation. AUD patients consumed more than twice as much ultra-processed food than HS. Fructan intake was negatively associated with anxiety (p = 0.04) adjusted for main confounders. Total DF, insoluble, soluble DF and galacto-oligosaccharide intakes were associated with higher sociability score. Soluble DF intake was associated with better satisfaction of bowel function (p = 0.02) and a lower intestinal discomfort (p = 0.04). CONCLUSIONS: This study reveals that insufficient DF intake is part of AUD-related malnutrition syndrome, and is associated with higher anxiety, lower sociability score and intestinal discomfort. Our results suggest that an adequate intake of DF might be beneficial for recovery from AUD. TRIAL REGISTRATION: NCT03803709, https://clinicaltrials.gov/ct2/show/NCT03803709.

Deficiency of Dietary Fiber Modulates Gut Microbiota Composition, Neutrophil Recruitment and Worsens Experimental Colitis.

Ulcerative colitis is an inflammatory disease of the colon that is associated with colonic neutrophil accumulation. Recent evidence indicates that diet alters the composition of the gut microbiota and influences host-pathogen interactions. Specifically, bacterial fermentation of dietary fiber produces metabolites called short-chain fatty acids (SCFAs), which have been shown to protect against various inflammatory diseases. However, the effect of fiber deficiency on the key initial steps of inflammation, such as leukocyte-endothelial cell interactions, is unknown. Moreover, the impact of fiber deficiency on neutrophil recruitment under basal conditions and during inflammation in vivo is unknown. Herein, we hypothesized that a fiber-deficient diet promotes an inflammatory state in the colon at baseline and predisposes the host to more severe colitis pathology. Mice fed a no-fiber diet for 14 days showed significant changes in the gut microbiota and exhibited increased neutrophil-endothelial interactions in the colonic microvasculature. Although mice fed a no-fiber diet alone did not have observable colitis-associated symptoms, these animals were highly susceptible to low dose (0.5%) dextran sodium sulphate (DSS)-induced model of colitis. Supplementation of the most abundant SCFA, acetate, prevented no-fiber diet-mediated enrichment of colonic neutrophils and colitis pathology. Therefore, dietary fiber, possibly through the actions of acetate, plays an important role in regulating neutrophil recruitment and host protection against inflammatory colonic damage in an experimental model of colitis.

Challenging the view that lack of fibre causes childhood constipation.

OBJECTIVES: To assess evidence supporting the view that 'low fibre causes childhood constipation'. DESIGN: Triangulation integrated three approaches: a systematic review NICE guideline CG99 examining effectiveness of increasing fibre; a cohort study, Avon Longitudinal Study of Parents and Children (ALSPAC), to assess if constipation (or hard stools) can precede fibre intake at weaning; and a literature search for twin studies to calculate heredity. SETTING: CG99 examined the literature regarding the effectiveness of increasing fibre. ALSPAC asked parents about: hard stools at 4 weeks, 6 months and 2.5 years and constipation at age 4-10 years, as well as fibre intake at 2 years. Twin studies and data from ALSPAC were pooled to calculate concordance of constipation comparing monozygotic and dizygous twin pairs. PARTICIPANTS: CG99 reported six randomised controlled trials (RCTs). ALSPAC hard stool data from 6796 children at 4 weeks, 9828 at 6 months and 9452 at 2.5 years plus constipation data on 8401 at 4-10 years were compared with fibre intake at 2 years. Twin studies had 338 and 93 twin pairs and ALSPAC added a further 45. RESULTS: Increasing fibre did not effectively treat constipation. Hard stools at 4 weeks predated fibre and at 6 months predicted lower fibre intake at 2 years (p=0.003). Heredity explained 59% of constipation. CONCLUSIONS: RCTs indicate that increasing fibre is not an effective treatment for constipation in children. Hard stools can precede and predict later fibre intake. Genetic inheritance explains most childhood constipation. Extended treatment with stool softeners may improve fibre intake and limit long-term damaging sequelae of constipation.

Deficiency of Prebiotic Fiber and Insufficient Signaling Through Gut Metabolite-Sensing Receptors Leads to Cardiovascular Disease.

BACKGROUND: High blood pressure (BP) continues to be a major, poorly controlled but modifiable risk factor for cardiovascular death. Among key Western lifestyle factors, a diet poor in fiber is associated with prevalence of high BP. The impact of lack of prebiotic fiber and the associated mechanisms that lead to higher BP are unknown. Here we show that lack of prebiotic dietary fiber leads to the development of a hypertensinogenic gut microbiota, hypertension and its complications, and demonstrate a role for G-protein coupled-receptors (GPCRs) that sense gut metabolites. METHODS: One hundred seventy-nine mice including C57BL/6J, gnotobiotic C57BL/6J, and knockout strains for GPR41, GPR43, GPR109A, and GPR43/109A were included. C57BL/6J mice were implanted with minipumps containing saline or a slow-pressor dose of angiotensin II (0.25 mg·kg-1·d-1). Mice were fed diets lacking prebiotic fiber with or without addition of gut metabolites called short-chain fatty acids ([SCFA)] produced during fermentation of prebiotic fiber in the large intestine), or high prebiotic fiber diets. Cardiac histology and function, BP, sodium and potassium excretion, gut microbiome, flow cytometry, catecholamines and methylation-wide changes were determined. RESULTS: Lack of prebiotic fiber predisposed mice to hypertension in the presence of a mild hypertensive stimulus, with resultant pathological cardiac remodeling. Transfer of a hypertensinogenic microbiota to gnotobiotic mice recapitulated the prebiotic-deprived hypertensive phenotype, including cardiac manifestations. Reintroduction of SCFAs to fiber-depleted mice had protective effects on the development of hypertension, cardiac hypertrophy, and fibrosis. The cardioprotective effect of SCFAs were mediated via the cognate SCFA receptors GPR43/GPR109A, and modulated L-3,4-dihydroxyphenylalanine levels and the abundance of T regulatory cells regulated by DNA methylation. CONCLUSIONS: The detrimental effects of low fiber Westernized diets may underlie hypertension, through deficient SCFA production and GPR43/109A signaling. Maintaining a healthy, SCFA-producing microbiota is important for cardiovascular health.

A Pilot and Feasibility Study of Oatmeal Consumption in Children to Assess Markers of Bowel Function.

Inadequate dietary fiber intake contributes to irregular bowel movements and may contribute to difficulty with defecation in children. Whole grain foods, such as oatmeal, may improve stool consistency and stool frequency in children; however, no studies have examined its effects. The purpose of this study was to investigate if 2 weeks of oatmeal consumption in children (ages 7-12 years) increases stool frequency, improves stool consistency, and gastrointestinal (GI) symptoms. In this single-arm intervention study, children who reported ≤5 bowel movements per week during screening, consumed two servings of instant oatmeal daily for 2 weeks. The primary outcome was stool frequency and secondary outcomes included stool consistency and GI symptoms. Participants recorded bowel movements daily, food intake, and GI symptoms during baseline and 2 intervention weeks. Photos of the children's stool were taken at three timepoints during the study to assess stool consistency. In total, 33 children (15 female and 18 male) completed the study. Linear mixed models were used to detect change between baseline and the intervention weeks and accounted for repeated measures within subjects. No statistical differences in stool frequency or consistency were observed between the intervention weeks vs. baseline; however, dietary fiber intake significantly increased during the 2 weeks of oatmeal consumption (P = .008). The addition of oatmeal to children's diets is an effective way to increase fiber consumption and may reduce some GI symptoms such as gas, straining, and feeling of incomplete evacuation. Trial identification number: NCT02868515.

The association between dietary fibre deficiency and high-income lifestyle-associated diseases: Burkitt's hypothesis revisited.

In 1969, Denis Burkitt published an article titled "Related disease-related cause?", which became the foundation for Burkitt's hypothesis. Working in Uganda, he noted that middle-aged people (40-60 years old) had a much lower incidence of diseases that were common in similarly aged people living in England, including colon cancer, diverticulitis, appendicitis, hernias, varicose veins, diabetes, atherosclerosis, and asthma, all of which are associated with lifestyles commonly led in high-income countries (HICs; also known as western diseases). Following Cleave's common cause hypothesis-which suggests that if a group of diseases occur together in the same population or individual, they are likely to have a common cause-Burkitt attributed these diseases to the small quantities of dietary fibre consumed in HICs due mainly to the over-processing of natural foods. Nowadays, dietary fibre intake in HICs is around 15 g/day (well below the amount of fibre Burkitt advocated of >50 g/day-which is associated with diets from rural, southern and eastern sub-Sahalean Africa). Since Burkitt's death in 1993, his hypothesis has been verified and extended by large-scale epidemiological studies, which have reported that fibre deficiency increases the risk of colon, liver, and breast cancer and increases all cancer mortality and death from cardiovascular, infectious, and respiratory diseases, diabetes, and all non-cardiovascular, non-cancer causes. Furthermore, mechanistic studies have now provided molecular explanations for these associations, typified by the role of short-chain fatty acids, products of fibre fermentation in the colon, in suppressing colonic mucosal inflammation and carcinogenesis. Evidence suggests that short-chain fatty acids can affect the epigenome through metabolic regulatory receptors in distant organs, and that this can reduce obesity, diabetes, atherosclerosis, allergy, and cancer. Diseases associated with high-income lifestyles are the most serious threat to health in developed countries, and public and governmental awareness needs to be improved to urge an increase in intake of fibre-rich foods. This Viewpoint will summarise the evidence that suggests that increasing dietary fibre intake to 50 g/day is likely to increase lifespan, improve the quality of life during the added years, and substantially reduce health-care costs.

A fiber-deprived diet disturbs the fine-scale spatial architecture of the murine colon microbiome.

Compartmentalization of the gut microbiota is thought to be important to system function, but the extent of spatial organization in the gut ecosystem remains poorly understood. Here, we profile the murine colonic microbiota along longitudinal and lateral axes using laser capture microdissection. We found fine-scale spatial structuring of the microbiota marked by gradients in composition and diversity along the length of the colon. Privation of fiber reduces the diversity of the microbiota and disrupts longitudinal and lateral gradients in microbiota composition. Both mucus-adjacent and luminal communities are influenced by the absence of dietary fiber, with the loss of a characteristic distal colon microbiota and a reduction in the mucosa-adjacent community, concomitant with depletion of the mucus layer. These results indicate that diet has not only global but also local effects on the composition of the gut microbiota, which may affect function and resilience differently depending on location.

Novel swine model of colonic diverticulosis.

The pathophysiology of colonic diverticulosis has not been completely understood. The development of appropriate animal models is essential to study diverticular disease. To date, no large animal models are available for this disease condition. The objective of this study was to develop a swine model by damaging the colon wall, combined with or without a low-fiber diet to mimic the pathogenesis of diverticulosis. To create a weakness on the colon wall, collagenase was applied in vivo to degrade the collagen in the colon wall. Three groups of Yucatan minipigs were included. Group 1 (n = 12) underwent collagenase injection (CI) with a low-fiber diet for 6 mo, group 2 (n = 8) underwent CI alone with a standard swine diet for 6 mo, and group 3 (n = 12) received a low-fiber diet alone for 6 mo. We found that diverticulosis occurred in 91.7% (11 of 12) of pigs in the CI + diet group and 100% (8 of 8) in CI-alone group. Moreover, around 30-75% of colon CI spots for each pig developed diverticular lesions. Diet alone for 6 mo did not induce diverticulosis. The endoscopic and histological examinations revealed the formation of multiple wide-mouthed diverticular lesions along the descending colon. Our results provide convincing evidence of the high efficacy of the reduced colon wall strength caused by CI in the development of a swine model of diverticulosis. Low-fiber diet consumption for 6 mo had no influence on the generation time or incidence rate of diverticulosis. In this model, digestion of the collagen in the colonic wall is sufficient to cause diverticulosis. NEW & NOTEWORTHY Effective large animal models of diverticulosis are currently lacking for the study of diverticular disease. This study marks the first time that a swine model of diverticulosis was developed by damaging colon wall structure, combined with or without a low-fiber diet. We found that a defect of colon wall could result in colon diverticular lesions within 6 mo in swine. This animal model mimicking the pathological process of diverticulosis is of great clinical value.

Gut microbiota profiling with differential tolerance against the reduced dietary fibre level in rabbit.

Dietary fibre is well acknowledged to be critical in maintaining the gut homeostasis in human and other monogastric animals. As a small monogastric herbivorous animal, rabbit is much sensitive to the reduced intake of dietary fibre and more interestingly shows individual difference in clinical tolerance. In the present study, we fed rabbits with fibre-deficiency diet for two weeks and successfully distinguished the individual tolerances according to clinical signs and gastrointestinal gross lesions. A total of 40 treatments were classified into three groups of the full health (N = 10), moderate intestinal disorder (N = 11) and severe intestinal disorder (N = 19). Together with three controls, 43 individuals were subjected to gut microbiota profiling by 16S rRNA gene sequencing. It was revealed that the Firmicutes/Bacteroidetes ratio steadily decreased from 1.74 in healthy group to 1.03 in severe group. However, the healthy individuals that showed complete tolerance still remained a comparable Firmicutes/Bacteroidetes ratio with controls. Notably, the class Alphaproteobacteria was found to be higher abundance in healthy group than controls and other treatment groups. The results would improve our understanding of the relationship among dietary fibre, gut microbiota and host health.

Deficiency of Dietary Fiber in Slc5a8-Null Mice Promotes Bacterial Dysbiosis and Alters Colonic Epithelial Transcriptome towards Proinflammatory Milieu.

Inflammatory bowel disease (IBD) is characterized by chronic inflammation in the intestinal tract due to disruption of the symbiotic relationship between the host immune system and microbiota. Various factors alter the gut microbiota which lead to dysbiosis; in particular, diet and dietary fibers constitute important determinants. Dietary fiber protects against IBD; bacteria ferment these dietary fibers in colon and generate short-chain fatty acids (SCFAs), which mediate the anti-inflammatory actions of dietary fibers. SLC5A8 is a high-affinity transporter in the apical membrane of colonic epithelium which mediates the entry of SCFAs from the lumen into cells in Na+-coupled manner. Due to the unique transport kinetics, the function of the transporter becomes important only under conditions of low dietary fiber intake. Here, we have examined the impact of dietary fiber deficiency on luminal microbial composition and transcriptomic profile in colonic epithelium in wild-type (WT) and Slc5a8-null (KO) mice. We fed WT and KO mice with fiber-containing diet (FC-diet) or fiber-free diet (FF-diet) and analyzed the luminal bacterial composition by sequencing 16S rRNA gene in feces. Interestingly, results showed significant differences in the microbial community depending on dietary fiber content and on the presence or absence of Slc5a8. There were also marked differences in the transcriptomic profile of the colonic epithelium depending on the dietary fiber content and on the presence or absence of Slc5a8. We conclude that absence of fiber in diet in KO mice causes bacterial dysbiosis and alters gene expression in the colon that is conducive for inflammation.

Denis Burkitt and the origins of the dietary fibre hypothesis.

For more than 200 years the fibre in plant foods has been known by animal nutritionists to have significant effects on digestion. Its role in human nutrition began to be investigated towards the end of the 19th century. However, between 1966 and 1972, Denis Burkitt, a surgeon who had recently returned from Africa, brought together ideas from a range of disciplines together with observations from his own experience to propose a radical view of the role of fibre in human health. Burkitt came late to the fibre story but built on the work of three physicians (Peter Cleave, G. D. Campbell and Hugh Trowell), a surgeon (Neil Painter) and a biochemist (Alec Walker) to propose that diets low in fibre increase the risk of CHD, obesity, diabetes, dental caries, various vascular disorders and large bowel conditions such as cancer, appendicitis and diverticulosis. Simply grouping these diseases together as having a common cause was groundbreaking. Proposing fibre as the key stimulated much research but also controversy. Credit for the dietary fibre hypothesis is given largely to Burkitt who became known as the 'Fibre Man'. This paper sets out the story of the development of the fibre hypothesis, and the contribution to it of these individuals.

Phosphorus bioavailability in increased-protein, reduced-fiber canola meal, conventional canola meal, and soybean meal fed to crossbred chicks.

Three experiments were conducted to evaluate 3 increased-protein, reduced-fiber canola meals (CM) (CMA, CMB, and Test CM), 2 conventional CM (CCM), and 2 soybean meals (SBM). For determination of P bioavailability in CM and SBM, a P-deficient cornstarch-dextrose-SBM basal diet was fed as Diet 1. The latter basal diet was then supplemented with 0.05 and 0.10% P from KH2PO4 or 12.5 and 25% of a CM or SBM. In addition, the effect of phytase enzyme on bioavailability of the P in CMA, Test CM, and one of the CCM was determined using P-deficient 45% CM-cornstarch-dextrose diets (0.11 to 0.15% non-phytate P), with a CM as the only source of dietary P. Additional diets contained 0.05 and 0.10% added P from KH2PO4 or 125 to 500 units phytase added per kg of diet. Crossbred chicks (New Hampshire X Columbian) were fed the experimental diets from 8 to 21 d post hatch in all experiments, and bioavailability of P was estimated using the slope ratio method in which tibia ash was regressed on supplemental P intake. A linear increase in tibia ash was observed as the P level increased by the addition of KH2PO4, CMA, CMB, or SBM. Based on the mean values of tibia ash in mg/tibia and tibia ash %, the mean bioavailabilities of P in the 3 increased-protein, reduced-fiber CM, 3 CCM, and 2 SBM relative to KH2PO4 were 18, 15, and 39%, respectively. A linear increase in weight gain and tibia ash was observed with addition of KH2PO4 or phytase to the P-deficient CM diets. It was estimated that 125 or 250 units/kg microbial phytase resulted in approximately 0.05 and 0.10% P being released from CM, respectively. In conclusion, the bioavailablity of the P in the new increased-protein, reduced-fiber CM was similar to that of CCM. Furthermore, phytase substantially and similarly increased the bioavailability of P in both types of CM.

Low dietary fiber intake increases Collinsella abundance in the gut microbiota of overweight and obese pregnant women.

The gut microbiota contributes to the regulation of glucose metabolism in pregnancy. Abundance of the genus Collinsella is positively correlated with circulating insulin; however, it is unclear what determines Collinsella abundance. This study aims to validate the correlation between Collinsella and insulin and to elucidate if macronutrient intake alters Collinsella abundance and gut microbiota composition. Gut microbiota profiles were assessed by 16S rRNA sequencing in 57 overweight and 73 obese pregnant women from the SPRING (Study of PRobiotics IN Gestational diabetes) trial at 16 weeks gestation and correlated with metabolic hormone levels and macronutrient intake. Gut microbiota composition in the top and bottom 10% of dietary fiber intake was evaluated through network analysis. Collinsella abundance correlated positively with circulating insulin (rho = 0.30, p = 0.0006), independent of maternal BMI, but negatively with dietary fiber intake (rho = -0.20, p = 0.025) in this cohort. Low dietary fiber intake was associated with a gut microbiota favoring lactate fermentation while high fiber intake promotes short-chain fatty acid-producing bacteria. Low dietary fiber may enable overgrowth of Collinsella and alter the overall fermentation pattern in gut microbiota. This suggests that dietary choices during pregnancy can modify the nutritional ecology of the gut microbiota, with potential deleterious effects on the metabolic and inflammatory health of the host. TRIAL REGISTRATION: ANZCTR 12611001208998, registered 23/11/2011.

Chronic transgenerational vitamin B12 deficiency of severe and moderate magnitudes modulates adiposity-probable underlying mechanisms.

We have demonstrated previously that severe but not moderate vitamin B12 deficiency altered body composition and induced adiposity in female C57BL/6 mice. This study aims to elucidate the effects of chronic transgenerational dietary vitamin B12 restriction on body composition and various biochemical parameters in the F1 generation offspring of our mouse models of severe and moderate vitamin B12 deficiency established earlier. Female weanling C57BL/6 mice received, ad libitum, for 4 weeks a (i) control diet, (ii) vitamin B12-restricted diet with pectin as dietary fiber (severely deficient diet), or (iii) vitamin B12-restricted diet with cellulose as dietary fiber (moderately deficient diet) and then mated with control males. The offspring of control and severely deficient dams continued on the respective diets of their mothers. Few moderately deficient dams were rehabilitated to control diet from parturition and their pups were weaned to control diet. Also, some offspring born to moderately B12 deficient dams were weaned to control diet, while others continued on the same diet as their mothers. Various parameters were determined in the F1 offspring after 12 and 36 weeks of feeding. The results indicate that both severe and moderate maternal vitamin B12 restrictions were associated with accelerated catch-up growth, increased body fat percentage, visceral adiposity, dyslipidemia, fasting hyperglycemia and insulin resistance in the F1 offspring. Inflammation, increased glucocorticoid and oxidative stress and poor antioxidant defence probably underlie these adverse effects. Rehabilitation from parturition but not weaning was beneficial in delaying the onset of the adverse outcomes in the offspring. © 2016 BioFactors, 43(3):400-414, 2017.

United States Guidelines for Diverticulitis Treatment.

Guidelines for diverticular disease management were last supported and published by the American Gastroenterology Association and the American College of Gastroenterology 2 decades ago. Guidelines have been published in other countries and by some societies. These guidelines are suggested as United States of America guidelines. In reality, they are what is practiced in Connecticut at Yale New Haven hospitals. The epidemiology and pathophysiology is described. This is still considered a dietary fiber-deficiency disease that results in high intracolonic pressure with resultant outpocketing of diverticula in the weakest point of the colon at the sites of vascular penetration with developing elastin deposition in the colon wall. The age and gender distribution is described. They are most common in the sigmoid. The guidelines of management are described according to accepted classification of the disease at all stages from onset, to early formation, to mild disease, to complicated disease, to rare specific states. The outcomes and mortality are discussed.

Impact of a High-Fat or High-Fiber Diet on Intestinal Microbiota and Metabolic Markers in a Pig Model.

To further elaborate interactions between nutrition, gut microbiota and host health, an animal model to simulate changes in microbial composition and activity due to dietary changes similar to those in humans is needed. Therefore, the impact of two different diets on cecal and colonic microbial gene copies and metabolic activity, organ development and biochemical parameters in blood serum was investigated using a pig model. Four pigs were either fed a low-fat/high-fiber (LF), or a high-fat/low-fiber (HF) diet for seven weeks, with both diets being isocaloric. A hypotrophic effect of the HF diet on digestive organs could be observed compared to the LF diet (p < 0.05). Higher gene copy numbers of Bacteroides (p < 0.05) and Enterobacteriaceae (p < 0.001) were present in intestinal contents of HF pigs, bifidobacteria were more abundant in LF pigs (p < 0.05). Concentrations of acetate and butyrate were higher in LF pigs (p < 0.05). Glucose was higher in HF pigs, while glutamic pyruvic transaminase (GPT) showed higher concentrations upon feeding the LF diet (p < 0.001). However, C-reactive protein (CRP) decreased with time in LF pigs (p < 0.05). In part, these findings correspond to those in humans, and are in support of the concept of using the pig as human model.

The intestinal microbiota of piglets fed with wheat bran variants as characterised by 16S rRNA next-generation amplicon sequencing.

The intestinal microbiota of piglets fed with a Control diet low in dietary fibre and modified wheat bran variants as an additional source of insoluble dietary fibre was characterised. In this context, variances in the microbiota of three different gut segments were assessed. Wheat bran was either included in its native form or modified by fermentation and extrusion before added at 150 g/kg to a basal diet for 48 piglets (12 animals per treatment). Total DNA was extracted from digesta samples from the jejunum, the end of the ileum and the colon ascendens. Samples were prepared accordingly for subsequent sequencing with the Illumina MiSeq. The obtained results revealed distinct location-specific differences in microbial composition. While Firmicutes were most predominant in all three gut segments, Bacteroidetes were additionally found in the colon at high abundance. The parameters of alpha and beta diversity analysis showed significant differences (p < 0.01) between the colon and the other two gut segments. Specialised bacterial groups like Prevotella and Ruminococcaceae were among the most predominant ones found in the colon, as they possess cellulolytic properties to degrade (at least partially) non-starch polysaccharides, while their abundance was negligible in the jejunum and the ileum. Conversely, the genera Lactobacillus, Bifidobacterium and Veillonella, for example, were among the most predominant groups in the jejunum and ileum, while in the colon they were hardly found. Although statistical taxonomical evaluation, following p-value correction, did not reveal pronounced differences in abundance related to bran modification, alpha and beta diversity analysis showed an influence regarding the various feeding strategies applied. Based on these findings, a more in-depth view on intestinal microbial composition within the gastrointestinal tract of young pigs fed with low- and high-fibre diets was generated.

Fermented and extruded wheat bran in piglet diets: impact on performance, intestinal morphology, microbial metabolites in chyme and blood lipid radicals.

The aim of the present study was to evaluate the influence of native, fermented and extruded wheat bran on the performance and intestinal morphology of piglets. Additionally, short-chain fatty acids (SCFA), biogenic amines, ammonia, lactic acid, pH as well as E. coli and lactic acid bacterial counts were analysed in digesta samples from three gut sections. Furthermore, the antioxidant potential in blood samples was evaluated based on the lipid radicals formed. For this purpose, 48 newly weaned piglets (28 d old) were allocated to one of the four different dietary treatment groups: no wheat bran (Control), native wheat bran, fermented wheat bran as well as extruded wheat bran. Wheat bran variants were included at 150 g/kg into the diets. All diets were mixed to reach the calculated isonitrogenic nutrient contents. Gut tissue and digesta samples were collected from the proximal jejunum, the terminal ileum and the colon ascendens, blood samples directly at slaughter. Although none of the dietary interventions had an impact on performance parameters, the amount of goblet cells in the ileum was increased upon feeding native and extruded wheat bran, compared to fermented bran (p < 0.05). The E. coli counts in colonic chyme were significantly lower (p < 0.05) in the Control group compared to the groups fed with wheat bran. The concentration of SCFA showed differences for minor compounds (p < 0.05), while linear contrast analyses revealed a reduced concentration of total SCFA in the colon following the feeding of modified wheat bran compared to native wheat bran. This may suggest that several compounds are more easily digested already in the ileum, resulting in a reduced nutrient flow into the large intestine and therefore less unexploited digesta is available as substrate for the microorganisms there. Fermentation also resulted in a significant decrease of methylamine in the colon (p < 0.05), while other biogenic amines in the ileum and colon showed no statistically significant differences. The formation of lipid radicals was decreased (p < 0.05) after feeding native wheat bran compared to the Control group. These results suggest that fermentation and extrusion of wheat bran exert some different impact regarding their physiological mode of action.