Niacin (nicotinic acid) in its non-physiological dose level is known to be an effective lipid-lowering agent; its potential risk as a therapeutic agent, however, has not been critically considered. Since niacin is excreted predominantly as methylated pyridones, requiring methionine as a methyl donor, the present study was undertaken to examine whether metabolism of the amino acid is altered in the presence of large doses of niacin. Male Sprague–Dawley rats were given a nutritionally adequate, semi-synthetic diet containing niacin at a level of either 400 or 1000 mg/kg diet (compared to 30 mg/kg in the control diet) for up to 3 months. Supplementation with niacin (1000 mg/kg diet) for 3 months resulted in a significant increase in plasma and urinary total homocysteine levels; this increase was further accentuated in the presence of a high methionine diet. The hyperhomocysteineaemia was accompanied by a significant decrease in plasma concentrations of vitamins B6 and B12, which are cofactors for the metabolism of homocysteine. The homocysteine-raising action of niacin, in particular, has an important toxicological implication, as hyperhomocysteineaemia is considered to be an independent risk factor for arterial occlusive disease. The niacin-associated change in homocysteine status may be an important limiting factor in the use of this vitamin as a lipid-lowering agent.

Flavanols are the most abundant flavonoids in the human diet where they exist as monomers, oligomers and polymers. In the present study, catechin, the procyanidin dimer B3 and a grapeseed extract containing catechin, epicatechin and a mixture of procyanidins were fed to rats in a single meal. After the meals, catechin and epicatechin were present in conjugated forms in both plasma and urine. In contrast, no procyanidins or conjugates were detected in the plasma or urine of any rats. Procyanidins were not cleaved into bioavailable monomers and had no significant effects on the plasma levels or urinary excretion of the monomers when supplied together in the grapeseed extract. We conclude that the nutritional effects of dietary procyanidins are unlikely to be due to procyanidins themselves or monomeric metabolites with the intact flavonoid-ring structure, as they do not exist at detectable concentrations in vivo. Future research should focus on other procyanidin metabolites such as phenolic acids and on the effects of the unabsorbed oligomers and polymers on the human gastrointestinal tract.

We aimed to improve the use of the human intestinal Caco-2 cell line for studying dietary lipid and cholesterol processing by using isolated pure clones (). Three clones (TC7, PD7 and PF11) were grown as monolayers on semi-permeable filters and compared for cell viability, fatty acid and cholesterol apical uptake or basolateral secretion, apolipoprotein B-48 basolateral secretion and 3-hydroxy-3-methylglutaryl (HMG)-CoA reductase activity. The TC7 clone showed the best viability upon apical incubation with mixed micelles and should be preferred for routine work. Short-term (3·0 h) rates of apical uptake of cholesterol were not different with the three clones, whereas the rate of apical uptake of oleic acid (18 : 1) was lower (P<0·05) with PF11 (250·6 nmol/mg) and the basolateral secretion of cholesterol and oleic acid was lower with the TC7 clone (0·40 and 29·1 nmol/mg respectively). The secretion of apolipoprotein B-48 basolaterally was about 2-fold lower than from PD7 clone. The basal levels of HMG-CoA reductase activity were significantly different (P<0·05; TC7>PF11>PD7). The down-regulation of the enzyme activity was moderate (range 13·8–21·0 %) and comparable in the presence of apical micellar cholesterol, but was much marked upon basolateral incubation with LDL (range 34·0–53·6 %), especially for the PD7 clone. In conclusion, the Caco-2 clones characterized here proved to be particularly suitable for studying lipid nutrients processing. Because these three clones exhibit some different metabolic capabilities, they provide a new tool to study intestinal response to lipid nutrients.

The aims of this study were to determine the total body phylloquinone and its metabolic turnover in human subjects using a tracer dose of [5-H3]phylloquinone containing 55·5×104 MBq/mmol. Seven subjects aged 22 to 49 years were given 0·3 μg isotopic phylloquinone intravenously on a control diet (75 μg phylloquinone/d) and blood, urine and faeces were sampled periodically for 6 d. Five of these subjects were studied a second time after 3–8 weeks on a low-vitamin K diet (8 μg/d). The changes in the radioactivity of plasma phylloquinone with time were analysed by the method of residuals and fitted to a curve composed of two exponential components. The size of the exchangeable body pool was calculated by isotope dilution. Plasma phylloquinone levels fell during vitamin K restriction but the vitamin K-dependent coagulation factors did not change. After injection the first exponential decay curve t1/2 was 1·0 (SD 0·47) H IN THE SUBJECTS ON THE CONTROL DIET AND 0·49 (sd 0·27) h after vitamin K restriction. On the control diet, the second exponential t1/2 was 27·6 (sd 124) h that did not change on the low-vitamin K diet (t1/2=25·1 (sd 13·5) h). These results indicate that the turnover time for phylloquinone in human subjects is about 1·5 d. Urinary excretion of 3H-metabolites ranged from 30 % of the administered dose on the control diet to 38 % on the restricted diet and had the same turnover rate as the second component of the plasma decay curves. The exchangeable body pool of phylloquinone declined from about 1·0 μg/kg before restriction to lower values after vitamin K restriction. The faecal excretion of phylloquinone and its metabolites fell from 32 % of the administered dose on the control diet to 13 % on the restricted diet.

Within Europe there are differences in cardiovascular disease (CVD) risk between countries and this might be related to dietary habits. Oxidative modification of LDL is suggested to increase the risk of CVD and both the fatty acid and antioxidant content of LDL can affect its oxidation. In the present study, concentration of LDL fatty acid and antioxidant micronutrients (tocopherols and carotenoids) and ex vivo oxidative resistance of LDL (lag phase) was compared in volunteers from five countries with different fruit and vegetable intakes and reported rates of CVD. Eighty volunteers (forty males, forty females per centre), age range 25–45 years, were recruited from France, Northern Ireland, UK, Republic of Ireland, The Netherlands, and Spain, and their LDL composition and lag phase were measured. There were some differences in LDL carotenoid and α-tocopherol concentrations between countries. α-Tocopherol was low and β- + γ-tocopherol were high (P<0·001) in the Dutch subjects. β-Carotene concentrations were significantly different between the French and Spanish volunteers, with French showing the highest and Spanish the lowest concentration. LDL lycopene was not different between centres in contrast to lutein, which was highest in French (twofold that in the Dutch and Spanish and threefold that in Northern Ireland and the Republic of Ireland, P<0·001). However absolute LDL saturated, monounsaturated, polyunsaturated and total unsaturated fatty acid concentrations were different between countries (P<0·001, total unsaturated highest in Northern Ireland) there was little difference in unsaturated:saturated fatty acid concentration ratios and no difference in polyunsaturated:saturated fatty acid concentration ratios. LDL from the Republic of Ireland (a region with a high rate of CVD) had greater resistance to Cu-stimulated oxidation than samples obtained from volunteers in other countries. In conclusion, LDL composition did not predict resistance to Cu-stimulated oxidation, nor is there evidence that LDL from volunteers in countries with lower rates of CVD have greater resistance to oxidation.

The effect of maternal phylloquinone supplementation on vitamin K in breast milk was studied to establish: (1) if phylloquinone is the source of menaquinone-4 in breast milk; (2) the dose–effect relationship between intake and obtainable levels. Four groups of lactating mothers with a full-term healthy infant participated and took oral phylloquinone supplements of 0·0 (n 8), 0·8 (n 8), 2·0 (n 8), and 4·0 (n 7) mg/d for 12 d, starting at day 4 post-partum. Milk samples were collected on days 4, 8, 16, and 19. Blood samples were collected on days 4 and 16. Vitamin K and vitamin E concentrations, the latter for reason of comparison, were assayed. Phylloquinone and menaquinone-4 were present in all milk samples: 5·84 (SD 2·31) AND 2·98 (sd 1·51) nmol/l (n 31) respectively, in colostrum (day 4 sample). A strong correlation between the vitamers was found (r 0·78, P<0·001). Breast-milk phylloquinone levels were raised in a dose-dependent manner: 4-, 12-, and 30-fold on day 16 for the 0·8, 2·0, and 4·0 mg group respectively. In addition, menaquinone-4 levels were higher: 2·5- (P<0·05) and 7-fold (P<0·001) in the 2·0 and 4·0 mg groups respectively. Plasma of supplemented subjects contained 3-, 5-, and 10-fold higher phylloquinone levels on day 16. Detectable menaquinone-4 was found in ten of thirty-one day 4 plasma samples. All day 16 plasma samples of the 4 mg supplemented group contained the vitamin. There was no correlation between the K-vitamers in plasma. Vitamin E and phylloquinone appear to differ in their distribution in breast milk, milk:plasma concentration ratios were ≤1 and 3–5 for vitamin E and phylloquinone respectively. The milk:plasma concentration ratio of menaquinone-4 was >10. In conclusion, dietary phylloquinone is a source of menaquinone-4 in breast milk. Phylloquinone supplementation to lactating mothers may be of benefit to the newborn infant, since both phylloquinone and menaquinone-4 are raised by supplementation.

Diet composition and energy content modulate free fatty acid (FFA) release. The aim of this study was to evaluate the dose–response effects of euenergetic variations in dietary carbohydrate and fat content on postabsorptive FFA release. The rate of appearance (Ra) of palmitate was measured by infusion of [2,2-2H2]palmitate after an overnight fast in six healthy men on three separate occasions, i.e. after 7 d on euenergetic control, high-carbohydrate and high-fat diets. The protein content and composition was identical for each diet. Postabsorptive plasma fatty acid concentrations were not different between the high-carbohydrate and control diets (0·36 (SE 0·07) V. 0·43 (se 0·04) mmol/l), but were increased after the high-fat diet (0·75 (se 0·09) mmol/l, (P<0·01 compared with the other diets). Ra palmitate was not different between the high-carbohydrate and control diets (1·36 (se 0·20) v. 1·47 (se 0·15) μmol/kg per min). However, Ra palmitate was increased to 2·36 (se 0·26) μmol/kg per min after the high-fat diet (P<0·01 compared with the other diets). The fatty acid flux and whole-body fat oxidation were not affected by the high-carbohydrate diet compared with the control diet, but were increased by 67 and 47 % respectively, on the high-fat diet (P<0·01 compared with the other diets). A euenergetic high-fat diet results in increased postabsorptive FFA release and fat oxidation, whereas a euenergetic high-carbohydrate diet does not affect these variables of fat metabolism.

The difference between vitamin K metabolism in the liver and that in the bone of vitamin K-deficient rats was examined. After 17 d administration of vitamin K-deficient food, vitamin K in the liver was almost depleted, and prothrombin time (PT) was prolonged. Serum total osteocalcin level was slightly decreased by vitamin K deficiency, whereas serum undercarboxylated osteocalcin level did not change. The level of menaquinone (MK)-4 as well as that of phylloquinone was decreased, but approximately 40 % of the initial level still existed in the femur after the 17 d period. A single-dose administration of vitamin K (250 nmol/kg body weight) markedly increased vitamin K level in the liver but not in the femur. These results suggest that the turnover of vitamin K in the bone is slower than that in the liver, and bone metabolism may be little affected by the short period of intake of vitamin K-deficient food. However, intake of a larger amount of vitamin K is required for its accumulation in the bone than in the liver. Furthermore, the counteracting effect of MK-7 on prolonged PT in vitamin K-deficient rats was found to be higher than phylloquinone or MK-4.

Vitamin C (ascorbic acid) is an essential nutrient that is involved in a number of cellular processes. However, unlike most mammals, man is unable to synthesize vitamin C and it must therefore be acquired from the diet. Absorption of vitamin C is achieved by two transporters, SVCT1 and SVCT2, recently cloned from rat and human kidney. SVCT1 is thought to be the predominant transporter in the intestine. Vitamin C supplements are increasingly common, thus contributing to an increased dietary load, and therefore the aim of the present study was to investigate the effect of high doses of ascorbic acid on SVCT1 expression. Using the Caco-2 TC7 cell model of small intestinal enterocytes, we measured the effects of ascorbic acid (4·5 mg/ml culture medium) on L-[14C]ascorbic acid uptake and SVCT1 expression (determined by reverse transcription-polymerase chain reaction). Ascorbic acid uptake was decreased significantly in Caco-2 TC7 cells exposed to ascorbate for 24 h (-50 %, P<0·0005). Expression of SVCT1 was also significantly reduced by exposure to elevated levels of ascorbate for 24 h (-77 %, P<0·005). Taken together these results suggest that high-dose supplements might not be the most efficient way of increasing the body pool of vitamin C.

This work was designed to investigate the effect of different lipid sources on ob gene expression and serum leptin levels in rats with two different feeding protocols: (1) free access to food; or (2) energy-controlled feeding. Male Wistar rats were fed diets containing 40 % energy as fat (olive oil, sunflower oil or beef tallow), for 4 weeks. In Expt 1 rats had free access to food, and in Expt 2 rats were fed a controlled amount of food (16 g/d, equivalent to 300 kJ/d). Insulin and leptin were determined by ELISA and ob mRNA by Northern blot. When rats had free access to food, ob mRNA levels were higher in animals fed either olive oil or sunflower oil than in those fed beef tallow. In marked contrast with feeding ad libitum, no differences were found among dietary fat groups in rats fed energy-controlled diets. When both feeding protocols were compared, free access to food induced an increased expression of ob mRNA in perirenal and/or epididymal adipose tissues from rats fed either olive oil or sunflower oil, but not from rats fed beef tallow. Dietary lipid type did not induce modifications in serum leptin concentrations. A tendency to higher serum leptin levels was observed more in rats with free access to food than in rats fed energy-controlled feeding. No differences were found in insulin levels. Dietary fat type importantly affects ob mRNA expression in rat white adipose tissue under hyperphagic conditions. Further study is needed in order to elucidate the mechanism underlying this effect.

Dietary fibre consists of remnants of edible plant cell polysaccharides and associated substances resistant to hydrolysis by human alimentary enzymes, which may benefit health through a wide range of physiological effects. Inulin and oligofructose are storage carbohydrates found in a number of vegetables, fruits and whole grains. They resist digestion and absorption in the stomach and small intestine of humans, as shown by their almost full recovery at the end of the ileum of healthy or ileostomised volunteers. Inulin and oligofructose thus enter into the large intestine where they are available to fermentation, as demonstrated by increased breath hydrogen. Fermentation of both substrates is complete and no residue is found in human stools. Inulin and oligofructose improve laxation. Their bulking capacity comprised between 1·2 and 2·1 g of stool per g of ingested substrate, results mainly from increases in microbial biomass in the colon. As water content of bacterial cells is high, stools are softer and easier to expulse. Stool frequency is thus increased, particularly in slightly constipated individuals. In addition, likely due to their fermentation properties, inulin and oligofructose also affect the intestinal epithelium (trophicity, mucin expression, etc.), that may strengthen mucosal protection and reduce the risk of gastrointestinal diseases. In summary, inulin and oligofructose are plant carbohydrates, resistant to digestion in the human small intestine and fermented by colonic bacteria. They exert several intestinal physiological effects contributing to maintenance of health. Therefore, inulin and oligofructose fit well within the current concept of dietary fibre.

Recent studies underline the importance of the immunoinflammatory processes in the pathology of Mg deficiency. Neutrophils possess a superoxide anion-generating NADPH oxidase and its inappropriate activation may result in tissue damage. The aim of the present study was to assess the effect of experimental Mg deficiency in the rat on polymorphonuclear leucocytes (PMN) activity and the role of increasing extracellular Mg. Weaning male Wistar rats were fed either a Mg-deficient or a control diet for 8 d. In Mg-deficient rats, the characteristic inflammatory response was accompanied by a marked increase in the number of PMN. Higher plasma interleukin 6 and NO concentrations and increased lipid peroxidation in the heart were found in Mg-deficient rats as compared with control rats. As shown by chemiluminescence studies, basal neutrophil activity from Mg-deficient rats was significantly elevated when compared with neutrophils from control rats. Moreover, the chemiluminescence of PMN from Mg-deficient rats was significantly higher than that of control rats following phorbol myristate acetate or opsonized zymosan activation. PMN from Mg-deficient rats also showed an increased activity of phagocytosis in comparison with neutrophils from control animals. Increasing extracellular Mg concentration in the incubating medium of PMN (0·8 v. 8·0 mM) decreased the chemiluminescence activity of PMN from control rats following opsonized zymosan activation. Chemiluminescence activities of PMN from Mg-deficient rats following phorbol myristate acetate or opsonized zymosan challenge were also decreased by high extracellular Mg concentration. From this work, it appears that PMN activation is an early consequence of Mg deficiency and that high extracellular Mg concentration inhibits free radicals generation.

The objectives of the present study were to investigate the recovery of [14C]allantoin in urine of sheep dosed intravenously and degradation of allantoin by rumen micro-organisms. The recovery of [14C]allantoin in the urine of eight sheep was measured during three periods in two experiments. Individual values of [14C]allantoin recovery varied from 66 to 95 % (mean value 83 (SE 1·6) %). The recovery of [14C]allantoin showed no relation to the level of feed intake. There was some evidence that glomerular filtration rate was an important factor affecting the amount of urinary allantoin recovered in one experiment. Incomplete recovery of plasma [14C]allantoin in the urine indicated losses of plasma [14C]allantoin via non-renal routes. This is supported by the disappearance of 14C from rumen contents incubated in vitro with [14C]allantoin for 48 h (88 %) and the presence of 14C in saliva in vivo from sheep sampled after dosing with [14C]allantoin. However, the amount of 14C activity in the saliva was very low (equivalent to only 1·5 % of the total dose in sheep producing saliva at a rate of 15 litres/d). The proportion of renal and non-renal excretion of purine derivatives was found to be unpredictable both between and within individual animals. The factors responsible for this variability need to be identified, and existing models of excretion of purine derivatives may need to be modified accordingly to improve their accuracy of prediction. A single intravenous injection of [4,5-14C]allantoin provides a simple alternative to infusion methods used to measure the proportion of plasma allantoin excreted in the urine of sheep. Using this method it may be feasible to validate PD excretion models in other ruminant livestock.

The bulking index (i.e. the increase in faecal fresh weight in gram per gram indigestible carbohydrate ingested) with oligofructose and inulin is similar to that produced with other easily fermented fibres such as pectins and gums. Most studies in man have been performed at a level of 15 g/d and more investigations on lower intakes are needed to appoint the least intake for an effect. Concerning short-chain fatty acids (SCFA) most studies have been using oligofructose and points at an increased butyric acid formation in the caecum of rats. In one study on rats with inulin high caecal proportions of propionic acid were obtained. As inulin has a higher molecular weight than oligofructose it might be speculated if this could be a reason to the different SCFA-profile formed. No effects on faecal concentrations of SCFA in humans have been revealed with inulin and oligofructose, which neither is expected as most of the SCFA formed during the fermentation already has been absorbed or utilized by the colonic mucosa.

Sweet lupin (Lupinus albus), a protein-rich legume devoid of anti-nutritional factors, is considered to have a high potential for protein nutrition in man. Results concerning the nutritional value of lupin protein are, however, conflicting in animals and very scarce in human subjects. Furthermore, where fibre-rich protein sources are concerned, the long-term nutritional results are often obscured, particularly since fibre-promoted colonic fermentation may bias the energy supply and redistribute N flux. We therefore studied, during the postprandial phase, the bioavailability and utilisation of lupin-flour protein in nine healthy men who had ingested a mixed meal containing intrinsically 15N-labelled lupin flour as the protein source (Expt 1). The real ileal digestibility (RID) and ileal endogenous N losses (IENL) were assessed using a perfusion technique at the terminal ileum, and the N content and 15N enrichment of ileal samples. Lupin flour exhibited a high RID of 91 (SD 3) % AND LOW IENL (5·4 (sd 1·3) mmol N/h). Postprandial dietary deamination was also assessed from body dietary urea and urinary dietary N excretion, and compared with results in nine healthy men following an isoenergetic meal containing a 15N-soyabean-protein isolate with a similar RID, as a control (Expt 2). Postprandial dietary deamination was similar after lupin and soyabean meals (17 (sd 2) and 18 (sd 4) % ingested N respectively). We therefore conclude that lupin protein is highly bioavailable, even if included in fibre-rich flour, and that it can be used with the same efficiency as soyabean protein to achieve postprandial protein gain in healthy human subjects.

Little is known about flavonoid metabolism and excretion in man. In the present study, the urinary excretion of a major flavonoid in wine, catechin, and its metabolites, were measured after nine human subjects each consumed 120 ml red wine (RW) on one day and de-alcoholized red wine (DRW) on a separate day. Both the RW and DRW contained 120 (SEM 3) ΜMOL CATECHIN (35 MG). GC–MS ANALYSES OF THE TRIMETHYLSILYLATED DERIVATIVES OF CATECHIN AND 3″ AND 4″ METHYLCATECHIN WERE PERFORMED BEFORE AND AFTER HYDROLYSIS OF CONJUGATES BY Β-GLUCURONIDASE AND SULFATASE. BASELINE URINE SAMPLES COLLECTED PRIOR TO WINE CONSUMPTION CONTAINED 0·013 (sem 0·005) μmol catechin and metabolites. During the 8 h period following consumption of RW and DRW, 6·6 (sem 0·9) and 5·3 (sem 0·6) μmol catechin and metabolites were excreted in 893 (sem 94) and 740 (sem 101) ml urine respectively. This corresponded to 3·0–10·3 % of the dose after RW and 2·1–8·2 % of the dose after DRW. The amount of catechin and metabolites excreted in urine was 20 % higher after RW compared with DRW (P=0·06). Catechin in all urine samples was present as metabolites and there were no differences in the proportions of individual metabolites after RW and DRW. As with other flavonoids, the fate of most ingested catechin is not yet known.

Fish-oil supplementation can reduce circulating triacylglycerol (TG) levels and cardiovascular risk. This study aimed to assess independent associations between changes in platelet eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) and fasting and postprandial (PP) lipoprotein concentrations and LDL oxidation status, following fish-oil intervention. Fifty-five mildly hypertriacylglycerolaemic (TG 1·5–4·0 mmol/l) men completed a double-blind placebo controlled cross over study, where individuals consumed 6 g fish oil (3 g EPA+DHA) or 6 g olive oil (placebo)/d for two 6-week intervention periods, with a 12-week wash-out period in between. Fish-oil intervention resulted in a significant increase in the platelet phospholipid EPA (+491 %, P<0·001) and DHA (+44 %, P<0·001) content and a significant decrease in the arachidonic acid (-10 %, P<0·001) and γ-linolenic acid (-24 %, P<0·001) levels. A 30 % increase in ex vivo LDL oxidation (P<0·001) was observed. In addition, fish oil resulted in a significant decrease in fasting and PP TG levels (P<0·001), PP non-esterified fatty acid (NEFA) levels, and in the percentage LDL as LDL-3 (P=0·040), and an increase in LDL-cholesterol (P=0·027). In multivariate analysis, changes in platelet phospholipid DHA emerged as being independently associated with the rise in LDL-cholesterol, accounting for 16 % of the variability in this outcome measure (P=0·030). In contrast, increases in platelet EPA were independently associated with the reductions in fasting (P=0·046) and PP TG (P=0·023), and PP NEFA (P=0·015), explaining 15–20 % and 25 % of the variability in response respectively. Increases in platelet EPA+DHA were independently and positively associated with the increase in LDL oxidation (P=0·011). EPA and DHA may have differential effects on plasma lipids in mildly hypertriacylglycerolaemic men.

4-Desmethylsterols and -stanols reduce plasma total cholesterol (TC) and LDL cholesterol by inhibition of intestinal cholesterol absorption, while the cholesterol-lowering potential of 4,4′-dimethylsterols is less well defined. The present study aimed to compare the effects of 4-desmethylsterols, -stanols, and 4,4′-dimethylsterols on plasma and hepatic cholesterol, sterol excretion and bile acid metabolism. Male golden Syrian hamsters were fed diets containing 13 g/100 g fat, 0·08 g/100 g cholesterol and 0 (control), 0·24 or 0·48 % (w/w) esterified 4-desmethylsterols (sterols) and esterified hydrogenated 4-desmethylsterols (stanols) from common vegetable oils or esterified 4,4′-dimethylsterols from rice bran oil for 5 weeks. Sterol and stanol esters at the dose of 0·24 % were equally effective and significantly (P<0·05) lowered TC by 15 %, while 0·24 % 4,4-dimethylsterols reduced TC by 10 %. Liver total and esterified cholesterol concentrations were significantly (P<0·05) lowered by 40, 22, 43 and 31 % in hamsters fed 0·48 % sterols, 0·24 % stanols, 0·48 % stanols or 0·48 % dimethylsterols, respectively. Daily faecal bile acid excretion and hepatic cholesterol 7α-hydroxylase activity were not altered, indicating that sterols, stanols and dimethylsterols had no effect on the intestinal re-absorption of bile acids or on hepatic bile acid synthesis. Daily excretion of cholesterol was significantly higher in hamsters fed esterified sterols and stanols, but was only slightly increased in those fed dimethylsterols. The results indicate that esterified sterols and stanols were equally effective in lowering plasma TC and LDL cholesterol, while dimethylsterol esters caused a weaker cholesterol-lowering effect. Sterols and stanols achieve their cholesterol-lowering effect by stimulating faecal cholesterol excretion through inhibiting intestinal cholesterol absorption, but do not affect bile acid excretion. Other mechanisms need to be considered to explain the effect on plasma and hepatic cholesterol of dimethylsterols.