Resistant starch, large bowel fermentation and a broader perspective of prebiotics and probiotics.

The metabolic end products of the large bowel microbiota contribute significantly to human health. After weaning to solid foods, some of the most important of these are the short chain fatty acids (SCFA) produced by the fermentation of undigested dietary components and endogenous secretions. The main SCFA are acetate, propionate and butyrate which have numerous documented effects promoting large bowel function. Of the major acids, butyrate seems especially important. It is a major metabolic fuel for colonocytes and promotes a normal phenotype in these cells, potentially lowering the risk of diseases such as colo-rectal cancer. Imbalances in the microbiota are thought to predispose to large bowel dysfunction and probiotics are being developed to correct this. However, most commercial products contain bacteria (lactobacilli and bifidobacteria) which are dominant species in milk-fed infants but have limited roles in adults. Prebiosis is defined usually by the specific stimulation of these bacteria. However, the end products of most probiotics do not include butyrate or propionate which raises questions about their effectiveness in promoting bowel health in adults. Resistant starch (RS) is a dietary fibre component and its fermentation generally favours butyrate production. Dietary RS intakes and faecal butyrate levels are high in populations at low risk of diet-related large bowel diseases. Conversely, RS intakes and faecal butyrate levels are very low in high risk groups. This raises the possibility that greater RS consumption could be of health benefit. RS is not regarded widely as a prebiotic but (according to the accepted definition) most forms show the requisite features in stimulating specific bacteria, giving raised total SCFA and butyrate levels and a consequent benefit to the host. Current efforts to improve public health through increasing RS consumption could be facilitated by greater recognition of its prebiotic role.

Short-chain fatty acids and human colonic function: roles of resistant starch and nonstarch polysaccharides.

Resistant starch (RS) is starch and products of its small intestinal digestion that enter the large bowel. It occurs for various reasons including chemical structure, cooking of food, chemical modification, and food mastication. Human colonic bacteria ferment RS and nonstarch polysaccharides (NSP; major components of dietary fiber) to short-chain fatty acids (SCFA), mainly acetate, propionate, and butyrate. SCFA stimulate colonic blood flow and fluid and electrolyte uptake. Butyrate is a preferred substrate for colonocytes and appears to promote a normal phenotype in these cells. Fermentation of some RS types favors butyrate production. Measurement of colonic fermentation in humans is difficult, and indirect measures (e.g., fecal samples) or animal models have been used. Of the latter, rodents appear to be of limited value, and pigs or dogs are preferable. RS is less effective than NSP in stool bulking, but epidemiological data suggest that it is more protective against colorectal cancer, possibly via butyrate. RS is a prebiotic, but knowledge of its other interactions with the microflora is limited. The contribution of RS to fermentation and colonic physiology seems to be greater than that of NSP. However, the lack of a generally accepted analytical procedure that accommodates the major influences on RS means this is yet to be established.

Coarse brown rice increases fecal and large bowel short-chain fatty acids and starch but lowers calcium in the large bowel of pigs.

Young male pigs were fed a diet formulated from human foods including either boiled white rice plus rice bran or heat-stabilized brown rice at equivalent levels of fiber for 3 wk. Stool and starch excretion were low in pigs fed white rice during the first 2 wk of the experiment. In pigs fed brown rice, their excretion was high during wk 1 but declined in wk 2 while short-chain fatty acid (SCFA) excretion was higher at both times. Large bowel digesta mass, measured during wk 3, was higher in pigs fed brown rice but only in the proximal colon. Large bowel and fecal starch concentrations were higher in pigs fed brown rice but the difference was insufficient to explain the increase in large bowel digesta mass. In pigs with a cecal cannula, digesta starch concentrations were equally higher when white or brown rice was fed compared with the corresponding rice which had been finely milled, indicating that particle size was a determinant of ileal digestibility. Concentrations and pools of total and individual SCFA were higher in all regions of the colon but not the cecum of pigs fed brown rice. Large bowel Ca(2+) concentrations were lower in pigs fed brown rice, suggesting greater absorption. The data confirm earlier findings that brown rice raises large bowel digesta mass and SCFA through greater fermentation of starch but show that starch itself makes a relatively small contribution to digesta and stool mass. Apparently, the rate of passage of digesta is a determinant of the concentrations and pools of SCFA in the distal colon and in feces.

Starches, resistant starches, the gut microflora and human health.

Starches are important as energy sources for humans and also for their interactions with the gut microflora throughout the digestive tact. Largely, those interactions promote human health. In the mouth, less gelatinised starches may lower risk of cariogensis. In the large bowel, starches which have escaped small intestinal digestion (resistant starch), together with proteins, other undigested carbohydrates and endogenous secretions are fermented by the resident microflora. The resulting short chain fatty acids contribute substantially to the normal physiological functions of the viscera. Specific types of resistant starch (e.g. the chemically modified starches used in the food industry) may be used to manipulate the gut bacteria and their products (including short chain fatty acids) so as to optimise health. In the upper gut, these starches may assist in the transport of probiotic organisms thus promoting the immune response and suppressing potential pathogens. However, it appears unlikely that current probiotic organisms can be used to modulate large bowel short chain fatty acids in adults although resistant starch and other prebiotics can do so. Suggestions that starch may exacerbate certain conditions (such as ulcerative colitis) through stimulating the growth of certain pathogenic organisms appear to be unfounded. Short chain fatty acids may modulate tissue levels and effects of growth factors in the gut and so modify gut development and risk of serious disease, including colo-rectal cancer. However, information on the relationship between starches and the microflora is relatively sparse and substantial opportunities exist both for basic research and food product development.

White and wholemeal flours from wheats of low and higher apparent metabolizable energy differ in their nutritional effects in rats.

Wheats used for feeding poultry differ considerably in the ratio of soluble to insoluble non-starch polysaccharides (NSP) and apparent metabolizable energy (AME). We have examined effects of whole and white flour from a wheat of low (12.02 MJ/kg of dry matter) and high (14.52 MJ/kg of dry matter) AME in rats fed a cholesterol-free diet. NSP concentrations were higher in whole flour from the low AME wheat but similar in both white flours. In contrast to chickens, food intake and body weight gain of rats were unaffected by diet. Plasma cholesterol concentrations were lower in rats fed whole wheat and low AME wheat. Cecal bile acids and neutral sterol pools were larger in rats fed whole wheat but were unaffected by wheat type. Negative correlations were found between digesta steroid pools and plasma cholesterol, consistent with greater fecal steroid excretion. Cecal digesta was greater in rats fed whole wheat and low AME wheat. Digesta pH was lower in rats fed whole wheat, but there was a significant interaction between wheat and flour type with lower pH in rats fed low AME white flour. Total volatile fatty acids (VFA) and acetate and butyrate pools were larger in rats fed whole wheat than in those fed white flour. Total and individual VFA pools were larger in rats fed low AME flours than in those fed high AME flours, apparently due to greater cecal starch fermentation in the former. Factors affecting wheat AME in chickens affect important metabolic variables in rats and may have similar actions in other species including humans.

Fecal numbers of bifidobacteria are higher in pigs fed Bifidobacterium longum with a high amylose cornstarch than with a low amylose cornstarch.

Twelve young male pigs consumed a purified diet containing wheat bran as fiber source. Starch provided 50% of total daily energy either as a low amylose cornstarch or as a high amylose (amylomaize) starch. The pigs were given a supplement of a freeze-dried probiotic organism (Bifidobacterium longum CSCC 1941). A block crossover design was used so that at any one time two groups of three pigs consumed either the high or low amylose cornstarch without probiotic and a further two groups of three pigs consumed either high or low amylose cornstarch with probiotic. Neither food intake nor body weight gain was affected by diet. Fecal output was higher when pigs were fed the high amylose cornstarch, but moisture content was unaffected. Fecal concentrations and excretion of total volatile fatty acids were higher when pigs were fed the high amylose cornstarch. Concentrations of acetate were unaffected by dietary starch, but those of propionate and butyrate were higher when the high amylose cornstarch was consumed. Fecal excretion of all three acids was higher during high amylose cornstarch feeding. Bifidobacteria were detected in the feces only when pigs were fed Bifidobacterium longum. Fecal bifidobacteria counts (expressed per gram of wet feces) and their daily fecal excretion were higher when pigs were fed high amylose cornstarch. Feeding the probiotic did not alter fecal starch or volatile fatty acids. None of the variables studied was affected by the order of feeding of starch or probiotic. The data show that a high amylose starch acts as a prebiotic in promoting the fecal excretion of probiotic organisms.

A high amylose (amylomaize) starch raises proximal large bowel starch and increases colon length in pigs.

Young male pigs consumed a diet of fatty minced beef, safflower oil, skim milk powder, sucrose, cornstarch and wheat bran. Starch provided 50% of total daily energy either as low amylose cornstarch, high amylose (amylomaize) cornstarch or as a 50/50 mixture of corn and high amylose starch. Neither feed intake nor body weight gain as affected by dietary starch. Final plasma cholesterol concentrations were significantly higher than initial values in pigs fed the 50/50 mixture of corn and high amylose starch. Biliary concentrations of lithocholate and deoxycholate were lower in pigs fed high amylose starch. Large bowel length correlated positively with the dietary content of high amylose starch. Concentrations of butyrate in portal venous plasma were significantly lower in pigs fed high amylose starch than in those fed cornstarch. Neither large bowel digesta mass nor the concentrations of total or individual volatile fatty acids were affected by diet. However, the pool of propionate in the proximal colon and the concentration of propionate in feces were higher in pigs fed amylose starch. Concentrations of starch were uniformly low along the large bowel and were unaffected by starch type. In pigs with cecal cannula, digesta starch concentrations were higher with high amylose starch than with cornstarch. Electron micrographic examination of high amylose starch granules from these animals showed etching patterns similar to those of granules obtained from human ileostomy effluent. It appears that high amylose starch contributes to large bowel bacterial fermentation in the pig but that its utilization may be relatively rapid.

Inflammatory mediators stimulate arginine transport and arginine-derived nitric oxide production in a murine breast cancer cell line.

Inflammatory mediators stimulate arginine-derived nitric oxide (NO) production in a variety of cells. The purpose of this study was to determine if the inflammatory mediators, endotoxin (LPS) and interferon gamma (IFN), stimulate arginine transport and nitric oxide production in a murine breast cancer cell line. We also investigated the effect of the nitric oxide synthase (NOS) inhibitors, omega-nitro-L-arginine methyl ester (LNAME) and aminoguanidine (AG), as well as the effect of varying the concentration of L-arginine in the cellular media, on arginine transport and NO production in these tumors cells. Confluent EMT-6 murine breast cancer cells were incubated with LPS (10 microgram/ml) and IFN (50 units/ml) in the presence or absence of the NOS inhibitors, L-NAME (2 mM) or AG (1 mM), and arginine transport (using L-[3H]arginine) and NO production (the stable end-product nitrite was assayed using the Greiss reagent) were measured at various time points. In addition, the effect of varying the concentration of L-arginine (0, 10, 100, 1000, 10,000 mM) in the cellular media on stimulated L-arginine transport and nitrite accumulation was assessed. Incubation of EMT-6 with LPS and IFN stimulated arginine transport approximately 70% over control levels at 12 hr and transport returned to basal levels at 24 hr. LPS/IFN-stimulated EMT-6 cells produced 25 microM nitrite at 24 hr and reached a plateau of 55 microM nitrite at 48 hr. The NO synthase inhibitors, L-NAME and AG, failed to inhibit basal and stimulated levels of arginine transport, but significantly inhibited nitrite accumulation, which was restored by 10 mM L-arginine. Finally, L-arginine was necessary in the media for nitrite accumulation by LPS/IFN-stimulated cells, with maximal accumulation at 1 mM L-arginine. In summary, LPS/IFN stimulate arginine transport and NO production in the EMT-6 breast cancer cell line. L-NAME and AG do not inhibit basal or stimulated arginine transport in this tumor cell line and extracellular L-arginine is required for NO synthesis in these cells. LPS/IFN stimulation of arginine transport may represent an adaptive response to provide increased substrate for enhanced tumor cell NO production.

Short-chain fatty acids produced by intestinal bacteria.

The colon is the major site of bacterial colonisation in the human gut and the resident species are predominantly anaerobes. They include potential pathogens but the greater proportion appear to be organisms which salvage energy through the metabolism of undigested carbohydrates and gut secretions. The major products of carbohydrate metabolism are the short chain fatty acids (SCFA), acetate, propionate and butyrate. In addition to general effects (such as lowering of pH) individual acids exert specific effects. All of the major SCFA appear to promote the flow of blood through the colonic vasculature while propionate enhances muscular activity and epithelial cell proliferation. Butyrate appears to promote a normal cell phenotype as well as being a major fuel for colonocytes. Important substrates for bacterial fermentation include non-starch polysaccharides (major components of dietary fibre) but it seems that starch which has escaped digestion in the small intestine (resistant starch) is the major contributor. Oligosaccharides are utilised by probiotic organisms and in the diet, act as prebiotics in promoting their numbers in faeces. High amylose starch is a form of RS and it appears to act as a prebiotic also. Although there is evidence that probiotics such as Bifidobacteria metabolise oligosaccharides and other carbohydrates, there appears to be little evidence to support a change in faecal SCFA excretion. It seems that any health benefits of probiotics are exerted through means other than SCFA.

Randomized trial of loperamide versus dose escalation of octreotide acetate for chemotherapy-induced diarrhea in bone marrow transplant and leukemia patients.

This study compares maximal daily doses of loperamide to escalating doses of continuous intravenous (CI) octreotide acetate in bone marrow transplant (BMT) and leukemia patients. Following chemotherapy, BMT and leukemia patients who developed > or = 600 ml of stool volume in a 24-hr period were randomized to receive loperamide 4 mg po q6h or octreotide 150 micrograms mixed in hyperalimentation solution or normal saline and administered CI. Patients were assessed at 48 hr intervals for decrease in stool volume from baseline. Complete response (CR) was defined as > or = 50% from baseline stool volume (BSV). Patients receiving octreotide who did not achieve a CR at 48 hr were dose escalated by doubling the dose to a maximum of 2,400 micrograms with evaluations at 48 hr intervals. Patients receiving loperamide who did not achieve a CR at 48 hr had treatment discontinued. A total of 36 patients were enrolled in the study. Of these, all were evaluable for intention to treat, and 31 were evaluable for initial response. Based on intent to treat at the initial 48 hr, patients receiving loperamide had a higher complete response rate (86% vs. 45%, P = 0.033) than did those who received octreotide. By treatment analysis (patients who actually received the drug), patients receiving loperamide had a higher complete response rate (92% vs. 56%, P = 0.0448) than did those who received octreotide at the 150 micrograms dosage level. Additional octreotide patients eventually achieved a CR at a higher dosage level (78%). Loperamide at maximal doses of 4 mg po q6h is more effective than octreotide 150 micrograms CI in treating diarrhea following chemotherapy in BMT and leukemia patients. Higher doses of octreotide may be required in a significant number of patients not responding to lower doses.

Feeding Australian Acacia gums and gum arabic leads to non-starch polysaccharide accumulation in the cecum of rats.

Exudative gums from two Australian Acacia species (A. pycnantha and A. baileyana) and gum arabic (from A. senegal) were fed to rats at graded levels (0, 20, 40, 80 g/kg), replacing cellulose in purified diets containing cholesterol plus cholic acid. Compared with consumption of the control diet containing cellulose only, consumption of the gums had no significant effects on concentrations of plasma or liver cholesterol. Plasma triacylglycerol concentrations were higher in rats fed gum arabic, whereas liver triacylglycerols were lower in rats fed the gums. The gums did not affect the total pool of volatile fatty acids in the ceca, as compared with results in controls, but did promote the relative contribution of propionate at the expense of acetate. In rats fed the diet containing cellulose (80 g/kg) the proportions of cecal acetate:propionate:butyrate were 76:15:9, whereas in the rats fed A. pycnantha gum, gum arabic and A. baileyana gum (80 g/kg) the ratios were 42:54: 4, 35:46:19 and 43:53:4, respectively. The low apparent fermentability of the gums was confirmed by the accumulation of non-starch polysaccharides in cecal digesta. In rats fed 80 g/kg A. pycnantha gum, 3.44 g of soluble non-starch polysaccharides was measured in the ceca, which was 58% of the dry weight of the cecal contents. We conclude that the biological activities of the Australian Acacia gums were similar to those of gum arabic and that these gums may have potential value as human food ingredients.

Oat bran, barley and malted barley lower plasma cholesterol relative to wheat bran but differ in their effects on liver cholesterol in rats fed diets with and without cholesterol.

Males rats were fed diets containing wheat bran, oat bran, barley or malted barley without or with 10 g/kg cholesterol + 1 g/kg cholic acid (referred to as "cholesterol"). Plasma total, HDL, and VLDL+LDL cholesterol concentrations were higher overall in rats fed cholesterol. There was a significant interaction between dietary cholesterol and cereal type. Higher concentrations of total and VLDL+LDL cholesterol were found in rats fed cholesterol with wheat bran than in those fed oat bran, barley or malted barley. HDL cholesterol concentrations were higher overall in rats fed wheat bran than in those fed oat bran or barley but not malted barley. Liver cholesterol pools were higher overall in rats fed cholesterol. In all animals fed oat bran, liver cholesterol was lower than in rats fed barley or malted barley. Hepatic HDL receptor activity was lower overall in rats fed cholesterol. There was no independent effect of cereal type on HDL receptor activity, but there was a significant interaction with dietary cholesterol. Activity tended to be higher in rats fed malted barley with cholesterol than in rats fed malted barley without cholesterol. LDL receptor activity was not affected by cereal type but was significantly lower overall in rats fed cholesterol.

Plasma lipids and large bowel volatile fatty acids in pigs fed on white rice, brown rice and rice bran.

Adult male pigs were fed on a diet containing (% of energy) fat 25 starch 55 from white rice and providing 20 g fibre/pig d (diet WR). In two other groups rice bran was added to the diet to provide 43 g fibre/d. One group received the diet unmodified (diet RB), but in another (diet RO) heat-stabilized unrefined rice oil replaced the palm oil. In a further group brown rice replaced white rice and provided 37 g fibre/pig per d (diet BR). Plasma cholesterol concentrations were similar with diets WR, RB and BR. With diet RO the concentration was significantly lower than with diets WR and BR but was not different from diet RB. Plasma high-density-lipoprotein-cholesterol and plasma triacylglycerols were unaffected by diet. In all groups, digesta mass rose from the caecum to the proximal colon but fell in the distal colon. Diet WR gave the lowest digesta mass while diet BR gave a significantly higher mass along the large bowel length. RB- and RO-fed pigs had equal masses of digesta which were intermediate between BR- and WR-fed pigs at all sampling sites. Pools of individual and total volatile fatty acids (VFA) in the proximal large bowel were unaffected by diet. Pools of total and individual VFA in the median and distal colon were lowest with diets WR and RB and significantly higher with diet BR. In these regions of the colon pools of acetate in RO-fed pigs did not differ from those in the BR-fed group but were higher than in other groups. However, pools of propionate and butyrate with the RO diet were significantly lower than with diet BR and the same as with diets WR and RB. Portal venous VFA concentrations were unaffected by diet. The higher large bowel digesta masses and VFA with diet BR may reflect the escape of starch from the small intestine.

Prevention of coprophagy does not alter the hypocholesterolaemic effects of oat bran in the rat.

Male rats were fed on either a non-purified rodent diet (JS) or cholesterol-free purified diets containing wheat bran (WB) or oat bran (OB). Some animals were allowed normal access to their faeces for coprophagy (coprophagy+), while in others coprophagy was prevented by placement of a plastic cup over the anus (coprophagy-). Direct ingestion of faeces from the anus was observed in the former groups. Food intake was unaffected by diet or coprophagy status and body weight gain was unchanged with OB- and JS- but was significantly lower with WB-. Plasma cholesterol was highest with WB and equally lower with OB and JS and was unaffected by coprophagy status. Plasma triacylglycerols were highest with OB and were unaffected by coprophagy status. Caecal digesta mass was highest with JS, intermediate with OB and lowest with WB. Digesta mass was unaffected by coprophagy status with WB and JS but was higher with OB-. Digesta moisture content was lowest with WB+ but highest with WB-. Digesta volatile fatty acid (VFA) concentrations were similarly lower with OB+ and OB-, but were significantly lower with JS- and WB- than in the corresponding coprophagy+ group. In all groups digesta butyrate concentrations were reduced by coprophagy prevention. Pools of total VFA, acetate and butyrate in the digesta were highest with JS. Pools of total VFA in digesta were highest with JS+, OB+ and OB- and lowest with WB+ and WB-. The propionate pool was highest with OB-, intermediate with OB+, and equally low in all other groups. The pool of butyrate was highest with JS+ and lowest with OB-.(ABSTRACT TRUNCATED AT 250 WORDS)

White wheat flour lowers plasma cholesterol and increases cecal steroids relative to whole wheat flour, wheat bran and wheat pollard in rats.

Plasma cholesterol concentrations were significantly lower in rats fed a cholesterol-free diet containing white wheat flour than those fed the diet with whole wheat or wheat bran. Concentrations of total bile acids and neutral sterols in cecal digesta were significantly higher in rats fed wheat flour than in those fed whole wheat, wheat pollard or wheat bran. Digesta bile acids and neutral sterol pools correlated negatively with plasma cholesterol, indicating that excretion was regulating plasma concentration. Total cecal volatile fatty acid (VFA) concentrations were unaffected by diet but cecal propionate was higher and butyrate lower in rats fed wheat flour than in those fed whole wheat. Cecal digesta butyrate concentrations correlated negatively with the cholesterol metabolite, coprostanol, and with secondary bile acids. Cecal propionate correlated negatively with plasma cholesterol concentration, but butyrate correlated equally positively, suggesting these VFA were indicators rather than regulators of altered cecal steroid metabolism. Effects of white wheat flour on steroid metabolism and cecal VFA resemble those of oat bran and support the observation that wheat flour might be hypocholesterolemic in humans.

Dietary non-starch polysaccharides interact with cholesterol and fish oil in their effects on plasma lipids and hepatic lipoprotein receptor activity in rats.

Male rats were fed the non-starch polysaccharides pectin, methylcellulose or guar gum with corn oil or with 60% of the corn oil replaced by fish oil. They were also fed these diets with or without cholesterol (+ cholic acid). Plasma total cholesterol concentration was higher overall in rats fed cholesterol and lower in those fed fish oil or fish oil + cholesterol. Plasma triacylglycerols were lower in rats fed fish oil with or without cholesterol. Hepatic LDL receptor activity was higher overall in rats fed fish oil or fish oil + cholesterol than in those fed cholesterol. Liver HDL receptor was lower overall in rats fed fish oil or cholesterol. Type of non-starch polysaccharide influenced these dietary effects so that in cholesterol-fed rats plasma cholesterol was highest in those fed methylcellulose, intermediate in those fed guar gum and in those fed pectin was unchanged from concentrations in rats fed pectin without cholesterol. Fish oil feeding lowered plasma cholesterol concentration in rats fed pectin or methylcellulose but not in those fed guar gum. Plasma triacylglycerols were lower in rats fed fish oil and all three non-starch polysaccharides, but concentrations were similar in rats fed pectin + fish oil + cholesterol and in those fed pectin. In rats fed methylcellulose + cholesterol and any non-starch polysaccharide + fish oils, HDL receptor activity was uniformly lower than in rats fed pectin, methylcellulose or guar gum. Low density lipoprotein receptor activity was higher in rats fed pectin + fish oil or pectin + fish oil + cholesterol than in rats fed pectin.

Dietary fat and fiber alter large bowel and portal venous volatile fatty acids and plasma cholesterol but not biliary steroids in pigs.

Male pigs were fed a low fiber beef diet (control) or that diet with additional fiber either as wheat bran, oat bran or baked beans. Total large bowel digesta and volatile fatty acid (VFA) pools were highest in pigs fed the diet with baked beans, intermediate in those fed the diets with oat bran and wheat bran and lowest in those fed the control diet. In all groups digesta mass and total VFA pools rose from the cecum and then fell to the distal colon, and incremental effects of diet were the same at all sampling sites. For acetate and propionate pools there was a significant interaction between diet and anatomical site, but data conversion to logarithms abolished this interaction, indicating that all dietary effects were proportionately the same across sections. Consumption of the diets with wheat bran, oat bran and baked beans increased the total large bowel butyrate pool compared with consumption of the control diet. Digesta H+ concentrations fell along the large bowel and correlated positively with VFA concentrations in the median colon. Portal venous VFA concentrations correlated with VFA in the proximal colon only. Plasma cholesterol and biliary steroids were unrelated to portal venous propionate concentrations.

Fish oil and oat bran in combination effectively lower plasma cholesterol in the rat.

Male rats were fed a semi-purified diet containing oat bran or wheat bran with or without a marine fish oil to investigate the effects of such combinations on lipid metabolism. Oat bran alone and wheat bran plus fish oil gave lower plasma cholesterol concentrations than wheat bran alone while oat bran plus fish oil gave the lowest. Oat bran increased plasma triacylglycerols compared with wheat bran but oat bran plus fish oil gave concentrations similar to those seen with wheat bran plus fish oil. Oat bran gave higher hepatic cholesterol synthesis rates and a higher activity of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase compared to wheat bran. The addition of fish oil to either bran diet decreased cholesterol synthesis but HMG CoA reductase activity was not reduced. Oat bran increased hepatic acyl coenzyme A:cholesterol acyl transferase (ACAT) activity and increased the ratio of esterified to unesterified cholesterol in hepatic microsomal membranes compared with wheat bran. Fish oil decreased hepatic LDL receptor activity and increased HDL binding activity when added to the wheat bran diet but these effects were not seen with oat bran. Oat bran also had no effect on hepatic lipoprotein receptor activity compared with wheat bran. These results show that fish oil and oat bran have complementary cholesterol lowering effects in the rat.

Soluble fiber polysaccharides: effects on plasma cholesterol and colonic fermentation.

Many soluble-fiber polysaccharides, used as stabilizers and thickeners by the food industry, lower plasma cholesterol and slow small intestinal transit and nutrient absorption. Although nondigestible by human enzymes, these polysaccharides are fermented by the large-bowel microflora, yielding short-chain fatty acids that are absorbed and contribute to energy. The caloric yield from fiber polysaccharides needs to be quantified. Short-chain fatty acid production from soluble fibers is modified by the presence of insoluble fibers but, in total, is probably less than from other carbohydrates, e.g., resistant starch. Short-chain fatty acids do not seem to mediate effects of fiber on plasma cholesterol, but in the large bowel they exert the trophic and antineoplastic effects of dietary fiber. The mechanism for cholesterol reduction by soluble fibers relates to enhanced steroid excretion and altered fat absorption and may be a function of the viscosity of these fibers in solution. The relationships between the chemical structure of soluble polysaccharides and their documented physiologic effects are not yet clear. By using polysaccharides of defined structure and properties, it should be possible to identify those characteristics that predict physiologic actions.