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(Journal of Nutrition. 1999;129:1424S-1427S.)
© 1999 The American Society for Nutritional Sciences

Supplement

Fiber, Inulin and Oligofructose: Similarities and Differences1

Barbara O. Schneeman

Department of Nutrition, University of California, Davis, CA 95616


   ABSTRACT
TOP
 ABSTRACT
INTRODUCTION
 Small intestine
 Large intestine
 CONCLUSION
 REFERENCES
 
The biological, chemical and physical properties of dietary fibers are associated with physiologic actions in the small and large intestine that have important metabolic implications for health. These properties of fiber include dispersibility in water, bulk, viscosity, adsorption and binding of compounds and fermentability. Dietary fructans share some of the properties of dietary fiber and thus are likely to have similar metabolic effects. Within the small intestine, properties such as dispersibility in water, bulking and viscosity are associated with slowing the digestion and absorption of carbohydrate and lipid and promoting nutrient absorption along a greater length of the small intestine. Both of these actions are related to cholesterol reduction and blunting of alimentary gylcemia. Although fructans are dispersible in water and will provide some bulk because they are nondigestible in the small intestine, they do not appear to be associated with significant increases in viscosity. Thus one would predict that any immediate effects on alimentary glycemia or on cholesterol reduction are likely to be modest compared with more viscous polysaccharides. Fermentability and bulking capacity of nondigestible carbohydrates define an essential role of fiber in maintaining gastrointestinal health. Within the large intestine, carbohydrates that are not digested in the small intestine are available for fermentation by the microflora present. Carbohydrates that are dispersible in the aqueous phase are more readily digested by microbes. A large body of evidence indicates that dietary fructans are digested in the large intestine, resulting in an increase in microbial mass and production of short-chain fatty acids.

KEY WORDS: • dietary fibers • inulin • oligofructose


   INTRODUCTION
TOP
 ABSTRACT
 INTRODUCTION
Small intestine
 Large intestine
 CONCLUSION
 REFERENCES
 
Consumption of foods rich in dietary fiber has been associated with reductions in plasma and LDL-cholesterol, blunting of the alimentary glycemic and insulin response, increases in stool bulk and improved laxation (Berger and Venhaus 1992Citation , Cummings et al. 1992Citation , Jenkins et al. 1978Citation , Read and Eastwood 1992Citation , Truswell and Beynen 1992Citation ). These physiologic responses to fiber consumption are the basis for associating high fiber diets with reduced risk of chronic diseases such as cardiovascular disease, diabetes and intestinal cancer. Dietary fiber is not digested by the enzymes in the mammalian small intestine; hence its effects on metabolism and disease risk are mediated through its chemical-physical properties as it passes through the gastrointestinal tract. These characteristics include the following: dispersibility in water or water-holding capacity, bulk due to nondigestibility, viscosity associated with certain polysaccharides, the ability to adsorb or bind bile acids and fermentability by microbes in the gut. Inulin and oligofructose are comparable to dietary fiber in that they are composed of multiple saccharide units, which are not digested by the enzymes found in the mammalian small intestine. This review will consider the similarities between dietary fiber and inulin and oligofructose on the basis of their effects on gastrointestinal function.


   Small intestine
TOP
 ABSTRACT
 INTRODUCTION
 Small intestine
Large intestine
 CONCLUSION
 REFERENCES
 
Within the small intestine, nutrients are digested and absorbed. The compounds and fluids in food are mixed with the secretions of the stomach, small intestine, pancreas and gallbladder. Although dietary fibers, as well as inulin and oligofructose, are not digested by the enzymes in the small intestine, their presence in the intestine may affect the physical characteristics of the gut contents. The water-holding capacity and nondigestibility of polysaccharides associated with fiber will directly affect the volume and bulk of small intestine contents. An increase in dry weight is directly related to the fact that, with consumption of fiber, nondigestible material is added to the small intestine, whereas the increase in volume of the small-intestinal contents is related to the water-holding capacity and viscosity of the polysaccharides in fiber (Ebihara and Schneeman 1989Citation , Gallaher and Schneeman 1986Citation , Schneeman 1982Citation ). Table 1Citation contains data from two studies and illustrates that the volume of the aqueous phase of the small-intestinal contents in rats fed guar gum or glucomannan was significantly higher than that of cellulose-fed rats. The high water-holding capacity of these two polysaccharides allowed this increase in volume. The ability to increase viscosity is a property associated with certain polysaccharides that have high water-holding capacity. These fibers are often referred to as soluble fibers, which typically refers to the fact that they are dispersible in water and increase viscosity. Not all polysaccharides that can be dispersed in water become viscous, which is important for understanding the variability in physiologic responses to different sources of fiber. Viscous polysaccharides also slow the rate of gastric emptying, resulting in an overall slower rate of digestion and absorption during the alimentary period (Lin et al. 1992 and 1997Citation Citation , Schwartz et al. 1982Citation ).


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  		Table 1. Volume in the small intestine contents of rats fed fiber1

 
The water-holding capacity, bulk and viscosity of fiber will interfere with mixing of the intestinal contents and diffusion of nutrients toward the epithelial cells or the absorptive surface of the gut. These characteristics of fiber are associated with a blunting of the insulin and/or glucose response to a carbohydrate load and the slower disappearance of lipids from the small intestine (Johnson and Gee 1981Citation ). These relationships among the properties of fiber, small-intestinal contents and their implications are summarized in Table 2Citation. As confirmation of the importance of this relationship, Gallaher's laboratory has reported the association of viscosity with cholesterol reduction in hamsters (Carr et al. 1996Citation , Gallaher and Hassel 1995Citation ). Tietyen et al. (1995)Citation demonstrated that hydrolysis of oat ß-glucan reduces its effectiveness in lowering hepatic cholesterol in cholesterol-fed rats. In a recent study we demonstrated that reverse cholesterol transport can be enhanced in human subjects fed barley pasta enriched in ß-glucan (Bourdon et al. 1999Citation ). Presumably this enhancement of reverse cholesterol transport is due to slower fat absorption in barley-fed subjects and will contribute to the ability of barley to lower plasma and LDL-cholesterol concentration when fed long term.


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  		Table 2. Characteristics of dietary fiber and their relationship to small intestine function

 
Certain sources of fiber interact with bile acids and increase their fecal excretion (Story and Furumoto 1990Citation ). A greater excretion of bile acids contributes to the plasma cholesterol–lowering ability of dietary fiber (Marlett 1997Citation ).

Inulin and oligofructose will share some but not all of the properties of fiber in the small intestine (Table 3Citation). They are soluble in water and not digested by mammalian enzymes. As a consequence, they may cause a slight increase in volume and some increase in the dry weight of intestinal contents. Although these properties may result in some effect on mixing and diffusing within the small intestine, the overall effect is unlikely to be very pronounced because in most cases, inulin and oligofructose do not appear to increase viscosity significantly. Several lines of experimental evidence illustrate the importance of viscosity in understanding the metabolic responses to certain types of fiber. Thus for those physiologic responses of fiber that are mediated through the small intestine, the effect of inulin and oligofructose is likely to be minimal, unless these compounds are modified in some manner so that they affect the physical characteristics of the small intestine contents.


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  		Table 3. Characteristics of inulin and oligofructose and their relationship to small intestine function

 

   Large intestine
TOP
 ABSTRACT
 INTRODUCTION
 Small intestine
 Large intestine
CONCLUSION
 REFERENCES
 
In the large intestine, water and electrolytes are absorbed, and microbial action breaks down the macronutrients in the residual material that passes from the small bowel. The characteristics of dietary fiber that are likely to affect the large intestine and their physiologic implications are summarized in Table 4Citation. Dietary fiber and undigested starch are the primary substrates for growth of the microflora in the large bowel (Cummings et al. 1992Citation , Cummings and Englyst 1995Citation ). Thus the bulk associated with undigested residue contributes directly to stool bulk as undigested material or indirectly through the growth of microflora, which are a part of the stool weight. Originally it was thought that the water-holding capacity of dietary fiber was important for maintaining water content of stool and stool bulk. However, water content of stool is relatively constant at about 25%. The dispersibility of polysaccharides in water and water-holding capacity determine the ability with which microorganisms can penetrate the undigested food residue and gain access to the polysaccharides for metabolism (Stephen and Cummings 1979Citation ). Thus water-holding capacity has a relationship to stool bulk but primarily through its effects on the fermentability of polysaccharides.


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  		Table 4. Characteristics of dietary fiber and their relationship to large intestine function

 
Fiber sources with high water-holding capacity tend to be more readily degraded or fermented by microbes in the large bowel. For example, in the stool of rats, very little residual sugar from polysaccharide remains when animals are fed gums or pectins, but a higher level is present when they are fed wheat bran, a source of relatively insoluble polysaccharides (Nyman and Asp 1982Citation , Nyman et al. 1986Citation ). In both cases, feeding the fiber source results in some increase in stool weight, but rats fed wheat bran have a significantly greater increase in stool weight than the ones fed more fermentable polysaccharides. Polysaccharides entering the large bowel are the primary substrates for fermentation and result in growth of the microflora or an increased microbial mass and production of products of fermentation, which include CO2, H2 and short-chain fatty acids (SCFA). SCFA, which include acetate, propionate and butyrate, are used as an energy source and appear to promote the health of the intestinal mucosa (Velázquez et al. 1997Citation ). Propionate has been reported to inhibit fatty acid, but not cholesterol synthesis in isolated hepatocytes (Nishina and Freedland 1990Citation ). Fatty acids synthesized in the liver are incorporated into VLDL. Further research is required to determine the role that propionate might have in triglyceride metabolism in human subjects consuming fermentable polysaccharides.

Because inulin and oligofructose are dispersible in water, they are likely to be readily degraded by microorganisms present in the large bowel. Table 5Citation summarizes the characteristics of inulin and oligofructose that might affect functioning of the large bowel. The fermentability of inulin and oligofructose provides a route by which they can increase stool weight because they would increase microbial mass in the colon. In addition, the fermentation can lower the pH of colon contents, and the production of SCFA is likely to affect the health of the intestinal mucosa. Further research is required to understand the effect that propionate production from fermentation of inulin and oligofructose might have on glucose and triglyceride metabolism. One of the more promising areas of investigation for inulin and oligofructose will be the effect of this fermentation relative to the distribution of microorganisms in the large intestine and the products of fermentation.


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  		Table 5. Characteristics of inulin and oligofructose and their relationship to large intestine function

 

   CONCLUSION
TOP
 ABSTRACT
 INTRODUCTION
 Small intestine
 Large intestine
 CONCLUSION
REFERENCES
 
A comparison of the properties of dietary fiber, inulin and oligofructose with respect to the characteristics that will affect gastrointestinal function is shown in TableCitation 6. Differences in properties are based on the ability of certain polysaccharides to increase the viscosity of intestinal contents and the ability of some polysaccharides to bind compounds such as bile acids. Even within the category of compounds classified as dietary fiber, these characteristics vary among fiber sources and polysaccharide structures. For example, hydrolyzed guar gum or ß-glucan are significantly less viscous than the intact molecules, and the hydrolyzed polysaccharides are less effective in reducing cholesterol levels. The characteristic that is common among dietary fiber, inulin and oligofructose is their nondigestibility by enzymes in the small intestine. In addition, most polysaccharides associated with dietary fiber, as well as inulin and oligofructose, can be fermented by microorganisms.


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  		Table 6. Dietary fibers, inulin, oligofructose: similarities and differences based on gastrointestinal function

 

   FOOTNOTES
 
1 Presented at the conference Nutritional and Health Benefits of Inulin and Oligofructose held May 18–19, 1998 in Bethesda, MD. This symposium was supported in part by educational grants from the National Institutes of Health Office of Dietary Supplements, the U.S. Department of Agriculture and Orafti Technical Service. Published as a supplement to The Journal of Nutrition. Guest editors for the symposium publication were John A. Milner, The Pennsylvania State University, and Marcel Roberfroid, Louvain University, Brussels, Belgium. Back


   REFERENCES
TOP
 ABSTRACT
 INTRODUCTION
 Small intestine
 Large intestine
 CONCLUSION
 REFERENCES
 

1. Berger M., Venhaus A. Dietary fibre in the prevention and treatment of diabetes mellitus. Schweizer T. F. Edwards C. A. eds. Dietary Fibre—A Component of Food 1992:280-293 Springer-Verlag London, UK

2. Bourdon I., Yokoyama W., Davis P., Hudson C., Backus R., Richter D., Knuckles B., Schneeman B. O. Postprandial lipid, glucose, insulin, cholecystokinin, responses in male subjects fed barley pasta enriched in beta-glucan. Am. J. Clin. Nutr. 1999;69:55-63[Abstract/Free Full Text]

3. Carr T., Gallaher D., Yang C. H., Hassel C. A. Increased intestinal contents viscosity reduces cholesterol absorption efficiency in hamsters fed hydroxypropyl methylcellulose. J. Nutr. 1996;126:1463-1469

4. Cummings J. H., Bingham S. A., Heaton K. W., Eastwood M. A. Fecal weight, colon cancer risk, and dietary intake of non-starch polysaccharides (dietary fiber). Gastroenterology 1992;103:1783-1789[Medline]

5. Cummings J. H., Englyst H. N. Gastrointestinal effects of food carbohydrate. Am. J. Clin. Nutr. 1995;61:938S-945S[Abstract/Free Full Text]

6. Ebihara K., Schneeman B. O. Interaction of bile acids, phospholipids, cholesterol and triglycerides with dietary fibers in the small intestine of rats. J. Nutr. 1989;119:1100-1106

7. Gallaher D. D., Hassel C. A. The role of viscosity in the cholesterol-lowering effect of dietary fiber. Kritchevsky D. Bonfield C. eds. Dietary Fiber in Health and Disease 1995:106-114 Plenum Press New York, NY

8. Gallaher D., Schneeman B. O. Intestinal interaction of bile acids, phospholipids, dietary fibers and cholestyramine. Am. J. Physiol. 1986;250:G420-G426[Medline]

9. Jenkins D.J.A., Wolever T.M.S., Leeds A. R., Gassull M. A., Haisman P., Dilawari J., Goff D. V., Metz G.L., Alberti Dietary fibres, fibre analogues, and glucose tolerance: importance of viscosity. Br. Med. J. 1978;1:1392-1394

10. Johnson L. R., Gee J. M. Effect of gel-forming gums on the intestinal unstirred layer and sugar transport in vitro. Gut 1981;22:398-403[Abstract/Free Full Text]

11. Lin H. C., Moller N. A., Wolinsky M. M., Kim B. H., Doty J. E., Meyer J. H. Sustained slowing effect of lentils on gastric emptying of solids in human and dogs. Gastroenterology 1992;102:787-792[Medline]

12. Lin H. C., Zhao X. T., Chu A. W., Lin Y. P., Wang L. Fiber-supplemented enteral formula slows intestinal transit by intensifying inhibitory feedback from the distal gut. Am. J. Clin. Nutr. 1997;65:1840-1844[Abstract/Free Full Text]

13. Marlett J. A. Sites and mechanisms for the hypocholesterolemic actions of soluble dietary fiber sources. Kritchevsky D. Bonfield C. eds. Dietary Fiber in Health and Disease 1997:109-121 Plenum Press New York, NY.

14. Nishina P. M., Freedland R. A. Effects of propionate on lipid biosynthesis in isolated rat hepatocytes. J. Nutr. 1990;120:668-673

15. Nyman M., Asp N.-G. Fermentation of dietary fibre components in the rat intestinal tract. Br. J. Nutr. 1982;47:357-366[Medline]

16. Nyman M., Asp N.-G., Cummings J. H., Wiggins H. Fermentation of dietary fibre in the intestinal tract: comparison between man and rat. Br. J. Nutr. 1986;55:487-496[Medline]

17. Read N. W., Eastwood M. A. Gastro-intestinal physiology and function. Schweizer T. F. Edwards C. A. eds. Dietary Fibre—A Component of Food 1992:103-117 Springer-Verlag London, UK.

18. Schneeman B. O. Pancreatic and digestive function. Vahouny G. Kritchevsky D. eds. Dietary Fiber in Health and Disease 1982:73-83 Plenum Press New York, NY.

19. Schwartz S. E., Levine R. A., Singh A., Scheidecker J. R., Track N. S. Sustained pectin ingestion delays gastric emptying. Gastroenterology 1982;83:812-817[Medline]

20. Stephen A. M., Cummings J. H. Water holding by dietary fibre in vitro and its relationship to faecal output in man. Gut 1979;20:722-729[Abstract/Free Full Text]

21. Story J., Furumoto E. J. Dietary fiber and bile acid metabolism. Kritchevsky D. Bonfield C. Anderson J. W. eds. Dietary Fiber 1990:365-373 Plenum Press New York, NY.

22. Tietyen J. L., Nevins D. L., Shoemaker C. F., Schneeman B. O. Hypocholesterolemic potential of oat bran treated with an endo- ß-D-glucanase from Bacillus subtilis. J. Food Sci. 1995;60:558-560, 579

23. Truswell A. S., Beynen A. C. Dietary fibre and plasma lipids: potential for prevention and treatment of hyperlipidaemias. Schweizer T.F. Edwards C.A. eds. Dietary Fibre—A Component of Food 1992:295-332 Springer-Verlag London, UK.

24. Velázquez O. C., Lederer H. M., Rombeau J. L. Butyrate and the colonocyte: production, absorption, metabolism and therapeutic implications. Kritchevsky D. Bonfield C. eds. Dietary Fiber in Health and Disease 1997:123-134 Plenum Press New York, NY.





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Copyright © 1999 by American Society for Nutrition