Short-chain fatty acid formation at fermentation of indigestible carbohydrates

Henningsson, Åsa; Björck, Inger; Nyman, Margareta

doi:10.3402/fnr.v45i0.1801

Cited by 54 publications

(53 citation statements)

References 53 publications

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“…SCFAs, primarily acetate, propionate and butyrate, are the end-products of microbial fermentation of carbohydrate in the large intestine which depends on the species, amounts of microflora present in the colon, substrate sources and transit time (Wong et al 2006). Different types of non-digestible carbohydrate have been shown to produce different SCFA ratios (Berggren et al 1993;Henningsson et al 2001). Several studies have shown that the acids plays a significant role in the process of inhibiting colon carcinogenesis by stimulating cell proliferation and inducing apoptosis, which in turn affects carcinogenesis (Ruemmele et al 2003;Fung et al 2011).…”

Section: Discussionmentioning

confidence: 99%

Hydrolysed inulin alleviates the azoxymethane-induced preneoplastic aberrant crypt foci by altering selected intestinal microbiota in Sprague–Dawley rats

Pattananandecha

Sirilun

Duangjitcharoen

et al. 2016

Pharmaceutical Biology

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Context Inulin, a non-digestible carbohydrate isolated from Helianthus tuberosus L. (Asteraceae), has been shown to alter the gut beneficial bacteria including Lactobacillus spp. and Bifidobacteria. Inulin also influences the activities of intestinal microbiota that could prevent the colon cancer development. Objective This study determines the effect of hydrolysed inulin with different degrees of polymerisation on alteration of intestinal microbiota and their activities on azoxymethane (AOM)-induced preneoplastic aberrant crypt foci (ACF) in rats. Materials and methods Seventy-two male Sprague-Dawley rats were randomly divided into six groups (three control and three AOM-treated groups) and the animal were fed with either a normal diet or diet containing 10% of long-chain inulin (InuL) or short-chain inulin (InuS), respectively, for 17 weeks. Colon cancer was induced in rats by injecting AOM subcutaneously at the 8th and 9th week of the study period. At the end of the experiment, cecal contents of rats were examined for selected microbiota, organic acids, putrefactive compounds and microbial enzymes. ACF formation was microscopically examined. Results The inulin diets significantly increased the weight and decreased the pH of the caecal content. The rats fed with InuL-supplemented diet showed approximately 2.9-and 6.8-fold increases in the biomass of Lactobacillus spp. and Bifidobacteria, respectively. Naive and AOMtreated rats fed with inulin-supplemented diet showed $1.3-and $2.2-fold decreases in the biomass of Escherichia coli and Salmonella enterica serovar Typhi, respectively. Inulins significantly decreased the colonic concentration of phenol, p-cresol and indole. Reduction in the activity of microbial enzymes such as b-glucuronidase, azoreductase and nitroreductase were observed in inulin-treated animals. Reduction in the ACF formation has been observed in inulin-treated groups. Discussion and conclusion The present study demonstrates that dietary administration of inulin reduces the formation of preneoplastic lesions in the colon, possibly by altering the microecology and microbial activities on carcinogenesis.ARTICLE HISTORY

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Section: Discussionmentioning

confidence: 99%

Hydrolysed inulin alleviates the azoxymethane-induced preneoplastic aberrant crypt foci by altering selected intestinal microbiota in Sprague–Dawley rats

Pattananandecha

Sirilun

Duangjitcharoen

et al. 2016

Pharmaceutical Biology

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“…Approximately 20 to 60 g of ingested carbohydrates escape digestion and absorption in the human small intestine each day and enters the colon as a potential source for fermentation (203). These carbohydrates are converted by colonic bacteria to volatile fatty acids (VFAs).…”

Section: Small Intestine Functional Hyperemia (Postprandial Hyperemia)mentioning

confidence: 99%

“…The major VFAs present in the colon are acetic, propionic, and butyric acids. While the relative proportion of VFAs produced from fermentation in the colon vary with the amount and type of indigestible carbohydrate consumed and the colonic microflora, acetate is generally the major anion generated, accounting for about 60% of the total VFA produced (203). It has been reported that intracolonic placement of acetic acid, at physiologically relevant concentrations, increases local colonic blood flow, while butyric, or propionic acids are without effect (286).…”

Section: Small Intestine Functional Hyperemia (Postprandial Hyperemia)mentioning

confidence: 99%

The Gastrointestinal Circulation: Physiology and Pathophysiology

Granger

Holm

Kvietys

2015

Comprehensive Physiology

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The gastrointestinal (GI) circulation receives a large fraction of cardiac output and this increases following ingestion of a meal. While blood flow regulation is not the intense phenomenon noted in other vascular beds, the combined responses of blood flow, and capillary oxygen exchange help ensure a level of tissue oxygenation that is commensurate with organ metabolism and function. This is evidenced in the vascular responses of the stomach to increased acid production and in intestine during periods of enhanced nutrient absorption. Complimenting the metabolic vasoregulation is a strong myogenic response that contributes to basal vascular tone and to the responses elicited by changes in intravascular pressure. The GI circulation also contributes to a mucosal defense mechanism that protects against excessive damage to the epithelial lining following ingestion of toxins and/or noxious agents. Profound reductions in GI blood flow are evidenced in certain physiological (strenuous exercise) and pathological (hemorrhage) conditions, while some disease states (e.g., chronic portal hypertension) are associated with a hyperdynamic circulation. The sacrificial nature of GI blood flow is essential for ensuring adequate perfusion of vital organs during periods of whole body stress. The restoration of blood flow (reperfusion) to GI organs following ischemia elicits an exaggerated tissue injury response that reflects the potential of this organ system to generate reactive oxygen species and to mount an inflammatory response. Human and animal studies of inflammatory bowel disease have also revealed a contribution of the vasculature to the initiation and perpetuation of the tissue inflammation and associated injury response.

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“…In this issue, fermentation is reviewed by Henningsson et al with emphasis on short-chain fatty acid formation (18). Langkilde (19) provides data on available substrates, based on ileostomy studies.…”

Section: Fermentationmentioning

confidence: 99%

Low intestinal lactase activity - a 40 years perspective

Asp

2001

Näringsforskning

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Low intestinal lactase activity (hypolactasia) was discovered in the early 1960s as a cause of lactose intolerance. Since then, it has become clear that hypolactasia in adults is a normal phenomenon in man as in other mammals. Lactase persistence is a dominant autosomal trait, enriched during thousands of years in cattle-raising populations, where continued high capacity to digest lactose might have been related to better health and more children. Hypolactasia is a cause of lactose intolerance, but it should be noted that most people with hypolactasia tolerate considerable amounts of milk products, especially when distributed throughout the day and taken with meals. Perceived intolerance to a few grams of lactose may be due to other food components or related to a general "sensitivity" of the gastrointestinal tract. Keywords: Hypolactasia, lactose intolerance, malabsorption, milk TerminologyThe original term lactase deficiency was questioned during the 70s, when it became clear that down-regulation of lactase is a normal phenomenon in man as in other mammals. Primary low intestinal lactase activity, hypolactasia and lactase restriction are terms considered more appropriate to describe the low lactase activity in adults due to down-regulation. Lactase persistence is a logical corresponding term for keeping a high intestinal lactase activity throughout life. Secondary hypolactasia means that the low intestinal lactase activity is due to damage of the small-intestinal mucosa as a result of infection, infestation, czliac disease, allergy or malnutrition. The "normal" lactase activity will then be restored when the underlying condition is cured.Lactose malabsorption or lactose maldigestion or low lactose digestion capacity means that lactose is incompletely absorbed in the small intestine, with the result that lactose passes to the large intestine. This is demonstrated through a lactose tolerance test, in which a standardised amount of lactose, usually 50 g, is given. A small blood-glucose elevation, a small blood-galactose elevation, or a small urinary galactose excretion in a lactose tolerance test with ethanol (to inhibit galactose metabolism), or an elevated breath hydrogen excretion (as a result of fermentation) are measurements used to demonstrate lactose malabsorption, which is almost always due to low intestinal lactase activity.Lactose intolerance means the experience of symptoms due to lactose malabsorption. Obviously, lactose intolerance is dosedependent, and it has been demonstrated repeatedly that hypolactasia does not always mean intolerance to normal amounts of milk products in the diet.Milk intolerance can be due to lactose intolerance, but also to milk protein allergy, and possibly related to other milk components.Pseudolactose intolerance not always means gastrointestinal symptoms related to milk in subjects with lactase persistence.

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Short-chain fatty acid formation at fermentation of indigestible carbohydrates

Cited by 54 publications

References 53 publications

Hydrolysed inulin alleviates the azoxymethane-induced preneoplastic aberrant crypt foci by altering selected intestinal microbiota in Sprague–Dawley rats

Hydrolysed inulin alleviates the azoxymethane-induced preneoplastic aberrant crypt foci by altering selected intestinal microbiota in Sprague–Dawley rats

The Gastrointestinal Circulation: Physiology and Pathophysiology

Low intestinal lactase activity - a 40 years perspective

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