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Guan, Z.;  Yu, E.;  Feng, Q. Soluble Dietary Fiber. Encyclopedia. Available online: (accessed on 22 June 2024).
Guan Z,  Yu E,  Feng Q. Soluble Dietary Fiber. Encyclopedia. Available at: Accessed June 22, 2024.
Guan, Zhi-Wei, En-Ze Yu, Qiang Feng. "Soluble Dietary Fiber" Encyclopedia, (accessed June 22, 2024).
Guan, Z.,  Yu, E., & Feng, Q. (2022, September 02). Soluble Dietary Fiber. In Encyclopedia.
Guan, Zhi-Wei, et al. "Soluble Dietary Fiber." Encyclopedia. Web. 02 September, 2022.
Soluble Dietary Fiber

Dietary fiber is a widely recognized nutrient for human health. Previous studies proved that dietary fiber has significant implications for gastrointestinal health by regulating the gut microbiota. Moreover, mechanistic research showed that the physiological functions of different dietary fibers depend to a great extent on their physicochemical characteristics, one of which is solubility.

soluble dietary fiber resistant oligosaccharide viscous fiber gut microbiota human health

1. Introduction

The dietary pattern is closely related to human health. Hu et al. identified two major dietary patterns, which are the Prudent and Western diets [1]. The Prudent diet is considered healthy and is characterized by higher intake of vegetables, fruit, legumes, whole grains, fish, and poultry. Compared to the Prudent diet, the Western diet is characterized by abundant red meat, fat, and refined carbohydrates [2][3]. The Western diet contributes to increased risk of non-communicable diseases, especially gastrointestinal diseases and metabolic diseases which are partially attributed to the deficiency of dietary fiber in the Western diet [4][5][6][7][8][9][10]. According to the widely accepted definition derived from Codex Alimentarius Alinorm in 2009, dietary fiber is considered as edible carbohydrate polymers with three or more monomeric units that are resistant to endogenous digestive enzymes and thus are neither hydrolyzed nor absorbed in the small intestine [11]. Based on their structures, dietary fibers can be classified into non-starch polysaccharides, resistant starches (RSs), and resistant oligosaccharides. Moreover, the non-carbohydrate polymer, lignin, which coexists with cellulose in plant cell walls, is also considered in this definition as dietary fiber. Based on the source, dietary fibers are mainly comprised three subgroups: (i) Carbohydrate polymers naturally existing in edible plants and consumed as vegetables, fruits, seeds, cereals, and tubers; (ii) edible carbohydrate polymers obtained from raw foods by physical, enzymatic, and chemical means that have a proven physiological benefit (e.g., resistant oligosaccharides, inulin, and psyllium); and (iii) synthetic carbohydrate polymers with a proven physiological benefit (e.g., methylcellulose). [11][12].

Dietary fibers from food pass through the small intestine into the large intestine, where they play physiological roles. Dietary fibers contain a variety of organic polymers, with different monomers linked by different glycosidic bonds, showing complex and heterogeneous structure [13]. To help correlate physicochemical characteristics of dietary fiber with their physiological functions, many ways in classifying dietary fiber were established, which include solubility, viscosity, and fermentability [14]. Depending on solubility, dietary fiber can be categorized as insoluble or soluble (SDFs) [15]. The sugar chains in insoluble dietary fiber associate with each other by dense hydrogen bonds, forming a hydrophobic and crystalline structure, which can resist the hydrolysis of exogenous glucosidases. As the most widely distributed and abundant insoluble fiber in nature, cellulose is a polysaccharide with high molecular weight, composed of β-glucose. It is the main structural component of plant cell walls, which usually combines with hemicellulose, pectin, and lignin [16]. A schematic diagram of molecular structure of cellulose is shown in Figure 1. Most insoluble dietary fibers, such as cellulose, hemi-cellulose, and lignin, have an effect on bulking fecal material, but are not or just slowly utilized by gut bacteria. On the contrary, SDFs can be readily and quickly metabolized by gut bacteria, in the process of which SDFs significantly influence the abundance and diversity of the human gut microbiota [17]. Studies confirmed that dietary fibers, especially SDFs, can positively regulate the gut microbiota and be metabolized to beneficial products, mainly short-chain fatty acids (SCFAs), thus providing many advantages to human health, such as reducing the risk of gastrointestinal diseases including irritable bowel syndrome (IBS), inflammatory bowel disease (IBD), diverticular disease, functional constipation, fecal incontinence, and colorectal cancer (CRC) [18][19][20].

Figure 1. Schematic diagram of the structures of representative insoluble dietary fiber and SDF. The representative insoluble dietary fiber, cellulose.

2. SDFs and Their Metabolites Display Important Physiological Effects on Human Health

Although SDFs hardly directly provide energy for humans, SDFs per se exhibits specific physiological functions as recognized nutrients. In addition to stimulating the production and secretion of mucus, SDFs and SCFAs have other important physiological functions. In this section, the researchers summarized the physiological functions of SDFs, including those that are attributed to SCFAs.

2.1. Increase Satiety and Reduce Energy Intake

Viscous SDFs retard the hydrolysis and absorption of energetic nutrients from food in the small intestine, such as starch and triglyceride. So, SDFs can significantly reduce the total intake of energy as well as glucose and cholesterol, so they contribute to slowing down the process of obesity, type 2 diabetes mellitus (T2DM), hyperlipidemia, and related metabolic diseases [21][22]. Then, the chyme gets to and stimulates the terminal ileum, where the mucosa responses and releases glucagon-like peptide-1 (GLP-1). The results from the experiments in human and pigs indicated that GLP-1 can inhibit gastric emptying and reduce intestinal peristalsis [23][24]. Therefore, viscous SDFs are helpful to control appetite, improve insulin sensitivity, and reduce weight.

2.2. Promote the Metabolism and Absorption of Active Substances

Many viscous SDFs can provide a platform for the metabolism of active substances. Take the bile acids as an example. Bile acids are produced in the liver and metabolized by enzymes from intestinal bacteria, which not only promote the absorption of dietary fat but also play indispensable roles in maintaining the healthy gut microbiota, balanced lipid and carbohydrate metabolism, insulin sensitivity, and innate immunity [25]. In the upper segment of the ileum and colon, conjugated primary bile acids combine with SDFs, where they are hydrolyzed to free primary bile acids by the bile salt hydrolase (BSH) from the intestinal bacteria, mainly Bacteroides and Lactobacilli [26]. Then, 7α-dehydroxylase also from the intestinal bacteria, such as Clostridium spp. and Eubacterium spp., catalyzes the free primary bile acids to secondary bile acids [27][28].
In addition to organic substrates, viscous SDFs can bind with inorganic nutrients such as metal ions. It was reported that after being bound with SDFs, calcium, magnesium, iron, copper, and zinc are transported to the distal colon. With the degradation of SDFs by the local bacteria, the ions are released and exhibit specific effects including resisting pathogens, increasing the diversity of the intestinal bacterial community, and protecting the gut from infection [29]. Furthermore, SCFAs produced via the gut microbiota fermenting SDFs combine with ions to form soluble salts, which are more prone to absorption by the colon [30][31].

2.3. SCFAs Act as Histone Deacetylase (HDAC) Inhibitors

Intracellular butyrate and propionate inhibit the activity of HDACs in colon cells and immune cells, leading to histone hyperacetylation, which in turn affects gene expression and cell differentiation, proliferation, and apoptosis [32]. Many studies have shown that SCFAs have important anti-inflammatory effects due to HDAC inhibition. For example, SCFAs can down-regulate proinflammatory cytokines such as interleukin-6 (IL-6) and IL-12 in colonic macrophages and differentiate dendritic cells from bone marrow stem cells [33][34]. Moreover, SCFAs can induce colonic regulatory T cells (Tregs) in mice [35]. There is also evidence that butyrate and propionate can induce the differentiation of Tregs, which can express the transcription factor Foxp3 via increasing the acetylation at the gene locus of foxP3. Foxp3 is found to play a crucial role in controlling intestinal inflammation in mice [36]. In addition, butyrate and propionate activate the AP-1 signaling pathway in human epithelial cells, which plays an important role in controlling proliferation and inducing apoptosis of colon cancer cells [37].
In brief, SCFAs, especially butyrate, not only provide the most energy for colon cells, but also aid to a large extent in the prevention of inflammation and CRC due to HDAC inhibition.

2.4. SCFAs Are Important Ligands for Specific G-Protein Coupled Receptors (GPCRs)

In addition to acting as HDAC inhibitors, SCFAs also exert important physiological functions as ligands for GPCRs. Three GPCRs (GPR41, GPR43, and GPR109A) involved in immune regulation were proven to specifically respond to free fatty acids. Therefore, GPR43 and GPR41 were also named FFAR (free fatty acid receptor) 2 and FFAR3, respectively [38].
In mice, butyrate can increase the secretion of Tregs, IL-18, and T cells producing IL-10 in intestinal epithelial cells via stimulating GPR109A [39]. Additionally, the study by Macia et al. in mice indicated that SCFAs derived from a high-fiber diet stimulated GPR43 and GPR109A to activate the NLRP3 inflammasome, which produces IL-18. This effect maintains intestinal homeostasis by decreasing the inflammatory response of the gut and maintaining the integrity of the mucosal barrier, which prevents bacterial invasion and infection [40]. In the intestine and white adipose tissue (WAT) of mice, SCFA-dependent GPR43 stimulation (especially acetate and propionate) displays beneficial effects in ameliorating the metabolism of glucose and lipids by GLP-1 secretion and anti-lipolytic activity, respectively [41]. GPR41 also plays a role in the regulating appetite. Samuel et al. reported that by binding with GPR41, SCFAs induce the production of peptide YY, which inhibits gastrointestinal motility and gastric acid secretion in mice [42].
The above studies indicated that SCFAs have significant immunologic and metabolic functions as ligands for GPCRs, affecting the incidence of IBD, CRC, and other cancers as well as chronic metabolic diseases.
The identified physiological effects of SDFs and SCFAs on human health are summarized in Figure 2.
Figure 2. Summary of identified physiological effects of SDF and SCFAs on human health.

3. Safety of SDFs

Although SDFs show excellent health effects, it cannot be ignored that inappropriate SDF intake may lead to certain health hazards, which depend on the type and quantity of SDFs as well as the physiological background of the host.
First, a sudden increase of SDF intake, even when consumed judiciously, may lead to abdominal distension, flatulence, constipation, diarrhea, and other syndromes of IBS [43][44]. Second, as mentioned above, the binding by SDFs can promote to a certain extent the absorption of certain micronutrients such as some metal ions in the colon. However, the study on six healthy young women by Riedl et al. indicated that the bioavailability of β-carotene, lycopene, and lutein, was markedly reduced by three different kinds of SDFs, pectin, guar gum, and alginate [45]. This suggests that excessive SDF intake may be disadvantageous to certain people with micronutrient deficiencies. In addition, Bruggencate et al. reported that the rapid fermentation of FOS by endogenous microbiota damaged the intestinal mucosal barrier and increased intestinal permeability, which caused pathogen infection in rats [46]. Moreover, the study by Singh et al. found that formulating a diet rich in refined inulin or other SDFs to feed TLR5-deficient (T5KO) mice with obesity caused by dysregulated gut microbiota, about 40% of mice had a lower weight than before. However, many mice suffered from icteric hepatocellular carcinoma (HCC). Further research revealed that SDF-induced HCC in mice developed via elevation of secondary bile acids in the systemic circulation, cholestasis, and hepatocyte death, followed by neutrophilic inflammation of the liver. Furthermore, fecal microbiota analysis by 16S rRNA sequencing showed that the HCC-prone mice exhibited gut dysbiosis characterized by a loss in species richness and diversity and an increase in the Proteobacteria phylum and the fiber-utilizing microbes including Clostridium spp. However, such HCC in T5KO mice cannot be induced by cellulose, the insoluble and non-fermentable fiber, and it was not observed in germ-free nor antibiotics-treated mice [47]. Although acting as a kind of metabolite with important physiological functions, certain bile acids, especially secondary bile acids, were proven to be cytotoxic and cancer-promoting, which have adverse effects on the structure and function of the colonic epithelium by many mechanisms including DNA oxidative damage, inflammation, NF-κB activation, reducing apoptosis, and differentiation, as well as enhancing cell proliferation [48]. Apart from HCC, the changed bile acid profile derived from dysregulated gut microbiota was demonstrated to be associated with a variety of digestive diseases. For example, many patients suffering from CRC exhibited abnormal bile acid metabolism characteristic of redundant secondary bile acids. These redundant secondary bile acids, including deoxycholic acid, lithocholic acid, and taurochenodeoxycholic acid, originate in the aberrant elevation of certain gut bacteria expressing BSH and 7α-dehydroxylase, whose proportion is significantly higher than that in the gut microbiota of healthy people [25]. These facts hinted that, despite notable physiological benefits, fortification of diets with SDFs should be done with great caution as it may cause severe digestive disorders, especially under the background of dysregulated gut microbiota.


  1. Hu, F.B.; Rimm, E.B.; Stampfer, M.J.; Ascherio, A.; Spiegelman, D.; Willett, W.C. Prospective study of major dietary patterns and risk of coronary heart disease in men. Am. J. Clin. Nutr. 2000, 72, 912–921.
  2. van Dam, R.M.; Rimm, E.B.; Willett, W.C.; Stampfer, M.J.; Hu, F.B. Dietary patterns and risk for type 2 diabetes mellitus in U.S. men. Ann. Intern. Med. 2002, 136, 201–209.
  3. Strate, L.L.; Keeley, B.R.; Cao, Y.; Wu, K.; Giovannucci, E.L.; Chan, A.T. Western Dietary Pattern Increases, and Prudent Dietary Pattern Decreases, Risk of Incident Diverticulitis in a Prospective Cohort Study. Gastroenterology 2017, 152, 1023–1030.e2.
  4. Christ, A.; Lauterbach, M.; Latz, E. Western Diet and the Immune System: An Inflammatory Connection. Immunity 2019, 51, 794–811.
  5. Sdona, E.; Georgakou, A.V.; Ekström, S.; Bergström, A. Dietary Fibre Intake in Relation to Asthma, Rhinitis and Lung Function Impairment—A Systematic Review of Observational Studies. Nutrients 2021, 13, 3594.
  6. Larrosa, S.; Luque, V.; Grote, V.; Closa-Monasterolo, R.; Ferré, N.; Koletzko, B.; Verduci, E.; Gruszfeld, D.; Xhonneux, A.; Escribano, J. Fibre Intake Is Associated with Cardiovascular Health in European Children. Nutrients 2020, 13, 12.
  7. O’Keefe, S.J. Diet, microorganisms and their metabolites, and colon cancer. Nat. Rev. Gastroenterol. Hepatol. 2016, 13, 691–706.
  8. Zhao, L.; Zhang, F.; Ding, X.; Wu, G.; Lam, Y.Y.; Wang, X.; Fu, H.; Xue, X.; Lu, C.; Ma, J.; et al. Gut bacteria selectively promoted by dietary fibers alleviate type 2 diabetes. Science 2018, 359, 1151–1156.
  9. Canfora, E.E.; Meex, R.C.R.; Venema, K.; Blaak, E.E. Gut microbial metabolites in obesity, NAFLD and T2DM. Nat. Rev. Endocrinol. 2019, 15, 261–273.
  10. Dinan, T.G.; Cryan, J.F. The Microbiome-Gut-Brain Axis in Health and Disease. Gastroenterol. Clin. N. Am. 2017, 46, 77–89.
  11. Stephen, A.M.; Champ, M.M.; Cloran, S.J.; Fleith, M.; van Lieshout, L.; Mejborn, H.; Burley, V.J. Dietary fibre in Europe: Current state of knowledge on definitions, sources, recommendations, intakes and relationships to health. Nutr. Res. Rev. 2017, 30, 149–190.
  12. Davani-Davari, D.; Negahdaripour, M.; Karimzadeh, I.; Seifan, M.; Mohkam, M.; Masoumi, S.J.; Berenjian, A.; Ghasemi, Y. Prebiotics: Definition, Types, Sources, Mechanisms, and Clinical Applications. Foods 2019, 8, 92.
  13. Lovegrove, A.; Edwards, C.H.; De Noni, I.; Patel, H.; El, S.N.; Grassby, T.; Zielke, C.; Ulmius, M.; Nilsson, L.; Butterworth, P.J.; et al. Role of polysaccharides in food, digestion, and health. Crit. Rev. Food Sci. Nutr. 2017, 57, 237–253.
  14. Williams, B.A.; Mikkelsen, D.; Flanagan, B.M.; Gidley, M.J. “Dietary fibre”: Moving beyond the “soluble/insoluble” classification for monogastric nutrition, with an emphasis on humans and pigs. J. Anim. Sci. Biotechnol. 2019, 10, 45.
  15. O’Grady, J.; O’Connor, E.M.; Shanahan, F. Review article: Dietary fibre in the era of microbiome science. Aliment. Pharmacol. Ther. 2019, 49, 506–515.
  16. Takahashi, T.; Karita, S.; Ogawa, N.; Goto, M. Crystalline cellulose reduces plasma glucose concentrations and stimulates water absorption by increasing the digesta viscosity in rats. J. Nutr. 2005, 135, 2405–2410.
  17. McRorie, J.W., Jr.; McKeown, N.M. Understanding the Physics of Functional Fibers in the Gastrointestinal Tract: An Evidence-Based Approach to Resolving Enduring Misconceptions about Insoluble and Soluble Fiber. J. Acad. Nutr. Diet. 2017, 117, 251–264.
  18. Gill, S.K.; Rossi, M.; Bajka, B.; Whelan, K. Dietary fibre in gastrointestinal health and disease. Nat. Rev. Gastroenterol. Hepatol. 2021, 18, 101–116.
  19. Staller, K.; Song, M.; Grodstein, F.; Whitehead, W.E.; Matthews, C.A.; Kuo, B.; Chan, A.T. Increased Long-Term Dietary Fiber Intake Is Associated with a Decreased Risk of Fecal Incontinence in Older Women. Gastroenterology 2018, 155, 661–667.e1.
  20. Koh, A.; De Vadder, F.; Kovatcheva-Datchary, P.; Bäckhed, F. From Dietary Fiber to Host Physiology: Short-Chain Fatty Acids as Key Bacterial Metabolites. Cell 2016, 165, 1332–1345.
  21. Burton-Freeman, B. Dietary fiber and energy regulation. J. Nutr. 2000, 130, 272S–275S.
  22. Howarth, N.C.; Saltzman, E.; Roberts, S.B. Dietary fiber and weight regulation. Nutr. Rev. 2001, 59, 129–139.
  23. Ratanpaul, V.; Williams, B.A.; Black, J.L.; Gidley, M.J. Review: Effects of fibre, grain starch digestion rate and the ileal brake on voluntary feed intake in pigs. Animal 2019, 13, 2745–2754.
  24. Benton, D.; Young, H.A. Reducing Calorie Intake May Not Help You Lose Body Weight. Perspect. Psychol. Sci. 2017, 12, 703–714.
  25. Jia, W.; Xie, G.; Jia, W. Bile acid-microbiota crosstalk in gastrointestinal inflammation and carcinogenesis. Nat. Rev. Gastroenterol. Hepatol. 2018, 15, 111–128.
  26. Ridlon, J.M.; Kang, D.J.; Hylemon, P.B. Bile salt biotransformations by human intestinal bacteria. J. Lipid Res. 2006, 47, 241–259.
  27. Chiang, J.Y. Bile acids: Regulation of synthesis. J. Lipid Res. 2009, 50, 1955–1966.
  28. Chiang, J.Y.L.; Ferrell, J.M. Bile Acids as Metabolic Regulators and Nutrient Sensors. Annu. Rev. Nutr. 2019, 39, 175–200.
  29. Makki, K.; Deehan, E.C.; Walter, J.; Backhed, F. The Impact of Dietary Fiber on Gut Microbiota in Host Health and Disease. Cell Host Microbe 2018, 23, 705–715.
  30. Baye, K.; Guyot, J.P.; Mouquet-Rivier, C. The unresolved role of dietary fibers on mineral absorption. Crit. Rev. Food Sci. Nutr. 2017, 57, 949–957.
  31. Bosscher, D.; Van Caillie-Bertrand, M.; Deelstra, H. Effect of thickening agents, based on soluble dietary fiber, on the availability of calcium, iron, and zinc from infant formulas. Nutrition 2001, 17, 614–618.
  32. Fung, K.Y.; Cosgrove, L.; Lockett, T.; Head, R.; Topping, D.L. A review of the potential mechanisms for the lowering of colorectal oncogenesis by butyrate. Br. J. Nutr. 2012, 108, 820–831.
  33. Chang, P.V.; Hao, L.; Offermanns, S.; Medzhitov, R. The microbial metabolite butyrate regulates intestinal macrophage function via histone deacetylase inhibition. Proc. Natl. Acad. Sci. USA 2014, 111, 2247–2252.
  34. Singh, N.; Thangaraju, M.; Prasad, P.D.; Martin, P.M.; Lambert, N.A.; Boettger, T.; Offermanns, S.; Ganapathy, V. Blockade of dendritic cell development by bacterial fermentation products butyrate and propionate through a transporter (Slc5a8)-dependent inhibition of histone deacetylases. J. Biol. Chem. 2010, 285, 27601–27608.
  35. Furusawa, Y.; Obata, Y.; Fukuda, S.; Endo, T.A.; Nakato, G.; Takahashi, D.; Nakanishi, Y.; Uetake, C.; Kato, K.; Kato, T.; et al. Commensal microbe-derived butyrate induces the differentiation of colonic regulatory T cells. Nature 2013, 504, 446–450.
  36. Arpaia, N.; Campbell, C.; Fan, X.; Dikiy, S.; van der Veeken, J.; deRoos, P.; Liu, H.; Cross, J.R.; Pfeffer, K.; Coffer, P.J.; et al. Metabolites produced by commensal bacteria promote peripheral regulatory T-cell generation. Nature 2013, 504, 451–455.
  37. Nepelska, M.; Cultrone, A.; Beguet-Crespel, F.; Le Roux, K.; Dore, J.; Arulampalam, V.; Blottiere, H.M. Butyrate produced by commensal bacteria potentiates phorbol esters induced AP-1 response in human intestinal epithelial cells. PLoS ONE 2012, 7, e52869.
  38. Brown, A.J.; Goldsworthy, S.M.; Barnes, A.A.; Eilert, M.M.; Tcheang, L.; Daniels, D.; Muir, A.I.; Wigglesworth, M.J.; Kinghorn, I.; Fraser, N.J.; et al. The Orphan G protein-coupled receptors GPR41 and GPR43 are activated by propionate and other short chain carboxylic acids. J. Biol. Chem. 2003, 278, 11312–11319.
  39. Singh, N.; Gurav, A.; Sivaprakasam, S.; Brady, E.; Padia, R.; Shi, H.; Thangaraju, M.; Prasad, P.D.; Manicassamy, S.; Munn, D.H.; et al. Activation of Gpr109a, receptor for niacin and the commensal metabolite butyrate, suppresses colonic inflammation and carcinogenesis. Immunity 2014, 40, 128–139.
  40. Macia, L.; Tan, J.; Vieira, A.T.; Leach, K.; Stanley, D.; Luong, S.; Maruya, M.; McKenzie, C.I.; Hijikata, A.; Wong, C.; et al. Metabolite-sensing receptors GPR43 and GPR109A facilitate dietary fibre-induced gut homeostasis through regulation of the inflammasome. Nat. Commun. 2015, 6, 6734.
  41. Kimura, I.; Ozawa, K.; Inoue, D.; Imamura, T.; Kimura, K.; Maeda, T.; Terasawa, K.; Kashihara, D.; Hirano, K.; Tani, T.; et al. The gut microbiota suppresses insulin-mediated fat accumulation via the short-chain fatty acid receptor GPR43. Nat. Commun. 2013, 4, 1829.
  42. Samuel, B.S.; Shaito, A.; Motoike, T.; Rey, F.E.; Backhed, F.; Manchester, J.K.; Hammer, R.E.; Williams, S.C.; Crowley, J.; Yanagisawa, M.; et al. Effects of the gut microbiota on host adiposity are modulated by the short-chain fatty-acid binding G protein-coupled receptor, Gpr41. Proc. Natl. Acad. Sci. USA 2008, 105, 16767–16772.
  43. Eswaran, S.; Muir, J.; Chey, W.D. Fiber and functional gastrointestinal disorders. Am. J. Gastroenterol. 2013, 108, 718–727.
  44. El-Salhy, M.; Gundersen, D. Diet in irritable bowel syndrome. Nutr. J. 2015, 14, 36.
  45. Riedl, J.; Linseisen, J.; Hoffmann, J.; Wolfram, G. Some dietary fibers reduce the absorption of carotenoids in women. J. Nutr. 1999, 129, 2170–2176.
  46. Ten Bruggencate, S.J.; Bovee-Oudenhoven, I.M.; Lettink-Wissink, M.L.; Van der Meer, R. Dietary fructooligosaccharides increase intestinal permeability in rats. J. Nutr. 2005, 135, 837–842.
  47. Singh, V.; Yeoh, B.S.; Chassaing, B.; Xiao, X.; Saha, P.; Olvera, R.A.; Lapek, J.D., Jr.; Zhang, L.; Wang, W.B.; Hao, S.; et al. Dysregulated Microbial Fermentation of Soluble Fiber Induces Cholestatic Liver Cancer. Cell 2018, 175, 679–694.e22.
  48. Bernstein, H.; Bernstein, C.; Payne, C.M.; Dvorak, K. Bile acids as endogenous etiologic agents in gastrointestinal cancer. World J. Gastroenterol. 2009, 15, 3329–3340.
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