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The scientific rationale for dietary fibre intake recommendations comes from the recognition of their benefits for health based on studies first published many years ago. It remains unclear which are the key physiological effects generated by dietary fibre in view of the diversity of the food components considered as dietary fibre, of the relevance of their classification (soluble and insoluble) and from the recent discoveries putting forward their interactions with the gut microbiota. The project FiberTAG (Joint Programming Initiative 'A Healthy Diet for a Healthy Life' 2017–2020 www.fibertag.eu/) aims to establish a set of biomarkers (markers of gut barrier function and bacterial co‐metabolites including volatile compounds and lipid derivatives), measured in different biological compartments (faeces, blood or breath) linking dietary fibre intake and gut microbiota‐related health effects. The FiberTAG consortium brings together academic and industrial partners from Belgium, France, Germany and Canada to share data and samples obtained from existing as well as new intervention studies in order to evaluate the relevance of such biomarkers. The FiberTAG consortium is currently working on five existing cohorts (prospective observational or nutritional interventions in healthy or obese patients), and a number of new intervention studies to analyse the effect of insoluble dietary fibre (wheat bran and chitin‐glucan, provided by the industrial partners) in healthy individuals or in obese patients at high cardiometabolic risk. [ABSTRACT FROM AUTHOR]

This review presents mechanistic studies performed in vitro and in animal models, as well as data obtained in patients that contribute to a better understanding of the impact of nutrients interacting with the gut microbiota on metabolic and behavioural alterations linked to obesity. The gut microbiota composition and function are altered in several pathological conditions including obesity and related diseases i.e. non-alcoholic fatty liver diseases (NAFLD). The gut-liver axis is clearly influenced by alterations of the gut barrier that drives inflammation. In addition, recent papers propose that specific metabolites issued from the metabolic cooperation between the gut microbes and host enzymes, modulate inflammation and gene expression in the liver. This review illustrates how dietary intervention with prebiotics or probiotics influences host energy metabolism and inflammation. Indeed, intervention studies are currently underway in obese and NAFLD patients to unravel the relevance of the changes in gut microbiota composition in the management of metabolic and behavioural disorders by nutrients interacting with the gut microbiota. In conclusion, diet is among the main triggers of NAFLD and the gut microbiota is modified accordingly, underlining the importance of the concomitant study of the nutrients and microbial impact on liver health and metabolism, in order to propose innovative, clinically relevant, therapeutic approaches. [ABSTRACT FROM AUTHOR]

Background:Metabolites released by the gut microbiota may influence host metabolism and immunity. We have tested the hypothesis that inulin-type fructans (ITF), by promoting microbial production of short-chain fatty acids (SCFA), influence cancer cell proliferation outside the gut.Methods:Mice transplanted with Bcr-Abl-transfected BaF3 cells, received ITF in their drinking water. Gut microbiota was analysed by 16S rDNA polymerase chain reaction (PCR)-denaturing gradient gel electrophoresis (DGGE) and qPCR. Serum Short-chain fatty acids were quantified by UHPLC-MS. Cell proliferation was evaluated in vivo, by molecular biology and histology, and in vitro.Results:Inulin-type fructans treatment reduces hepatic BaF3 cell infiltration, lessens inflammation and increases portal propionate concentration. In vitro, propionate reduces BaF3 cell growth through a cAMP level-dependent pathway. Furthermore, the activation of free fatty acid receptor 2 (FFA2), a Gi/Gq-protein-coupled receptor also known as GPR43 and that binds propionate, lessens the proliferation of BaF3 and other human cancer cell lines.Conclusion:We show for the first time that the fermentation of nutrients such as ITF into propionate can counteract malignant cell proliferation in the liver tissue. Our results support the interest of FFA2 activation as a new strategy for cancer therapeutics. This study highlights the importance of research focusing on gut microbes-host interactions for managing systemic and severe diseases such as leukaemia. [ABSTRACT FROM AUTHOR]

This article explores the potential role of inulin-type fructans in the human diet, focusing on scientific developments presented at the 5th Orafti Research Conference held at the Harvard Medical School in 2006, with special emphasis on the effects of inulin and oligofructose on the modulation of the gut microbiota and their effects on human health. [ABSTRACT FROM AUTHOR]

Nondigestible but fermentable dietary fructans such as oligofructose exert many effects on gut physiology through their fermentation end products such as short-chain fatty acids. Could other metabolites be produced in the gut and contribute to the physiologic effects of dietary fructans? The aim of the study was to evaluate the influence of oligofructose on putrescine, spermidine and spermine concentrations in the cecum, the portal vein and the liver of rats and to assess their involvement in cecal enlargement and the modulation of hepatic lipid metabolism. Putrescine, spermidine and spermine were quantified by HPLC in samples obtained from male Wistar rats fed a nonpurified standard diet (controls) or the same diet enriched with 10 g/100 g oligofructose (OFS) for 4 wk. OFS-fed rats had significantly greater cecal content and tissue weights. OFS almost doubled the concentration of putrescine in the cecal contents. The concentration of all three polyamines in the cecal tissue was significantly greater than in controls. The concentration of spermidine in portal plasma was lower in rats fed OFS, whereas the treatment did not affect the polyamine concentrations in the liver. The fermentation of dietary fructans contributed to an increase in the concentration of putrescine in the gut without modifying putrescine concentration in either the portal blood or liver. Moreover, the greater levels of polyamines in cecal tissue may be related to the cell proliferation resulting from OFS fermentation in the gut. [ABSTRACT FROM AUTHOR]

We studied the influence of oligofructose (OFS), a nondigestible fructan, on lipid metabolism in obese fa/fa Zucker rats. The addition of 10 g/100 g OFS to the diet slowed the increase in body weight without modifying serum triglycerides or glucose concentrations after 7 wk of treatment. However, an oral load of 2 g glucose and 5 g corn oil/kg body weight increased triglyceridemia more in OFS-fed rats than in control rats. After 10 wk, OFS decreased the hepatic concentration of triglycerides 57% relative to controls. The less severe steatosis was confirmed by histologic analysis. Among the key enzymes involved in fatty acid synthesis and esterification, only malic enzyme activity was significantly lower in OFS-fed rats than in controls. The epididymal fat mass was significantly lower in OFS-fed rats. In conclusion, dietary enrichment with OFS can counteract both the fat mass development and the hepatic steatosis that occur in obese Zucker rats. Future studies will be designed to clarify in obese animals the influence of dietary OFS on postprandial triglyceridemia, which is an important variable associated with the development of atherosclerosis in humans, and to analyze the biochemical mechanism underlying the "hepatoprotective" effect of OFS. [ABSTRACT FROM AUTHOR]

Oligofructose (OFS), a mixture of nondigestible/fermentable fructooligosaccharides, decreases serum triacylglycerol (TAG) when it is included in the standard, fiber-free or high fat diet of rats. This paper summarizes in vivo and in vitro data to establish a biochemical mechanism underlying the hypolipidemic effect of OFS. When OFS is added to the standard (carbohydrate-rich) diet of rats at the dose of 10 g/100 g, a TAG-lowering action occurs as a consequence of a reduction of de novo liver fatty acid synthesis. The depression in the activity of all lipogenic enzymes and fatty acid synthase mRNA suggests that OFS modifies the gene expression of lipogenic enzymes. Through its modulation of de novo lipogenesis, OFS can protect against liver lipid accumulation induced by providing 10% fructose-enriched water for 48 h. OFS also significantly decreases serum insulin and glucose, which are both known to participate in the nutritional regulation of lipogenesis. It also increases the intestinal production of incretins, namely, glucose-dependent insulinotropic peptide and glucagon-like peptide 1. This latter phenomenon results mainly from promotion of intestinal tissue proliferation by oligofructose fermentation end-products. Collectively, a link likely exists between the modulation of hormone and incretin production by OFS, and its antilipogenic effect. [ABSTRACT FROM AUTHOR]

Focuses on the rate of inulin-type fructans in the gastrointestinal tract. Nondigestibility in the upper gastrointestinal tract; Effect on mineral absorption; Effect on uremia and nitrogen disposal.

Dietary supplementation with oligofructose (OFS; 100 g/kg), a non-digestibleoligomer of β-D-fructose, decreases serum triacylglycerols in serum and VLDL of rats. In order to investigate the role of hepatic metabolism in the hypolipidaemic effect of OFS, male Wistar rats were fed on a standard diet with or without 1OOg Raftilose® P95/kg as OFS source for 30 d. OFS feeding (1) significantly decreased triacylglycerol and phospholipid concentrations in both blood and liver, (2) increased the glycerol-3-phosphate liver content but decreased the hepatic activity of glycerol-3-phosphate acyltransferase (EC 2.3.1.15), suggesting a decrease in acylglycerol synthesis, (3) did not affect the blood non-caterified fatty acid concentrations, but (4) reduced by 54% the capacity of isolated hepatocytesto synthesize and secrete triacylglycerols from labelled acetate; the activity of fatty acid synthase, a key lipogenic enzyme was also significantly decreased. These findings suggest that OFS decreases serum triacylglycerols by reducing de nova fatty acid synthesis in the liver; the lower insulin level in the serum of OFS-fed rats could explain, at least partly, the metabolic effect induced by such nondigestible carbohydrates. [ABSTRACT FROM PUBLISHER]