Fiber-deficient Diet Research Articles

Probiotic Clostridium butyricum ameliorates cognitive impairment in obesity via the microbiota-gut-brain axis

Obesity is a risk factor for cognitive dysfunction and neurodegenerative disease, including Alzheimer's disease (AD). The gut microbiota-brain axis is altered in obesity and linked to cognitive impairment and neurodegenerative disorders. Here, we targeted obesity-induced cognitive impairment by testing the impact of the probiotic Clostridium butyricum, which has previously shown beneficial effects on gut homeostasis and brain function. Firstly, we characterized and analyzed the gut microbial profiles of participants with obesity and the correlation between gut microbiota and cognitive scores. Then, using an obese mouse model induced by a Western-style diet (high-fat and fiber-deficient diet), the effects of Clostridium butyricum on the microbiota-gut-brain axis and hippocampal cognitive function were evaluated. Finally, fecal microbiota transplantation was performed to assess the functional link between Clostridium butyricum remodeling gut microbiota and hippocampal synaptic protein and cognitive behaviors. Our results showed that participants with obesity had gut microbiota dysbiosis characterized by an increase in phylum Proteobacteria and a decrease in Clostridium butyricum, which were closely associated with cognitive decline. In diet-induced obese mice, oral Clostridium butyricum supplementation significantly alleviated cognitive impairment, attenuated the deficit of hippocampal neurite outgrowth and synaptic ultrastructure, improved hippocampal transcriptome related to synapses and dendrites; a comparison of the effects of Clostridium butyricum in mice against human AD datasets revealed that many of the genes changes in AD were reversed by Clostridium butyricum; concurrently, Clostridium butyricum also prevented gut microbiota dysbiosis, colonic barrier impairment and inflammation, and attenuated endotoxemia. Importantly, fecal microbiota transplantation from donor-obese mice with Clostridium butyricum supplementation facilitated cognitive variables and colonic integrity compared with from donor obese mice, highlighting that Clostridium butyricum’s impact on cognitive function is largely due to its ability to remodel gut microbiota. Our findings provide the first insights into the neuroprotective effects of Clostridium butyricum on obesity-associated cognitive impairments and neurodegeneration via the gut microbiota-gut-brain axis.

Fiber-deficient diet inhibits colitis through the regulation of the niche and metabolism of a gut pathobiont

Exclusive enteral nutrition (EEN) with fiber-free diets is an effective steroid-sparing treatment to induce clinical remission in children with Crohn's disease (CD). However, the mechanism underlying the beneficial effects of EEN remains obscure. Using a model of microbiota-dependent colitis with the hallmarks of CD, we find that the administration of a fiber-free diet prevents the development of colitis and inhibits intestinal inflammation in colitic animals. Remarkably, fiber-free dietalters the intestinal localization of Mucispirillum schaedleri, a mucus-dwelling pathobiont, which is required for triggering disease. Mechanistically, the absence of dietary fiber reduces nutrient availability and impairs the dissimilatory nitrate reduction to ammonia (DNRA) metabolic pathway of Mucispirillum, leading to its exclusion from the mucus layer and disease remission. Thus, appropriate localization of the specific pathobiont in the mucus layer is critical for disease development, which is disrupted by fiber exclusion. These results suggest strategies to treat CD by targeting the intestinal niche and metabolism of disease-causing microbes.

Scytosiphon lomentaria fucoidan ameliorates DSS-induced colitis in dietary fiber-deficient mice via modulating the gut microbiota and inhibiting the TLR4/NF-κB/MLCK pathway

The prevalence of ulcerative colitis (UC) poses a serious threat to human health. This study showed that fiber-deficient diet (FD) increased the susceptibility of mice to low dosage of DSS-induced UC, and a UC model was established by feeding mice with DSS and FD to evaluate the effect of Scytosiphon lomentaria fucoidan (SLF) on UC. SLF ameliorated the symptoms of UC, as evidenced by increases in colon length, goblet cells and glycoprotein and reduction in inflammatory cell infiltration and intestinal epithelial injury. SLF alleviated oxidative stress and inhibited colonic inflammation by reducing the levels of lipopolysaccharides and pro-inflammatory cytokines and suppressing the activation of nuclear factor kappa B pathway. SLF protected tight junction integrity by reducing the level of myosin light chain kinase and increasing the levels of claudin, zonula occludens-1 and occludin. SLF improved serum metabolites profile and affected multiple metabolic pathways that are crucial to human health, e.g. butanoate metabolism. The underlying mechanism can be associated with modulation of the gut microbiota and metabolites, including increases in short chain fatty acids and reduction in Proteobacteria, Bacteroides and Romboutsia. It suggests that SLF could be developed as a prebiotic polysaccharide to benefit human health by improving intestinal microecology.

Butyrate Attenuates Hepatic Steatosis Induced by a High-Fat and Fiber-Deficient Diet via the Hepatic GPR41/43-CaMKII/HDAC1-CREB Pathway.

Hepatic steatosis is a major health issue that can be attenuated by a healthy diet. This study investigates the effects and molecular mechanisms of butyrate, a dietary fiber metabolite of gut microbiota, on lipid metabolism in hepatocytes. This study examines the effects of butyrate (0-8mM) on lipid metabolism in primary hepatocytes. The results show that butyrate (2mM) consistently inhibits lipogenic genes and activates lipid oxidation-related gene expression in hepatocytes. Furthermore, butyrate modulates lipid metabolism genes, reduces fat droplet accumulation, and activates the calcium/calmodulin-dependent protein kinase II (CaMKII)/histone deacetylase 1 (HDAC1)-cyclic adenosine monophosphate response element binding protein (CREB) signaling pathway in the primary hepatocytes and liver of wild-type (WT) mice, but not in G-protein-coupled receptor 41 (GPR41) knockout and 43 (GPR43) knockout mice. This suggests that butyrate regulated hepatic lipid metabolism requires GPR41 and GPR43. Finally, the study finds that dietary butyrate supplementation (5%) ameliorates hepatic steatosis and abnormal lipid metabolism in the liver of mice fed a high-fat and fiber-deficient diet for 15 weeks. This work reveals that butyrate improves hepatic lipid metabolism through the GPR41/43-CaMKII/HDAC1-CREB pathway, providing support for consideration of butyrate as a dietary supplement to prevent the progression of NAFLD induced by the Western-style diet.

A fiber-deprived diet causes cognitive impairment and hippocampal microglia-mediated synaptic loss through the gut microbiota and metabolites

BackgroundCognitive impairment, an increasing mental health issue, is a core feature of the aging brain and neurodegenerative diseases. Industrialized nations especially, have experienced a marked decrease in dietary fiber intake, but the potential mechanism linking low fiber intake and cognitive impairment is poorly understood. Emerging research reported that the diversity of gut microbiota in Western populations is significantly reduced. However, it is unknown whether a fiber-deficient diet (which alters gut microbiota) could impair cognition and brain functional elements through the gut-brain axis.ResultsIn this study, a mouse model of long-term (15 weeks) dietary fiber deficiency (FD) was used to mimic a sustained low fiber intake in humans. We found that FD mice showed impaired cognition, including deficits in object location memory, temporal order memory, and the ability to perform daily living activities. The hippocampal synaptic ultrastructure was damaged in FD mice, characterized by widened synaptic clefts and thinned postsynaptic densities. A hippocampal proteomic analysis further identified a deficit of CaMKIId and its associated synaptic proteins (including GAP43 and SV2C) in the FD mice, along with neuroinflammation and microglial engulfment of synapses. The FD mice also exhibited gut microbiota dysbiosis (decreased Bacteroidetes and increased Proteobacteria), which was significantly associated with the cognitive deficits. Of note, a rapid differentiating microbiota change was observed in the mice with a short-term FD diet (7 days) before cognitive impairment, highlighting a possible causal impact of the gut microbiota profile on cognitive outcomes. Moreover, the FD diet compromised the intestinal barrier and reduced short-chain fatty acid (SCFA) production. We exploit these findings for SCFA receptor knockout mice and oral SCFA supplementation that verified SCFA playing a critical role linking the altered gut microbiota and cognitive impairment.ConclusionsThis study, for the first time, reports that a fiber-deprived diet leads to cognitive impairment through altering the gut microbiota-hippocampal axis, which is pathologically distinct from normal brain aging. These findings alert the adverse impact of dietary fiber deficiency on brain function, and highlight an increase in fiber intake as a nutritional strategy to reduce the risk of developing diet-associated cognitive decline and neurodegenerative diseases.2_wgC4CVAKtYwCNZbg5Y4xVideo

Dietary Fiber Is Essential to Maintain Intestinal Size, L-Cell Secretion, and Intestinal Integrity in Mice.

Dietary fiber has been linked to improved gut health, yet the mechanisms behind this association remain poorly understood. One proposed mechanism is through its influence on the secretion of gut hormones, including glucagon-like peptide-1 (GLP-1) and glucagon-like peptide-2 (GLP-2). We aimed to: 1) investigate the impact of a fiber deficient diet on the intestinal morphological homeostasis; 2) evaluate L-cell secretion; and 3) to ascertain the role of GLP-1, GLP-2 and Takeda G protein-receptor-5 (TGR5) signaling in the response using GLP-1 receptor, GLP-2 receptor and TGR5 knockout mice. Female C57BL/6JRj mice (n = 8) either received a standard chow diet or were switched to a crude fiber-deficient diet for a short (21 days) and long (112 days) study period. Subsequent identical experiments were performed in GLP-1 receptor, GLP-2 receptor and TGR5 knockout mice. The removal of fiber from the diet for 21 days resulted in a decrease in small intestinal weight (p < 0.01) and a corresponding decrease in intestinal crypt depth in the duodenum, jejunum and ileum (p < 0.001, p < 0.05, and p < 0.01, respectively). Additionally, colon weight was decreased (p < 0.01). These changes were associated with a decrease in extractable GLP-1, GLP-2 and PYY in the colon (p < 0.05, p < 0.01, and p < 0.01). However, we could not show that the fiber-dependent size decrease was dependent on GLP-1 receptor, GLP-2 receptor or TGR5 signaling. Intestinal permeability was increased following the removal of fiber for 112 days. In conclusion, our study highlights the importance of dietary fiber to maintain intestinal weight, colonic L-cell secretion and intestinal integrity.

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.

\u03b2-glucan attenuates cognitive impairment via the gut-brain axis in diet-induced obese mice

Background“Western” style dietary patterns are characterized by a high proportion of highly processed foods rich in fat and low in fiber. This diet pattern is associated with a myriad of metabolic dysfunctions, including neuroinflammation and cognitive impairment. β-glucan, the major soluble fiber in oat and barley grains, is fermented in the lower gastrointestinal tract, potentially impacting the microbial ecosystem and thus may improve elements of cognition and brain function via the gut-brain axis. The present study aimed to evaluate the effect of β-glucan on the microbiota gut-brain axis and cognitive function in an obese mouse model induced by a high-fat and fiber-deficient diet (HFFD).ResultsAfter long-term supplementation for 15 weeks, β-glucan prevented HFFD-induced cognitive impairment assessed behaviorally by object location, novel object recognition, and nesting building tests. In the hippocampus, β-glucan countered the HFFD-induced microglia activation and its engulfment of synaptic puncta, and upregulation of proinflammatory cytokine (TNF-α, IL-1β, and IL-6) mRNA expression. Also, in the hippocampus, β-glucan significantly promoted PTP1B-IRS-pAKT-pGSK3β-pTau signaling for synaptogenesis, improved the synaptic ultrastructure examined by transmission electron microscopy, and increased both pre- and postsynaptic protein levels compared to the HFFD-treated group. In the colon, β-glucan reversed HFFD-induced gut barrier dysfunction increased the thickness of colonic mucus (Alcian blue and mucin-2 glycoprotein immunofluorescence staining), increased the levels of tight junction proteins occludin and zonula occludens-1, and attenuated bacterial endotoxin translocation. The HFFD resulted in microbiota alteration, effects abrogated by long-term β-glucan supplementation, with the β-glucan effects on Bacteroidetes and its lower taxa particularly striking. Importantly, the study of short-term β-glucan supplementation for 7 days demonstrated pronounced, rapid differentiating microbiota changes before the cognitive improvement, suggesting the possible causality of gut microbiota profile on cognition. In support, broad-spectrum antibiotic intervention abrogated β-glucan’s effects on improving cognition, highlighting the role of gut microbiota to mediate cognitive behavior.ConclusionThis study provides the first evidence that β-glucan improves indices of cognition and brain function with major beneficial effects all along the gut microbiota-brain axis. Our data suggest that elevating consumption of β-glucan-rich foods is an easily implementable nutritional strategy to alleviate detrimental features of gut-brain dysregulation and prevent neurodegenerative diseases associated with Westernized dietary patterns.Ajj4hQzaw2wK1LZwmZvEcmVideo

Recovery of the Gut Microbiota after Antibiotics Depends on Host Diet, Community Context, and Environmental Reservoirs

Antibiotics alter microbiota composition and increase infection susceptibility. However, the generalizable effects of antibiotics on and the contribution of environmental variables to gut commensals remain unclear. To address this, we tracked microbiota dynamics with high temporal and taxonomic resolution during antibiotic treatment in a controlled murine system by isolating variables such as diet, treatment history, and housing co-inhabitants. Human microbiotas were remarkably resilient and recovered during antibiotic treatment, with transient dominance of resistant Bacteroides and taxa-asymmetric diversity reduction. In certain cases, invitro sensitivities were not predictive of invivo responses, underscoring the significance of host and community context. A fiber-deficient diet exacerbated microbiota collapse and delayed recovery. Species replacement through cross housing after ciprofloxacin treatment established resilience to a second treatment. Single housing drastically disrupted recovery, highlighting the importance of environmental reservoirs. Our findings highlight deterministic microbiota adaptations to perturbations and the translational potential for modulating diet, sanitation, and microbiota composition during antibiotics.

Recovery of the Gut Microbiota after Antibiotics Depends on Host Diet and Environmental Reservoirs

That antibiotics alter microbiota composition and increase infection susceptibility is well known, but their generalizable effects on the gut commensal community and dependence on environmental variables remain open questions. Here, we systematically compared antibiotic responses in gnotobiotic and conventional mice across antibiotics, microbiotas, diets, and housing status. We identify remarkable resilience, whereby a humanized microbiota recovers before drug administration ends, with transient oligodominance and taxa-asymmetric reduction in diversity. In general, in vitro sensitivities were not predictive of in vivo responses, underscoring the significance of community context. A fiber-deficient diet exacerbated collapse of the microbiota. We also observed response reprogramming, in which species replacement after ciprofloxacin treatment established resilience to a second treatment, as did transmission through cross-housing. Single-housing drastically disrupted recovery, highlighting the importance of sanitation and environmental reservoirs. Our findings highlight the ability of the commensal microbiota to deterministically adapt to large perturbations, and the translational potential for modulating diet, sanitation, and microbiota composition during antibiotics.

The genetic epidemiology of diverticulosis and diverticular disease: Emerging evidence.

Diverticular disease (DD) is one of the most prevalent gastrointestinal disorders. The pathogenesis of diverticulosis and DD is controversially discussed. Current studies call the traditional concept of a fibre-deficient diet causing the development of diverticula into question. Data from two recent twin studies have provided conclusive evidence for a strong genetic component to diverticulosis. Although genomewide association studies have provided new insights into the polygenic architecture of human diseases, genomic research in diverticulosis and DD has just been started. This is an astonishing fact given the high morbidity and mortality of the disease, as well as the substantial economic burden on health care systems. For this review, we provide an update of the molecular pathobiology and summarise recent evidence supporting the hypothesis that distinct, yet unidentified genetic variants contribute to the development of diverticulosis and DD.

Single Nucleotide Polymorphisms of NLRP12 Gene and Association with Non-specific Digestive Disorder in Rabbit.

The NLRP12 (NLR family, pyrin domain containing 12) serves as a suppressor factor in the inflammatory response and protects the host against inflammation-induced damage. In the present study, we aimed to study the polymorphisms of NLRP12 gene and its association with susceptibility to non-specific digestive disorder (NSDD) in rabbits. We re-sequenced the entire coding region of the rabbit NLRP12 gene and detected a total of 19 SNPs containing 14 synonymous and five non-synonymous variations. Among them, the coding SNP (c.1682A>G), which would carry a potential functional implication, was subsequently subjected to genotyping for case-control association study (272 cases and 267 controls). The results revealed that allele A was significantly protective against NSDD with an odds ratio value of 0.884 (95% confidence interval, 0.788 to 0.993; p = 0.038). We also experimentally induced NSDD in growing rabbits by feeding a fibre-deficient diet and subsequently investigated NLRP12 mRNA expression. The mRNA expression of NLRP12 in healthy status was significantly higher than that in severe NSDD (p = 0.0016). The highest expression was observed in individuals carrying the protective genotype AA (p = 0.0108). These results suggested that NLRP12 was significantly associated with the NSDD in rabbits. However, the precise molecular mechanism of NLRP12 involving in the development of rabbit NSDD requires further research.

Case–control study and mRNA expression analysis reveal the MyD88 gene is associated with digestive disorders in rabbit

As in humans, significant associations between Toll-like receptor 4 (TLR4) and digestive disorders have been identified in rabbit and dog. However, as an essential adaptor downstream of TLR4, the genetic variation of myeloid differentiating factor 88 (MyD88) and its association with digestive disorders have remained unknown. In this study, we detected 10 single nucleotide polymorphisms (SNPs) in the entire genomic region of rabbit MyD88. The genetic variation in susceptibility to digestive disorders for the only coding SNP (synonymous c.699T>C) was studied in Yaan (183 cases and 142 controls) and Chengdu populations (145 cases and 140 controls). A case-control association study revealed that individuals with the C allele had significant protection against digestive disorders in the Yaan population (OR=0.71; 95% CI, 0.51-0.99; P<0.05), the Chengdu population (OR=0.55; 95% CI, 0.39-0.78; P<0.01) and for joint analysis (OR=0.62; 95% CI, 0.49-0.79; P<0.01). We also experimentally induced digestive disorders by feeding a fiber-deficient diet and found that increased susceptibility was significantly associated with higher MyD88 mRNA expression (P<0.05). The lowest MyD88 mRNA expression was observed in individuals carrying the protective CC genotype. These results suggest that MyD88 is one of the most plausible candidate genes in relation to digestive disorders in rabbit. Further studies are required to explore the biological implications of MyD88 in the pathogenesis of digestive disorders.

Polymorphism of NLRP3 Gene and Association with Susceptibility to Digestive Disorders in Rabbit.

NLR family pyrin domain containing 3 (NLRP3) is a key component of the inflammasome, whose assembly is a crucial part of the innate immune response. The aim of the present study was to evaluate the association between exon 3 polymorphisms of NLRP3 and the susceptibility to digestive disorders in rabbits. In total, five coding single-nucleotide polymorphisms (cSNPs) were identified; all of which are synonymous. Among them, c.456 C> and c.594 G> were further genotyped for association analysis based on case-control design (n =162 vs n =102). Meanwhile, growing rabbits were experimentally induced to digestive disorders by feeding a fiber-deficient diet, subsequently they were subjected to mRNA expression analysis. Association analysis revealed that haplotype H1 (the two cSNPs: GT) played a potential protective role against digestive disorders (p<0.001). The expression of NLRP3 in the group H1HX1 (H1HX1 is composed of H1H1, H1H3 and H1H4) was the lowest among four groups which were classified by different types of diplotypes. Those results suggested that the NLRP3 gene was significantly associated with susceptibility to digestive disorders in rabbit.

Genetic variability of the resistance for three types of enteropathy in the growing rabbit

This paper describes the genetic variability for the resistance to three digestive stresses in the growing rabbit: after inoculation of coccidia (trial “coccidia”), with a fibre deficient diet (trial “FD”), and after experimental reproduction of epizootic rabbit enteropathy (trial “ERE”). Genetic variability was analysed from a sample of 48 sires, which produced the experimental young rabbits. These animals were examined on D0, D4, D11, D18, D25 and D32 after weaning (at 30 days old). Three clinical symptoms were checked: bloated abdomen, diarrhoea and mucus. Mortality and clinical symptoms were used to assess an individual response to each digestive stress. Two binary indexes were defined to describe this rabbit individual response. The first one (“Alive”) dealt with mortality. The second (“Tolerant”) dealt with mortality and morbidity. “Alive”, and “tolerant” percentages were low for the “coccidia” trial (61% and 23% respectively), high for the “FD” trial (75% and 36% respectively) and intermediate for the “ERE” trial (66% and 37% respectively). The sire effect was significant for each index in the “coccidia” and the “FD” trials. The sire effect was significant for the “tolerant” index in the “ERE” trial. Correlations between sire rankings for the two indexes of one trial were often significant. Correlations between sire rankings for indexes of “coccidia” and “FD” trials were weakly significant. Our results demonstrate that there is a genetic variability for the resistance to three different enteropathies.

Effects of Age and Dietary Fibre Level on Caecal Microbial Communities of Conventional and Specific Pathogen-Free Rabbits

Caecal community structure in conventional and specific pathogen-free (SPF) rabbits was assessed by performing dot-blot hybridization with 16S rRNA targeted oligonucleotide probes. The variation of the caecal flora was analysed according to age (18–70 days old), nutritional status (acid detergent fibre=19% in standard and 9% in fibre-deficient diet) and rabbit health (healthy vs diarrhoeic). Caecal flora was stabilized at around 25–28 days. Bacteria and archaea represented 73% and 22%, respectively, of the total microbial communities at weaning (28 days). Cellulolytic bacteria ( Ruminococcus albus, R. flaefaciens, Fibrobacter succinogenes and F. intestinalis ) represented <7% of total bacteria, with a predominance of R. flaefaciens and R. albus , respectively, for conventional and SPF rabbits. Bacterial and archaeal rRNAs were twofold higher in conventional than in SPF rabbits, fed standard diet (p<0.001). In conventional rabbits, archaeal community was twofold higher with standard diet than with fibre-deficient diet. In both types of rabbits, quantities of Flexibacter-Cytophaga-Bacteroides rRNA were twofold higher with fibre-deficient diet than with standard diet. In diarrhoeic conventional rabbits, the proportion of eukaryal rRNA increased 4-fold, but proportions of bacterial and archaeal rRNA decreased by 1-, 2- and 6-fold, respectively. The quantities of rRNA of F. succinogene s and F. intestinalis in conventional rabbits were, respectively 17 and 5 times higher in sick than in healthy animals, and decreased by 7-fold for R. albus . This study shows some microbial interactions according to nutrition and health of the rabbit. Key words : rabbit, caecal flora, fibre deficiency, oligonucleotide probes, enteropathy, specific pathogen-free, microbial community balance.

Microbial activity in the caecum of the rabbit around weaning: impact of a dietary fibre deficiency and of intake level

The current study was designed to evaluate the caecal microbial activity in the young rabbit, as influenced by dietary fibre concentration and feed intake level. Caecal fermentative activity and bacterial fibrolytic activity were measured before and after weaning (28-day old) in young (six litters of eight per diet) fed before weaning a fibre deficient diet “DF” (92 g acid detergent fibre (ADF) kg −1), or a standard fibre diet (165 g ADF kg −1) containing either a standard (diet SF) or an excessive methionine level (diet MSF). The effect of the dietary fibre level on microbial activity was evaluated by comparing DF and SF groups. The fibre effect itself, without change in intake level, was estimated by comparing DF and MSF groups, since a high level of methionine reduces the intake level in rabbits. Feed intake (from 28 to 42 days) was 13% lower for MSF than for SF group, but was similar to DF group. Between 21 days of age and weaning, caecal volatile fatty acid (VFA) concentration doubled and then slightly increased until 42 days of age. A linear reduction for propionate and, conversely, an increase in butyrate molar proportions were observed with age. Until weaning, VFA concentrations were similar between the three diets, although it tended to be lower for DF ( P=0.067). Subsequently, VFA concentration of SF group increased, while for DF it decreased (respectively, 72 mM l −1 versus 40 mM l −1 at 42 days, P<0.05). Pectinase, xylanase and cellulase activity of bacteria increased by 80% between 25 and 34 days of age. The bacterial fibrolytic activity was not significantly affected by the reduction of the intake (MSF versus SF), while fermentative parameters of MSF group were intermediate between SF and DF, suggesting that fibre effect partly depended on the intake level.

Impact of fibre deficiency and sanitary status on non-specific enteropathy of the growing rabbit

The effects of a sharp reduction in dietary fibre level (19 to 9% ADF resp. for S and D diet) were studied on the health status and performances of two groups of rabbits with different sanitary statuses: conventional ( n = 224) and specified pathogen free 'SPF' ( n = 72) from 28 to 70 days of age. Digestive pathology was monitored daily and individually along the whole fattening period (28-70 d old) to precisely quantify the impact of a fibre deficiency on rabbit health. Diarrhoea was the most common symptom of enteritis due to fibre deficiency (90% of cases). The major diges- tive lesions were dilatation of the caeco-colic segment (30%) and a watery intestinal and caecal digesta (60%). The digestive troubles had a similar expression with respect to sanitary status or diet effect. The mortality and the Health Risk index (HRi = mortality + morbidity rate) respectively reached 25 and 60% with the fibre deficient diet D (28-70 d period) compared to 9 and 41% for the standard diet S ( P < 0.05). The digestive disturbances appeared mainly during the period 28-42 d for SPF rabbits, and later for the C rabbits (43-56 d). Morbidity, HRi and the duration of diarrhoea were respectively 7, 2 and 3 times higher for C rabbits as compared to the SPF rabbits. A syner- getic effect of fibre deficiency and conventional sanitary status was observed on the incidence and inten- sity of digestive troubles. For individually caged rabbits, morbidity seemed to be mainly linked to the sanitary status of the animal (SPF or conventional), while the mortality level was enhanced by a fibre deficiency. The fibre supply thus seemed to prevent morbidity from evolving into mortality. In conclusion, non-specific enteropathy depends jointly on sanitary and nutritional status of the animals. rabbit / fibre deficiency / sanitary status / digestive pathology / nutrition

An association between maternal diet and colonic diverticulosis in an animal model.

Maternal diet may have an effect on the health of the offspring in middle and later life. This study used the laboratory rat as an animal model to examine whether the fibre content of the maternal diet during pregnancy affected subsequent development of colonic diverticula in the offspring fed lifelong fibre deficient or higher fibre diets. The parents of experimental animals were fed either a diet that was known to predispose to colonic diverticulosis or a control diet for one month prior to mating. The offspring were fed one of these diets for 18 months. The incidence of colonic diverticulosis, submucosal collagen content, collagen solubility in weak acid, and the composition of intestinal contents were then measured. Offspring of rats fed a higher fibre diet from higher fibre diet fed parents had 0% incidence of colonic diverticulosis. When offspring (regardless of parental diet) were fed a low fibre diet for life the acid solubility was lowered compared with rats fed lifelong higher fibre diet mean (SD) (0.044 (0.0007) v 0.073 (0.0015) sigmoid colon (ratio of soluble:insoluble collagen)); 21.1% had diverticulosis and there was reduced fibre fermentation. However, when the diet of the parents of the fibre deficient diet fed rats was considered, the animals whose mothers had a fibre deficient diet had lower acid solubility (0.032 (0.0007)) and an increased incidence of colonic diverticulosis (42.1%) than the animals fed a fibre deficient diet from higher fibre diet fed parents (p < 0.01 in all instances). Maternal diet and the subsequent nutrition of the progeny seem to be of importance in the development of colonic diverticulosis in the rat.

Collagen alteration in an animal model of colonic diverticulosis.

Changes in the structure and integrity of the colon dependent on collagen content and crosslinkage occur with age. This study using an animal model examines colonic collagen content and crosslinkage over the lifetime of rats on fibre deficient and higher fibre diets. Two groups of 20 rats were fed either a fibre deficient diet (1.7 g NSP (non-starch polysaccharide)/100 g) or a higher fibre diet (13.3 g NSP/100 g) for 18 months. Diverticula were identified by postmortem examination. Caecal and colonic contents were weighed and assayed for short chain fatty acids. Collagen solubility in weak acid was measured to give an indication of the nature and amount of crosslinks in the collagen of the bowel wall. The incidence of colonic diverticula was greater (42.1% fibre deficient rats; 0% higher fibre rats). Colonic collagen solubility index in fibre deficient rats was significantly lower than higher fibre diet fed rats (p < 0.001 in all four sections of the large bowel). Rats with diverticula had the lowest solubility index (p < 0.001 in all four sections of the large bowel). Higher fibre diet rats had increased caecal and colonic contents, caecal and colonic tissue wet weights, and greater caecal short chain fatty acids. Fibre deficient diet fed rats had more pathological abnormalities. This animal model permits a study of the relation between collagen crosslinkage and the development of colonic diverticulosis. A higher fibre diet protects against collagen crosslinking and this is related to a decreased incidence of diverticula.