Thesis (Ph.D.)--University of Wisconsin--Madison, 2006 / Includes bibliographical references (p. 186-199). Also available on the Internet.

This document only includes an excerpt of the corresponding thesis or dissertation. To request a digital scan of the full text, please contact the Ruth Lilly Medical Library's Interlibrary Loan Department (rlmlill@iu.edu).

Brush border and basolateral membrane vesicles were isolated by subjecting homogenized mucosal cells from bovine small intestine to a divalent cation aggregation followed by a series of differential and density gradient centrifugations. Membrane marker enzyme assays were used to monitor the effectiveness of the fractionation procedure. Enrichments were determined by comparing the enzyme specific activities of the membrane fractions to the homogenate. Sodium-potassium adenosine triphosphatase and alkaline phosphatase served as the enzyme markers for the basolateral and brush border membranes, respectively. Basolateral membrane vesicles enriched 11.1 fold were isolated from the interface of the 31 and 34% sucrose bands of a discontinuous sucrose gradient. Brush border membranes enriched 10.1 fold were isolated from the surface of the 28% sucrose band of a discontinuous sucrose gradient. The use of frozen rather than fresh mucosal tissue in the isolation procedures was found to enhance the purification of basolateral and brush border membrane fractions. The transport capabilities of vesicles were demonstrated by incubating vesicles with radiolabeled substrate, then separating the vesicles and transported substrate from the incubation buffer by filtration. Substrate uptakes were quantified by liquid scintillation counting. Basolateral membrane vesicles were observed to accumulate substrate into an osmotically active space and to have Na⁺-dependent alanine transport capabilities. The use of basolateral and brush border membrane vesicles as tools to investigate nutrient uptake allows the investigator to manipulate both the extravesicular and intravesicular environments, thus making possible the evaluation of the complex interactions which are involved in nutrient transport mechanisms. / M.S.

A series of experiments was conducted to evaluate the effects of amylase supplementation upon the endogenous amylase levels and growth performance of male turkey poults. [In the first experiment, a multi-enzyme supplement containing amylase and an additional protease supplement were added to diets of low (24%) and high (28%) protein content. Enzyme supplements Significantly improved performance of birds on the low, but not on the high protein diet. Even with the improvement from enzyme addition, the performance of poults fed the low protein diet was not equal to poults fed the high protein diet. The second experiment was designed to evaluate the effect of varying levels of amylase and xylanase on bird performance, and to determine optimal level of enzyme inclusion in the basal corn-soybean meal diet. Feed utilization or growth of birds did not differ between the amylase diets, however 200 units of amylase per kilogram of feed produced numerically optimal growth and feed efficiency values. Xylanase inclusion greater than 160 units per kilogram of feed appeared to be detrimental to bird growth and feed efficiency. In the third experiment, endogenous amylase levels were measured to determine if supplemental amylase produced a quantitative, qualitative, or inhibitory effect upon the endogenous amylase activity. Amylase supplementation was found to be additive to the endogenous levels and did not inhibit endogenous activity. Amylase supplemented diets decreased body weight and feed efficiency loss due to weighing and handling stress on the birds when compared to the control and xylanase diets. Villi lengths within the jejunal and ileal sections of the small intestine were longer during the first three weeks for amylase supplemented birds when compared to intestinal villi of either the control or xylanase fed poults. The fourth experiment was conducted to compare the effect on growth and feed utilization of the serial addition of various enzyme preparations to corn-soybean poult diets. In retrospect, due to the serial application of the supplements, assessment of the benefits of a given supplement within a composite application was futile. Amylase, however, was present within the composite supplements fed to poults with the highest growth performance values. These experiments suggest that the addition of amylase to conventional corn-soybean meal turkey poult starter diets can be effective in improving growth and feed utilization during the first few weeks. The addition of amylase supplements to basal diets did not inhibit the poult endogenous amylase activity levels and were associated with increased intestinal villus length corresponding to increased utilization and absorption of nutrients. Xylanase appeared to be a detrimental enzyme additive to corn-soybean meal diets fed to male poults. / Ph. D.

Transport properties of bovine intestinal brush border membranes were investigated. Isolation of brush border membrane vesicles involved magnesium precipitation followed by a sucrose density gradient. Characterization by alkaline phosphatase activity (the brush border marker enzyme) showed 7 fold enrichment over homogenate at the interface between 38 and 42% sucrose. This fraction was employed to study transport of sugars and amino acids. Transport of D-glucose into an osmotically active space, was sodium stimulated, and inhibited by phloridzin, D-galactose, and D-xylose. Transport of L-alanine was sodium stimulated and mediated by at least two systems. Apparent affinities for L-alanine transport were .039, and .943 mM. Maximum velocities were 29.2, and 53.4 pmoles/mg protein/sec, for the two systems. Transport of L-proline, L-lysine, L-methionine, and L-phenylalanine were sodium stimulated. Data indicated sodium independent transport accounted for more influx of L-lysine, L-methionine, and L-phenylalanine than sodium dependent transport. Sodium dependent and sodium independent fluxes were equal for uptake of L-proline. Amino acid inhibition data indicated a common transporter for methionine, alanine, and phenylalanine. There was an additional methionine transport system not shared by alanine or phenylalanine. None of the amino acids effectively inhibited methionine uptake. Data indicated praline was transported by system(s) not shared by the other amino acids. Bovine brush border membranes transported the amino acid analog alpha-methyl-aminoisobutyric acid by sodium stimulated processes. / Ph. D.

Crohn's disease is a chronic inflammatory bowel disease which may affect any part of the gastrointestinal tract with a preference for the terminal ileum and ileocaecal region. The disease was first described in 1932 and has increased during the last decades. The clinical manifestations could be referred to as inflammation, malabsorption and obstruction. The annual incidence of Crohn's disease in the county of Västerbotten, North Sweden, was found to be 4.9/105 inhabitants. In a study of 87 patients in a medical gastrointestinal unit, 23% of non-operated patients and 66% of resected patients had increased fecal fat excretion. D-xylose test and lactose tolerance test were abnormal 1n 19% and 24% respectively of the non-operated patients. No clear relation could be found between the outcome of these malabsorption tests and localization, extension or activity of the disease. This suggests the cause of malabsorption 1n Crohn's disease to be complex and multi- factorial . The morphology of jejunal biopsies from 18 patients with Crohn's disease elsewhere 1n the gastrointestinal tract demonstrated an abnormal picture 1n 13 patients when assessed by light microscopy and scanning electron microscopy. A high proportion of these patients had abnormal Intestinal absorptive tests. Skeletal muscle biopsies were performed 1n 13 patients showing a depletion of muscle potassium content and more Infrequently low skeletal muscle magnesium content. This depletion 1s not reflected by subnormal plasma concentration. In the Initial clinical assessment of a new gamma labelled synthetic bile ac1d-SeHCAT, 45 patients, 19 of whom had Crohn's disease, were studied. The outcome of the test correlated well with the excretion of fecal bile acids. It was possible to discriminate patients with terminal Ileal disease from other patient groups. In a follow-up study, the SeHCAT test was modified as to make it simpler and to shorten the test period. Nine patients with Crohn's disease were tested, showing a suffi cent accuracy of the outcome of the test within 48 hours, using simple equipment available in many hospitals. The elimination of radioactivity was calculated as WBR50*» the time for 50% of the administered dose to be excreted. This gives information as to the rate of excretion, reflecting the degree of terminal ileal malfunction. / <p>S. 1-41: sammanfattning, s. 43-115: 5 uppsatser</p> / digitalisering@umu

No description available.

The consequences of ingesting different carbohydrate solutions on fluid movement and availability have not been systematically examined. In addition, the role of carbohydrate in the post-exercise rehydration period has received little attention despite the need for substrate replenishment following exercise and the role of carbohydrates in stimulating water absorption in the intestine. The aims of this thesis were to assess fluid absorption characteristics and availability of solutions containing increasing concentrations of glucose and to evaluate their role in the restoration and maintenance of fluid balance following a period of exercise-induced dehydration. The ingestion of a single bolus of a commercially available hypertonic 18% carbohydrate solution (chapter 3) and a hypertonic 10% glucose solution (chapter 4) resulted in reductions in plasma volume that are most likely due to acute net secretion of water into the intestinal lumen. When investigating recovery of whole body hydration status after sweat loss, a hypertonic 10% glucose-electrolyte solution maintained whole body fluid balance for a longer period than a hypotonic 2% glucose-electrolyte solution and an electrolyte only solution when a fixed volume of fluid was consumed during a rehydration period of one hour following cycle exercise in the heat (chapter 5). When fluid was consumed ad libitum over a two hour period following similar cycle exercise in the heat, a hypertonic 10% glucose-electrolyte solution was as effective in restoring and maintaining fluid balance as a 2% hypotonic glucose-electrolyte solution and an electrolyte only solution (chapter 6). The reduced rate of gastric emptying that accompanies the ingestion of high carbohydrate solutions was likely to be the primary cause for the difference in urine production reported between thetrials during this study (chapter 7). In conclusion, ingestion of hypertonic carbohydrate solutions results in a reduction in extracellular fluid volume that is most likely due to secretion of water into the intestinal lumen and the carbohydrate content of an ingested solution is of importance in the post-exercise rehydration period.

Zhang Li. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2003. / Includes bibliographical references (leaves 148-159). / Abstracts in English and Chinese. / Acknowledgements --- p.I / Abstract --- p.II / Abstract (in Chinese) --- p.IV / Publications --- p.V / List of Abbreviations --- p.VI / List of Tables --- p.VII / List of Figures --- p.VIII / Table of Contents --- p.XIII / Chapter Chapter One. --- Introduction --- p.1 / Chapter 1.1 --- Flavonoids --- p.1 / Chapter 1.2 --- Tea --- p.4 / Chapter 1.2.1 --- Composition of green tea catechins (GTC) --- p.4 / Chapter 1.2.2 --- Pharmacological activity --- p.6 / Chapter 1.2.2.1 --- Anticarcinogenic activity --- p.6 / Chapter 1.2.2.2 --- Antioxidative activity --- p.7 / Chapter 1.2.2.3 --- Radical scavenge --- p.7 / Chapter 1.2.2.4 --- Cardiovascular activity --- p.8 / Chapter 1.2.3 --- Pharmacokinetics of GTC --- p.8 / Chapter 1.2.3.1 --- Absorption --- p.10 / Chapter 1.2.3.2 --- Distribution --- p.11 / Chapter 1.2.3.3 --- Elimination --- p.11 / Chapter 1.2.3.4 --- Metabolism --- p.12 / Chapter 1.2.3.4.1 --- Metabolism in the small intestine --- p.12 / Chapter 1.2.3.4.2 --- Metabolism in the liver --- p.13 / Chapter 1.2.3.5 --- Summary of the pharmacokinetics of GTC --- p.13 / Chapter 1.3 --- Hawthorn --- p.14 / Chapter 1.3.1 --- Composition of hawthorn --- p.14 / Chapter 1.3.2 --- Pharmacological activity --- p.16 / Chapter 1.3.2.1 --- Inotonic activity --- p.16 / Chapter 1.3.2.2 --- Antiarrhythmic activity --- p.17 / Chapter 1.3.2.3 --- Hypolipidemic activity --- p.17 / Chapter 1.3.2.4 --- Antihypertensive activity --- p.18 / Chapter 1.3.2.5 --- Antioxidative activity --- p.18 / Chapter 1.3.3 --- Pharmacokinetics of HF --- p.18 / Chapter 1.3.3.1 --- Absorption --- p.19 / Chapter 1.3.3.2 --- Distribution and elimination --- p.21 / Chapter 1.3.3.3 --- Summary of pharmacokinetic of HF --- p.22 / Chapter 1.4 --- Mechanisms of intestinal absorption --- p.22 / Chapter 1.4.1 --- Passive transcellular transport --- p.23 / Chapter 1.4.2 --- Paracellular transport --- p.23 / Chapter 1.4.3 --- Carrier-mediated transport --- p.23 / Chapter 1.5 --- ABC transporters --- p.24 / Chapter 1.5.1 --- Cellular location and tissue distribution --- p.25 / Chapter 1.5.2 --- Substrates and inhibitors of ABC transporters --- p.26 / Chapter 1.6 --- Oral absorption models --- p.31 / Chapter 1.6.1 --- Ussing chamber --- p.31 / Chapter 1.6.2 --- In situ intestinal perfusion model --- p.33 / Chapter 1.6.3 --- Cell culture model --- p.34 / Chapter 1.7 --- Aims of the study --- p.36 / Chapter Chapter Two. --- Transport mechanism of green tea catechins --- p.37 / Chapter 2.1 --- Introduction --- p.37 / Chapter 2.2 --- Materials --- p.38 / Chapter 2.2.1 --- Chemicals --- p.38 / Chapter 2.2.2 --- Materials for cell culture --- p.38 / Chapter 2.2.3 --- Instruments --- p.39 / Chapter 2.3 --- Methods --- p.39 / Chapter 2.3.1 --- Analytical methods --- p.39 / Chapter 2.3.1.1 --- Analytical methods for validation of Caco-2 model --- p.39 / Chapter 2.3.1.1.1 --- Fluorescence analysis of lucifer yellow --- p.39 / Chapter 2.3.1.1.2 --- HPLC analysis of propranolol --- p.39 / Chapter 2.3.1.1.3 --- HPLC analysis of verapamil --- p.40 / Chapter 2.3.1.1.4 --- HPLC analysis of quinidine --- p.40 / Chapter 2.3.1.2 --- Analytical methods for samples contained GTC --- p.41 / Chapter 2.3.1.2.1 --- HPLC analysis for each GTC --- p.41 / Chapter 2.3.1.2.2 --- Preparation of calibration curves for each GTC --- p.42 / Chapter 2.3.1.2.3 --- HPLC/MS analysis of samples containing mixtures of four GTC --- p.42 / Chapter 2.3.1.2.4 --- Preparation of calibration curves for samples containing GTC mixture --- p.43 / Chapter 2.3.1.2.5 --- Validation of the HPLC methods --- p.43 / Chapter 2.3.1.3 --- Identification of metabolites with HPLC/MS --- p.44 / Chapter 2.3.2 --- Determination of stability profile of GTC in phosphate buffer --- p.44 / Chapter 2.3.3 --- Cell culture --- p.45 / Chapter 2.3.4 --- Validation of Caco-2 cell monolayer model --- p.46 / Chapter 2.3.4.1 --- Integrity of Caco-2 cell monolayer at pH 6.0 --- p.46 / Chapter 2.3.4.2 --- Permeability of paracellular and transcellular markers at pH 6.0 --- p.46 / Chapter 2.3.4.3 --- Validation of the existence of P-glycoprotein (P-gp) transporterin Caco-2 monolayer model --- p.46 / Chapter 2.3.4.4 --- Cytotoxicity test --- p.47 / Chapter 2.3.5 --- Transport study of GTC using Caco-2 cell monolayer model --- p.48 / Chapter 2.3.5.1 --- Bi-directional transport experiment --- p.48 / Chapter 2.3.5.2 --- Preparation of different dosing formulations of GTC --- p.48 / Chapter 2.3.5.2.1 --- Preparation of individual pure GTC solutions --- p.48 / Chapter 2.3.5.2.2 --- Preparation of cocktail 1 solution --- p.49 / Chapter 2.3.5.2.3 --- Preparation of green tea extract solution --- p.49 / Chapter 2.3.5.2.4 --- Preparation of cocktail 2 solution --- p.50 / Chapter 2.3.5.3 --- Sample treatment --- p.50 / Chapter 2.3.5.3.1 --- Samples for direct analysis --- p.50 / Chapter 2.3.5.3.2 --- Samples for enzymatic hydrolysis treatment --- p.51 / Chapter 2.3.5.4 --- Further investigation of the transport mechanism of GTC --- p.51 / Chapter 2.3.5.4.1 --- Inhibition transport of EC and EGC --- p.51 / Chapter 2.3.5.4.2 --- Transport mechanism of metabolites of EC and EGC --- p.52 / Chapter 2.3.5.4.3 --- Metabolic competition between EGC and the other GTC --- p.52 / Chapter 2.3.6 --- Calculation --- p.53 / Chapter 2.3.7 --- Data analysis --- p.54 / Chapter 2.4 --- Results --- p.55 / Chapter 2.4.1 --- Validation of the HPLC methods --- p.55 / Chapter 2.4.2 --- Stability of the GTC --- p.55 / Chapter 2.4.3 --- Extract of green tea leaves --- p.55 / Chapter 2.4.4 --- Validation of Caco-2 model --- p.59 / Chapter 2.4.4.1 --- Integrity of Caco-2 cell monolayer --- p.59 / Chapter 2.4.4.2 --- Permeability of paracellular and transcellular markers at pH 6.0 --- p.59 / Chapter 2.4.4.3 --- Validation of P-glycoprotein --- p.60 / Chapter 2.4.4.4 --- Cytotoxicity test --- p.61 / Chapter 2.4.5 --- Transport study of GTC --- p.63 / Chapter 2.4.5.1 --- Bi-directional transport of individual pure GTC --- p.63 / Chapter 2.4.5.2 --- Bi-directional transport of GTC in different dosing formulations --- p.66 / Chapter 2.4.5.2.1 --- Absorption transport profile of GTC in different dosing formulations --- p.66 / Chapter 2.4.5.2.2 --- Secretion transport profile of GTC in different dosing formulations --- p.66 / Chapter 2.4.5.3 --- Identification of metabolites of each GTC formed during the transport in Caco-2 cell model --- p.71 / Chapter 2.4.6 --- Further investigation of the transport mechanism of GTC --- p.82 / Chapter 2.4.6.1 --- Inhibition transport of EC and EGC --- p.82 / Chapter 2.4.6.2 --- Transport mechanism of metabolites of EC and EGC --- p.82 / Chapter 2.4.6.3 --- Metabolic competition between EGC and the other GTC --- p.85 / Chapter 2.4.6.4 --- Contribution of GTC on the metabolism of EGC --- p.89 / Chapter 2.5 --- Discussion --- p.92 / Chapter 2.5.1 --- Stability of the four GTC --- p.92 / Chapter 2.5.2 --- Validation of Caco-2 cell model --- p.92 / Chapter 2.5.3 --- Bi-directional transport of GTC --- p.93 / Chapter 2.5.4 --- Structure related efflux --- p.97 / Chapter 2.5.5 --- Metabolism of GTC --- p.98 / Chapter 2.5.6 --- Relationship between metabolism and efflux transport of GTC --- p.99 / Chapter 2.5.7 --- Bi-directional transport of GTC in different dosing formulations …… --- p.100 / Chapter 2.5.7.1 --- Absorption transport profile of different dosing formulations --- p.100 / Chapter 2.5.7.2 --- Secretion transport profile of different dosing formulations --- p.101 / Chapter 2.6 --- Conclusion --- p.105 / Chapter Chapter Three. --- Transport mechanism of hawthorn flavonoids --- p.106 / Chapter 3.1 --- Introduction --- p.106 / Chapter 3.2 --- Materials --- p.107 / Chapter 3.2.1 --- Chemicals --- p.107 / Chapter 3.2.2 --- Materials for cell culture --- p.108 / Chapter 3.2.3 --- Instruments --- p.108 / Chapter 3.3 --- Methods --- p.109 / Chapter 3.3.1 --- Analytical methods for HF --- p.109 / Chapter 3.3.1.1 --- Analytical methods of individual pure compound of HF --- p.109 / Chapter 3.3.1.1.1 --- HPLC analysis of HP and IQ --- p.109 / Chapter 3.3.1.1.2 --- HPLC analysis of EC --- p.109 / Chapter 3.3.1.2 --- Preparation of calibration curves for individual pure HF --- p.109 / Chapter 3.3.1.3 --- HPLC/MS analysis of three HF in mixture --- p.110 / Chapter 3.3.1.4 --- Preparation of the calibration curves of three HF in mixture --- p.111 / Chapter 3.3.1.5 --- Validation of HPLC methods --- p.111 / Chapter 3.3.2 --- Analytical methods for identification of metabolites with HPLC/MS --- p.111 / Chapter 3.3.3 --- Cell culture --- p.112 / Chapter 3.3.4 --- Cytotoxicity test --- p.113 / Chapter 3.3.5 --- Transport studies of HF using Caco-2 monolayer model --- p.113 / Chapter 3.3.5.1 --- Bi-directional transport experiment --- p.113 / Chapter 3.3.5.2 --- Preparation of loading solutions in different dosing formulations of HF for Caco-2 cell model --- p.114 / Chapter 3.3.5.2.1 --- Preparation of individual pure HF solutions --- p.114 / Chapter 3.3.5.2.2 --- Preparation of cocktail 1 solution --- p.114 / Chapter 3.3.5.2.3 --- Preparation of hawthorn extract solution --- p.114 / Chapter 3.3.5.2.4 --- Preparation of cocktail 2 solution --- p.114 / Chapter 3.3.5.3 --- Sample treatment --- p.115 / Chapter 3.3.5.4 --- Further study of the transport mechanism of HF --- p.115 / Chapter 3.3.5.4.1 --- "Inhibition transport of EC, IQ, and HP" --- p.115 / Chapter 3.3.5.4.2 --- "Transport mechanisms of the metabolites of EC, HP, IQ" --- p.116 / Chapter 3.3.6 --- Calculation --- p.116 / Chapter 3.3.7 --- Data analysis --- p.117 / Chapter 3.4 --- Results --- p.118 / Chapter 3.4.1 --- Validation of the HPLC methods --- p.118 / Chapter 3.4.2 --- Cytotoxicity test --- p.118 / Chapter 3.4.3 --- Transport study of HF --- p.122 / Chapter 3.4.3.1 --- Bi-directional transport of individual pure HF --- p.122 / Chapter 3.4.3.2 --- Bi-directional transport of the HF in different formulations --- p.123 / Chapter 3.4.3.2.1 --- Absorption transport of different formulations of HF --- p.123 / Chapter 3.4.3.2.2 --- Secretion transport of different dosing forms --- p.123 / Chapter 3.4.3.3 --- Identification of metabolites of each HF formed during their transport in Caco-2 model --- p.126 / Chapter 3.4.4 --- Further study on the transport mechanism --- p.136 / Chapter 3.4.4.1 --- "Inhibition transport of EC, HP, IQ" --- p.136 / Chapter 3.4.4.2 --- Transport mechanism of metabolites of HF --- p.136 / Chapter 3.4.4.3 --- Transport profiles of HF metabolites upon the loading of different dosing formulations of HF --- p.138 / Chapter 3.5 --- Discussion --- p.140 / Chapter 3.5.1 --- Bi-directional transport of each HF --- p.140 / Chapter 3.5.2 --- Bi-directional transport of HF in different formulations --- p.141 / Chapter 3.6 --- Conclusion --- p.142 / Chapter Chapter Four. --- Limitations of the current study --- p.143 / Chapter Chapter Five. --- Overall conclusions --- p.146 / References --- p.148 / Appendices --- p.160

Les vitamines D et K sont des micronutriments liposolubles qui participent au bon fonctionnement de l’organisme. Elles jouent des rôles clés dans la prévention de trouble de l'hémostase et de la coagulation, des pathologies osseuses, métaboliques et cardiovasculaires. Cependant, même si ces vitamines sont apportées en quantités suffisantes par notre alimentation, leurs effets bénéfiques sont étroitement conditionnés par leur biodisponibilité. Or, mieux connaitre les mécanismes d’absorption permettrait d’appréhender leur biodisponibilité. Nous avons tout d’abord montré que l’absorption de la vitamine K implique des transporteurs du cholestérol, SR-B1 et CD36. Nous avons également montré que l’entérocyte est non seulement capable d’effluer les vitamines D et K néo-absorbées mais également d’excréter ces vitamines du compartiment sanguin vers la lumière intestinale. Ce phénomène bien connu pour le cholestérol (excrétion transintestinale du cholestérol) implique des transporteurs communs, dont ABCB1 et ABCG5/G8. Dans un second temps, dans le cadre de la relance de la consommation des légumineuses, nous avons mis en évidence que la présence de légumineuses dans un repas limite la biodisponibilité de ces vitamines. En effet, les fibres, phytates, saponines et tanins diminuent leur bioaccessibilité et/ou leur captage. La méthode de cuisson des légumineuses, en affectant leur composition nutritionnelle, peut moduler l’incorporation des vitamines D et K au sein des micelles mixtes et donc affecter leur biodisponibilité. Ces données soulignent ainsi le fait que les légumineuses doivent être cuites de manière appropriée et consommés dans des repas riches en micronutriments. / Vitamin D and K are fat-soluble micronutrients that participate to the proper functioning of the organism. They are essential to prevent bleeding, bone, metabolic and cardiovascular disorders. However, even if those vitamins are provided in sufficient quantities in our diet, their health effects are closely linked to their bioavailability. A better knowledge of their absorption mechanisms would help to optimize their bioavailability.Firstly, we showed that vitamin K absorption involves the cholesterol transporters SR-B1 and CD36. We also showed that enterocytes can not only efflux newly absorbed vitamins D and K but also excrete vitamin D and K from the blood compartment to the intestinal lumen. This phenomenon of transintestinal excretioninvolves the cholesterol membrane transporters ABCB1 and ABCG5/G8.Secondly, we showed that the presence of pulses within a meal limits vitamin D and K bioavailability. Indeed, fibers, phytates, saponins and tannins can decrease bioaccessibility and/or uptake of vitamin K. By modulating the nutritional profile of pulses, the cooking method can impact on fat-soluble vitamin transfer to mixed micelles, and in turn affect their bioavailability. These data suggest that pulses must be cooked in an appropriate manner and consumed in micronutrient-rich meals.Keywords: vitamin D, vitamin K, bioaccessibility, intestinal absorption, pulses.