Hypercholesterolaemia is a risk factor for CVD, which is a leading cause of death in industrialised societies. The biosynthetic pathways for cholesterol metabolism are well understood; however, the regulation of circulating cholesterol by diet is still not fully elucidated. The present study aimed to gain more comprehensive understanding of the relationship between circulating cholesterol levels and molecular effects in target tissues using the hamster model. Male golden Syrian hamsters were fed with chow or diets containing 36 % energy from fat with or without 1 % cholesteyramine (CA) as a modulator of circulating cholesterol levels for 35 d. It was revealed that the expression of lanosterol 14α-demethylase (CYP51) instead of 3-hydroxy-3-methyl-glutaryl (HMG)-CoA reductase mRNA expression was responsive to circulating cholesterol in hamsters fed hypercholesterolaemic diets. The high-fat diet increased circulating cholesterol and down-regulated CYP51, but not HMG-CoA reductase. The CA diet decreased cholesterol and increased CYP51 expression, but HMG-CoA reductase expression was not affected. The high-fat diet and CA diet altered the expression level of cholesterol, bile acids and lipid metabolism-associated genes (LDL receptor, cholesterol 7α-hydroxylase (CYP7A1), liver X receptor (LXR) α, and ATP-binding cassette subfamily G member 5/8 (ABCG5/8)) in the liver, which were significantly correlated with circulating cholesterol levels. Correlation analysis also showed that circulating cholesterol levels were regulated by LXR/retinoid X receptor and PPAR pathways in the liver. Using the hamster model, the present study provided additional molecular insights into the influence of circulating cholesterol on hepatic cholesterol metabolism pathways during hypercholesterolaemia.

The rational search of novel bioactive molecules against pathogens with immunomodulatory activity is presently one of the most significant approaches to discover and design new therapeutic agents for effective control of infectious diseases, such as the infection caused by Leishmania parasites. In the present study, we evaluated the therapeutic efficacy of the recently characterized immunomodulatory compound 11α,19β-dihydroxy-7-acetoxy-7-deoxoichangin, a seco-limonoid derived from the bark of Raputia heptaphylla (Pittier) using: (1) peritoneal macrophages and (2) Mesocricetus auratus hamsters infected with Leishmania (V.) panamensis and Leishmania (L.) amazonensis. We observed the ability of this seco-limonoid to induce the effective control of the parasite either in vitro [determining an effective concentration 50 (EC50) of 59 µ m at the infection model] and in vivo (inducing clinical improvement or even cure in infected animals treated compared with the groups of animals treated with vehicle solution or meglumine antimoniate).

Essential oil components from turmeric (Curcuma longa L.) are documented for neuroprotective, anti-cancer, anti-thrombotic and antioxidant effects. The present study aimed to investigate the disease-modifying potential of curcuma oil (C. oil), a lipophilic component from C. longa L., in hyperlipidaemic hamsters. Male golden Syrian hamsters were fed a chow or high-cholesterol (HC) and fat-rich diet with or without C. oil (30, 100 and 300 mg/kg) for 28 d. In HC diet-fed hamsters, C. oil significantly reduced plasma total cholesterol, LDL-cholesterol and TAG, and increased HDL-cholesterol when compared with the HC group. Similar group comparisons showed that C. oil treatment reduced hepatic cholesterol and oxidative stress, and improved liver function. Hyperlipidaemia-induced platelet activation, vascular dysfunction and repressed eNOS mRNA expression were restored by the C. oil treatment. Furthermore, aortic cholesterol accumulation and CD68 expression were also reduced in the C. oil-treated group. The effect of C. oil at 300 mg/kg was comparable with the standard drug ezetimibe. Delving into the probable anti-hyperlipidaemic mechanism at the transcript level, the C. oil-treated groups fed the chow and HC diets were compared with the chow diet-fed group. The C. oil treatment significantly increased the hepatic expression of PPARα, LXRα, CYP7A1, ABCA1, ABCG5, ABCG8 and LPL accompanied by reduced SREBP-2 and HMGCR expression. C. oil also enhanced ABCA1, ABCG5 and ABCG8 expression and suppressed NPC1L1 expression in the jejunum. In the present study, C. oil demonstrated an anti-hyperlipidaemic effect and reduced lipid-induced oxidative stress, platelet activation and vascular dysfunction. The anti-hyperlipidaemic effect exhibited by C. oil seems to be mediated by the modulation of PPARα, LXRα and associated genes involved in lipid metabolism and transport.

Glucose intolerance and dyslipidaemia are independent risk factors for endothelium dysfunction and CVD. The aim of the present study was to analyse the preventive effect of n-3 PUFA (EPA and DHA) on lipid and carbohydrate disturbances and endothelial dysfunction. Three groups of adult hamsters were studied for 20 weeks: (1) control diet (Control); (2) high-fat diet (HF); (3) high-fat diet enriched with n-3 PUFA (HFn-3) groups. The increase in body weight and fat mass in the HF compared to the Control group (P < 0·05) was not found in the HFn-3 group. Muscle TAG content was similar in the Control and HF groups, but significantly lower in the HFn-3 group (P = 0·008). Glucose tolerance was impaired in the HF compared to the Control group, but this impairment was prevented by n-3 PUFA in the HFn-3 group (P < 0·001). Plasma TAG and cholesterol were higher in the HF group compared to the Control group (P < 0·001), but lower in the HFn-3 group compared to the HF group (P < 0·001). HDL-cholesterol was lower in the HFn-3 group compared to the Control and HF groups (P < 0·0005). Hepatic secretion of TAG was lower in the HFn-3 group compared to the HF group (P < 0·005), but did not differ from the Control group. Hepatic gene expression of sterol regulatory element-binding protein-1c, diacylglycerol O-acyltransferase 2 and stearyl CoA desaturase 1 was lower in the HFn-3 group, whereas carnitine palmitoyl transferase 1 and scavenger receptor class B type 1 expression was higher (P < 0·05). In adipocytes and adipose macrophages, PPARγ and TNFα expression was higher in the HF and HFn-3 groups compared to the Control group. Endothelium relaxation was higher in the HFn-3 (P < 0·001) than in the HF and Control groups, and was correlated with glucose intolerance (P = 0·03) and cholesterol (P = 0·0003). In conclusion, n-3 PUFA prevent some metabolic disturbances induced by high-fat diet and improve endothelial function in hamsters.

The effectiveness of conjugated linoleic acid (CLA) as a weight-loss nutraceutical continues to be debatable, suggesting that there may be value in exploring the physiological effects of the lesser-known isomers. The effects of the minor isomer, trans-8, cis-10 (t8, c10)-CLA, in the form of an equimolar mixture with the cis-9, trans-11 (c9, t11) isomer, on body weight and body composition, circulating glucose and lipid concentrations, and liver weights were studied in sixty male Syrian golden hamsters. Animals were randomised to receive for 28 d a semi-purified, hypercholesterolaemic diet (5 % dietary fat and 0·25 % cholesterol) supplemented at the 2 % level with either the t8, c10+c9, t11-CLA mixture, c9, t11-CLA or trans-10, cis-12 (t10, c12)-CLA replacing lard and safflower-seed oil (control). Results show that compared with control, the t8, c10+c9, t11-CLA mixture and t10, c12-CLA-fed animals had lower (P < 0·0001) fat mass following supplementation. Animals consuming t10, c12-CLA also possessed higher lean mass compared with control and c9, t11-CLA groups (P < 0·001). However, the livers of these animals were larger (P < 0·0001) compared with those in the control and other CLA groups. Body weights of the hamsters did not differ across the experimental groups. CLA treatments had no effect on serum glucose or lipid profile, except for inducing higher (P < 0·05) non-HDL-cholesterol concentration with t10, c12-CLA compared with the c9, t11 isomer. Overall, these results indicate that in male hamsters fed a hypercholesterolaemic diet, the t8, c10+c9, t11-CLA mixture does not have an impact on blood lipid profile, but is able to effectively reduce fat mass, without incurring an accompanying liver enlargement.

Neurocysticercosis is a public health problem in many developing countries and is the most frequent parasitic disease of the brain. The human tapeworm carrier is the main risk factor for acquiring neurocysticercosis. Since the parasite lodges only in the human intestine, experimental models of Taenia solium taeniosis have been explored. Macaques, pigs, dogs, cats and rabbits are unsuccessful hosts even in immunodepressed status. By contrast, rodents are adequate hosts since tapeworms with mature, pregravid and, in some cases, gravid proglottids develop after infection. In this review, information that has been generated with experimental models of taeniosis due to T. solium is discussed. Initially, the use of the model for immunodiagnosis of human taeniosis and evaluation of intervention measures is summarized. Next, descriptions of tapeworms and comparison of hamsters, gerbils and other mammals as experimental models are discussed, as well as data on the humoral immune response, the inflammatory reaction and the production of cytokines associated to Th1 and Th2 responses in the intestinal mucosa. Finally, evaluation of protection induced against the development of tapeworms by recombinant T. solium calreticulin in hamsters is summarized and compared to other studies.

In mice, hepatic functions can be greatly affected by dietary trans-10, cis-12-conjugated linoleic acid (CLA). However, this phenomenon has been less documented in hamsters. In the present study, male hamsters were fed two doses of the trans-10, cis-12-CLA (0·5 and 1 %, w/w diet) or linoleic acid (0·5 %) for 6 weeks. The effects on the liver were examined by measuring the expression of thirty-six genes representing key metabolic pathways. CLA-responsive genes and their relationships with physiological outcomes were examined by a multivariate analysis procedure. Compared with control hamsters, those receiving either 0·5 or 1 % CLA exhibited similar fat loss (15–24 %; P ≤  0·05) and liver enlargement (21–28 %; P ≤ 0·05), with no signs of steatosis. We also observed a dose-dependent increase in the transcription of genes involved in lipid breakdown and lipid harvesting from blood, and in genes related to the oxidative stress and inflammatory responses. These responsive genes varied in parallel with cell membrane lipids (R2 0·31–0·42) and to a lesser extent with liver enlargement (R2 0·22) (all P < 0·05). We conclude that in hamsters, liver enlargement induced by trans-10, cis-12-CLA is accompanied by an increased metabolic potential to process fatty acids from mobilised adipose stores. This elevated metabolic activity, comprised of anabolic pathways and their catabolic counterparts, can trigger inflammation and the oxidant stress defence pathways in a dose-dependent manner. These results provide novel insights into the mechanisms by which trans-10, cis-12-CLA affects pathways related to liver function.

Very little evidence exists concerning the effects of conjugated linoleic acid (CLA) on body fat reduction induced by energy restriction. Moreover, although an effect of trans-10, cis-12-CLA on lipolysis has been suggested, it has not been consistently shown. The aims of the present study were to determine whether trans-10, cis-12-CLA increases the reduction of body fat induced by energy restriction, and to analyse its effect on lipolysis and adipose tissue lipase expression (hormone-sensitive lipase (HSL) and adipose tissue TAG lipase (ATGL)). Male Syrian Golden hamsters were fed a high-fat diet during 7 weeks in order to make them fatter. Then they were submitted to a mild energy restriction (25 %) without or with supplementation of 0·5 % trans-10, cis-12-CLA for 3 weeks. Basal glycerol release and lipolysis stimulated by several drugs acting at different levels of the lipolytic cascade were measured in epididymal adipose tissue. The expression of HSL and ATGL was assessed by real-time RT-PCR. No differences were found in adipose tissues size between the experimental groups. Medium adipocyte size and total number of adipocytes were similar in both experimental groups. Animals fed the CLA-enriched diet showed similar lipolytic rates as well as HSL and ATGL expressions to the controls. In conclusion, trans-10, cis-12-CLA does not promote adipose tissue lipid mobilisation nor does it heighten body fat reduction induced by energy restriction. Consequently, this CLA isomer does not seem to be a useful tool to be included in body weight-loss strategies followed in obesity treatment.

This study tested the hypothesis that protein source is a factor determining the impact of the diet on lipid metabolism in hamsters. Twenty-eight hamsters of similar body weight were assigned for a period of 8 weeks to one of the following four diets (seven per group) containing either 20 % (w/w) casein (CAS), beef protein (BF), wheat gluten (WG) or soya protein (SOY). The fat composition of the diet was the same (15·5 % w/w) in all groups and provided SFA, MUFA and PUFA representative of the average Canadian diet. After an overnight fast, blood and liver were collected for the measurement of serum lipids, fatty acid composition of liver phospholipids and mRNA levels of selected genes involved in lipid metabolism. WG resulted in lower total cholesterol, HDL-cholesterol and non-HDL-cholesterol but, along with SOY, in higher mRNA levels of cholesterol 7 α-hydroxylase and LDL receptor. Furthermore, both WG and SOY resulted in lower 18 : 3n-3, 20 : 4n-6, total n-6 PUFA, 18 : 1n-9 and total MUFA, but higher 22 : 6n-3, total n-3 PUFA, 22 : 6n-3/18 : 3n-3 and 22 : 5n-3/18 : 3n-3 ratios in liver phospholipids, and higher hepatic Δ6-desaturase mRNA levels. These results show that the impact of dietary protein on lipid metabolism is source-dependent and associated with changes in mRNA abundances of key hepatic enzymes and receptors.

The hypolipidaemic effects of plant sterols are well established. However, mechanisms by which plant sterols lower plasma cholesterol levels, particularly at the molecular level, have not been clearly elucidated. The objective of the present study was to determine whether different plant sterol analogues reduce plasma cholesterol levels by up regulating the sterol transporters ABCG5 and ABCG8 in the liver and/or small intestine. Male Golden Syrian hamsters were divided into eight groups. Groups 1 and 2 were fed a maize starch–casein–sucrose-based diet that did not contain cholesterol (control; Con) or the Con diet with the addition of 0·25 % cholesterol (Ch-Con). Groups 3–8 were fed the Ch-Con diet supplemented with 1 % plant sterols, 1 % plant stanols, 1 % of a plant sterol and stanol mixture (50:50), 1·76 % plant sterol–fish oil esters, or 0·71 or 1·43 % stanol–ascorbic acid esters, respectively. After 5 weeks, the Ch-Con diet up regulated the ABCG5 mRNA expression and tended (P = 0·083) to increase ABCG8 mRNA expression in the liver, but did not affect both genes’ expression in the small intestine compared with the Con diet. Hamsters fed 0·7 % stanol esters showed lower plasma cholesterol levels (P < 0·001) and also lower liver ABCG5 mRNA expression (P < 0·05) compared with the Ch-Con diet. Plant stanols, stanol esters, and sterol esters did not affect the ABCG5 or ABCG8 mRNA expressions in the liver and intestine although they reduced plasma cholesterol levels. These results suggest that plant sterols and their derivatives reduce plasma cholesterol levels independently from the mRNA expression of ABCG5 and ABCG8 transporters.

Conjugated linoleic acids (CLAs) such as rumenic acid (RA) have the potential to alter blood lipid profiles in animals and in humans. In contrast, physiological effects of conjugated α-linolenic acids (CLnAs), which concomitantly are omega-3 and conjugated fatty acids, are still unknown. The aim of this study was to evaluate the potential of CLnA to interfere in early steps of atherosclerosis by altering lipoprotein profiles and fatty streaks in the aortas. F1B hamsters were fed a control or one of the three hypercholesterolemic (HC) diets: HC-control, HC-RA (18:2 cis-9, trans-11) or HC-CLnA (CLnA: equimolar mixture of 18:3 cis-9, trans-11, cis-15 and cis-9, trans-13, cis-15) diet. In low-cholesterol control-fed hamsters, the proportion of high-density lipoprotein cholesterol (HDL-C) was around 45% while in HC-fed hamsters, HDL-C was around 10% and cholesterol was mostly (80%) carried by triglyceride-rich lipoproteins (TRL). Low-density lipoprotein (LDL) triglycerides (TGs) increased by approximately 60% in hamsters fed either HC-RA or HC-CLnA compared with HC-controls but not compared with the low-cholesterol control diet. HDL cholesterol decreased by 24% and 16% in hamsters fed HC-RA and HC-CLnA, respectively. Small dense LDL-cholesterol increased by approximately 60% in hamsters fed HC-RA and HC-CLnA compared with the HC-control group and by more than a 100% compared with hamsters on the control diet. The relative percentage of liver cholesteryl ester content increased by 88% in hamsters fed HC diets compared with the control diet. Significant differences in fatty streaks were observed between control and HC-diet-fed hamsters. However, no significant difference was observed among the HC-diet-fed hamsters. This study shows that animals fed any one of the HC diets developed an adverse lipoprotein profile compared with a normolipidic diet. Also, HC-RA or HC-CLnA diets altered lipoprotein profile compared with animals fed the HC-control diet but had no beneficial effects on atherosclerosis.

The aim of our present study was to compare the efficiency of conjugated linoleic acids (CLA) and fish oil in modulating atherogenic risk markers. Adult male hamsters were given a cholesterol-rich diet (0·6 g/kg) for 8 weeks; the diet was supplemented with 5 g cis-9,trans-11-CLA isomer/kg, 12 g CLA mixture (CLA-mix)/kg, 12 g fish oil/kg or 12 g fish oil + 12 g CLA-mix/kg. The plasma cholesterol status was improved only with the cis-9,trans-11-CLA (HDL-cholesterol and HDL-cholesterol:LDL-cholesterol ratio, P<0·05), but was of borderline significance for CLA-mix (HDL-cholesterol:LDL-cholesterol ratio, P=0·06), with an increase (33–40 %) in the liver lipoprotein receptors (scavenger receptor-type I and LDL ApoB/E receptor) and HDL-binding protein 2 (P<0·05). A 100 % pigment gallstones incidence and a slight insulin resistance (homeostatic model assessment index) were observed in the CLA-mix-fed hamsters (P=−0·031). In comparison, fish-oil feeding alone improved merely the scavenger receptor-type I and HDL-binding protein 2 liver status and faeces sterol output. For most of our present observations, the concomitant intake of fish oil and CLA-mix gave dominant effects that were exclusive and specific to one or the other oil. In conclusion, part of the beneficial effects of CLA in the present study can be ascribed to the cis-9,trans-11-isomer, and these did not generally overlap with those of fish oil. In addition, the CLA-mix effects are clearly affected by the marine (n-3) fatty acids.

In order to study the mechanism by which increasing unsaturation of dietary fat lowers HDL-cholesterol levels, we studied various measures of HDL metabolism in hamsters fed with fats with different degrees of saturation. Hamsters were fed on a cholesterol-enriched (1 g/kg) semipurified diet containing 200 g/kg of maize oil, olive oil, or palm oil for 9 weeks. Increasing saturation of dietary fat resulted in increasing concentrations of total plasma cholesterol (4·29 (SD 0·51), 5·30 (sd 0·67) and 5·58 (sd 0·76) mmol/l respectively, n 12) and HDL-cholesterol (3·31 (sd 0·50), 3·91 (sd 0·12) and 3·97 (sd 0·43) mmol/l) and these concentrations were significantly higher (P < 0·05) in the palm-oil and olive-oil-fed hamsters compared with the maize-oil group. Total plasma triacylglycerol levels also increased with increasing fat saturation (1·01 (sd 0·59), 1·56 (sd 0·65) and 2·75 (sd 1·03) mmol/l) and were significantly higher (P < 0·05) in the palm-oil group compared with the olive-oil and maize-oil-fed hamsters. The three diets did not have differential effects on plasma activity levels of lecithin: cholesterol acyltransferase (LCAT) and cholesteryl ester transfer protein (CETP). Levels of phospholipid transfer protein (PLTP) tended to be higher with increasing fat saturation but this effect was not significant. The capacity of liver membranes to bind human HDL3 was significantly higher (P < 0·05) in the hamsters fed with maize oil (810 (sd 100) ng HDL3 protein/mg membrane protein, n 4) compared with those fed on palm oil (655 (sd 56) ng/mg), whereas the olive-oil group had intermediate values (674 (sd 26) ng/mg). The affinity of HDL3 for the binding sites was not affected by the type of dietary fat. Hepatic lipase (EC 3.1.1.3) activity, measured in liver homogenates, increased with increasing fat saturation. We conclude that dietary maize oil, when compared with either olive oil or palm oil, may lower HDL-cholesterol concentrations by enhancing HDL binding to liver membranes.

In order to study the mechanism by which increasing unsaturation of dietary fat lowers HDL-cholesterol levels, we studied various measures of HDL metabolism in hamsters fed with fats with different degrees of saturation. Hamsters were fed on a cholesterol-enriched (1 g/kg) semipurified diet containing 200 g/kg of maize oil, olive oil, or palm oil for 9 weeks. Increasing saturation of dietary fat resulted in increasing concentrations of total plasma cholesterol (4·29 (SD 0·51), 5·30 (sd 0·67) and 5·58 (sd 0·76) mmol/l respectively, n 12) and HDL-cholesterol (3·31 (sd 0·50), 3·91 (sd 0·12) and 3·97 (sd 0·43) mmol/l) and these concentrations were significantly higher (P < 0·05) in the palm-oil and olive-oil-fed hamsters compared with the maize-oil group. Total plasma triacylglycerol levels also increased with increasing fat saturation (1·01 (sd 0·59), 1·56 (sd 0·65) and 2·75 (sd 1·03) mmol/l) and were significantly higher (P < 0·05) in the palm-oil group compared with the olive-oil and maize-oil-fed hamsters. The three diets did not have differential effects on plasma activity levels of lecithin: cholesterol acyltransferase (LCAT) and cholesteryl ester transfer protein (CETP). Levels of phospholipid transfer protein (PLTP) tended to be higher with increasing fat saturation but this effect was not significant. The capacity of liver membranes to bind human HDL3 was significantly higher (P < 0·05) in the hamsters fed with maize oil (810 (sd 100) ng HDL3 protein/mg membrane protein, n 4) compared with those fed on palm oil (655 (sd 56) ng/mg), whereas the olive-oil group had intermediate values (674 (sd 26) ng/mg). The affinity of HDL3 for the binding sites was not affected by the type of dietary fat. Hepatic lipase (EC 3.1.1.3) activity, measured in liver homogenates, increased with increasing fat saturation. We conclude that dietary maize oil, when compared with either olive oil or palm oil, may lower HDL-cholesterol concentrations by enhancing HDL binding to liver membranes.

Results from earlier experiments indicate that different species of rodent vary both in the number of cone types found in their retinas and in the spectral sensitivities of the cone pigments. These features have now been examined in two types of hamster commonly used for research purposes: Syrian golden hamsters (Mesocricetus auratus) and Siberian dwarf hamsters (Phodopus sungorus). Electroretinogram (ERG) flicker photometry, behavioral discrimination tasks, and opsin antibody labeling were used to investigate hamster photoreceptors and their visual consequences. Results from the three approaches support the following conclusions: (1) The retinas of both species have an abundant population of rods containing a photopigment with peak sensitivity of about 498–500 nm; (2) Siberian dwarf hamsters have two classes of cone: one with maximum sensitivity in the ultraviolet (c. 360 nm), the other with peak sensitivity closely similar to that of its rod; and (3) Syrian golden hamsters have a class of cone with peak sensitivity at about 506 nm, but they lack a second cone type. Implications of these alternative arrangements are discussed.

The effects of rye bran, oat bran and soya-bean fibre on serum lipids, bile composition and gallstone formation were studied in male Syrian golden hamsters (Mesocricetus auratus). The control groups received fibre-free stone-provoking (O1 diet) or non-stone-provoking (O2 diet) diets. The serum cholesterol levels were lower for all groups fed on the diets supplemented with the dietary fibre sources compared with the control groups. The total content of bile acids in bile was higher in groups given ryebran diets compared with the corresponding controls. The proportion of cholic acid was higher and that of chenodeoxycholic and lithocholic acid lower in the groups given rye-bran-, oat-bran- or soya-bean-fibre-supplemented diets, compared with the corresponding controls. The secondary: primary bile acid ratio was lower in the group given the rye-bran-supplemented O1 diet. The lithocholic:deoxycholic acid ratio was lower in the groups given rye-bran-, oat-bran- or soya-bean-fibre-supplemented diets than in the corresponding controls. A lower frequency of gallstones was observed only for the group receiving the rye-bran-supplemented O1 diet while the lithogenic index was lower in the groups given the rye-bran-supplemented O2 diet. A decreased epithelial volume density of the gall-bladder and an increased smooth muscular volume density were observed in animals given oat-bran- and rye-bran-supplemented O1 diets, whereas for the soya-bean-fibre-supplemented O1 diet, only the smooth muscular volume density was increased.

The effects of bran and starchy endosperm fractions of oat and rye on faecal weight and on biliary and faecal bile acids were studied in Syrian golden hamsters (Mesocricetus auratus). The animals fed on diets supplemented with steam-flaked oat bran, oat bran or rye bran had higher wet and dry weights of faeces compared with the animals fed on the fibre-free or low-fibre endosperm diets. A higher mean percentage of biliary cholic acid and a lower mean percentage of chenodeoxycholie and lithocholic (LCA) acids was observed in the bran-supplemented dietary groups. Animals fed on the bran-supplemented diets had increased daily faecal excretion of both total saponifiable and total free bile acids compared with the animals fed on fibre-free or endosperm-supplemented diets. The mean percentage of total saponifiable bile acids in the faeces was higher, and that of free bile acids lower in the animals fed on bran-supplemented diets. A significantly lower concentration of faecal free LCA was observed in the animals fed on the rye-bran diet. Both bran and endosperm diets reduced the faecal LCA: deoxycholic acid compared with the fibre-free diet, but the bran diets had a more pronounced effect than endosperm diets.