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Journal articles on the topic 'Intestinal absorption'

Author: Grafiati

Published: 4 June 2021

Last updated: 30 July 2024

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1

Fuqua, Brie K., Christopher D. Vulpe, and Gregory J. Anderson. "Intestinal iron absorption." Journal of Trace Elements in Medicine and Biology 26, no. 2-3 (June 2012): 115–19. http://dx.doi.org/10.1016/j.jtemb.2012.03.015.

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2

Kockx, Maaike, and Leonard Kritharides. "Intestinal cholesterol absorption." Current Opinion in Lipidology 29, no. 6 (December 2018): 484–85. http://dx.doi.org/10.1097/mol.0000000000000558.

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3

Iqbal, Jahangir, and M. Mahmood Hussain. "Intestinal lipid absorption." American Journal of Physiology-Endocrinology and Metabolism 296, no. 6 (June 2009): E1183—E1194. http://dx.doi.org/10.1152/ajpendo.90899.2008.

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Our knowledge of the uptake and transport of dietary fat and fat-soluble vitamins has advanced considerably. Researchers have identified several new mechanisms by which lipids are taken up by enterocytes and packaged as chylomicrons for export into the lymphatic system or clarified the actions of mechanisms previously known to participate in these processes. Fatty acids are taken up by enterocytes involving protein-mediated as well as protein-independent processes. Net cholesterol uptake depends on the competing activities of NPC1L1, ABCG5, and ABCG8 present in the apical membrane. We have considerably more detailed information about the uptake of products of lipid hydrolysis, the active transport systems by which they reach the endoplasmic reticulum, the mechanisms by which they are resynthesized into neutral lipids and utilized within the endoplasmic reticulum to form lipoproteins, and the mechanisms by which lipoproteins are secreted from the basolateral side of the enterocyte. apoB and MTP are known to be central to the efficient assembly and secretion of lipoproteins. In recent studies, investigators found that cholesterol, phospholipids, and vitamin E can also be secreted from enterocytes as components of high-density apoB-free/apoAI-containing lipoproteins. Several of these advances will probably be investigated further for their potential as targets for the development of drugs that can suppress cholesterol absorption, thereby reducing the risk of hypercholesterolemia and cardiovascular disease.

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4

Dawson, Paul A., and Lawrence L. Rudel. "Intestinal cholesterol absorption." Current Opinion in Lipidology 10, no. 4 (August 1999): 315–20. http://dx.doi.org/10.1097/00041433-199908000-00005.

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5

Granger, D. N., R. J. Korthuis, P. R. Kvietys, and P. Tso. "Intestinal microvascular exchange during lipid absorption." American Journal of Physiology-Gastrointestinal and Liver Physiology 255, no. 5 (November 1, 1988): G690—G695. http://dx.doi.org/10.1152/ajpgi.1988.255.5.g690.

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The forces and membrane coefficients governing transcapillary and lymphatic fluid fluxes were measured in the cat jejunum before and during perfusion of the gut lumen with oleic acid (5 mM) solubilized with taurocholic acid (10 mM). Net transmucosal fluid flux, lymph flow, capillary pressure (Pc), blood flow, capillary filtration coefficient (Kf,c), and lymph and plasma oncotic pressures were measured under absorptive and nonabsorptive conditions. Interstitial fluid pressure was calculated for the two conditions from measured parameters. Stimulation of lipid absorption resulted in a fivefold increase in lymph flow, a threefold increase in Kf,c, a doubling of blood flow, a 2.5 mmHg increase in Pc, and a 1.0 mmHg reduction in interstitial (lymph) oncotic pressure. Lipid absorption was associated with a 3.6 mmHg increase in interstitial fluid pressure. During lipid absorption, approximately 35% of the absorbed fluid is removed from the mucosal interstitium by lymphatics while capillaries remove the remaining 65%. The results of this study indicate that the effects of lipid absorption on microvascular and lymphatic fluid dynamics are quantitatively different than those produced by glucose absorption. These differences can be largely explained by lipid absorption-induced increases in blood flow and microvascular permeability.

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6

Ji, Yong, Xiaoming Li, and Patrick Tso. "Intestinal Fatty acid Absorption." Immunology‚ Endocrine & Metabolic Agents in Medicinal Chemistry 9, no. 1 (March 1, 2009): 60–73. http://dx.doi.org/10.2174/187152209788009832.

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7

Nakamura, Tsutomu, Motohiro Yamamori, and Toshiyuki Sakaeda. "Pharmacogenetics of Intestinal Absorption." Current Drug Delivery 5, no. 3 (July 1, 2008): 153–69. http://dx.doi.org/10.2174/156720108784911749.

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8

Said, Hamid M., and Chandira Kumar. "Intestinal absorption of vitamins." Current Opinion in Gastroenterology 15, no. 2 (March 1999): 172. http://dx.doi.org/10.1097/00001574-199903000-00015.

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9

Lewis, Stephen J., Robert E. Oakey, and Kenneth W. Heaton. "Intestinal absorption of oestrogen." European Journal of Gastroenterology & Hepatology 10, no. 1 (January 1998): 33–40. http://dx.doi.org/10.1097/00042737-199801000-00007.

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10

Ferraris, Ronaldo P., Jun-yong Choe, and Chirag R. Patel. "Intestinal Absorption of Fructose." Annual Review of Nutrition 38, no. 1 (August 21, 2018): 41–67. http://dx.doi.org/10.1146/annurev-nutr-082117-051707.

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Increased understanding of fructose metabolism, which begins with uptake via the intestine, is important because fructose now constitutes a physiologically significant portion of human diets and is associated with increased incidence of certain cancers and metabolic diseases. New insights in our knowledge of intestinal fructose absorption mediated by the facilitative glucose transporter GLUT5 in the apical membrane and by GLUT2 in the basolateral membrane are reviewed. We begin with studies related to structure as well as ligand binding, then revisit the controversial proposition that apical GLUT2 is the main mediator of intestinal fructose absorption. The review then describes how dietary fructose may be sensed by intestinal cells to affect the expression and activity of transporters and fructolytic enzymes, to interact with the transport of certain minerals and electrolytes, and to regulate portal and peripheral fructosemia and glycemia. Finally, it discusses the potential contributions of dietary fructose to gastrointestinal diseases and to the gut microbiome.

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11

Dahlqvist, Arne. "INTESTINAL ABSORPTION OF SUCROSE." Acta Medica Scandinavica 192, S542 (April 24, 2009): 13–18. http://dx.doi.org/10.1111/j.0954-6820.1972.tb05314.x.

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12

Lester, Roger. "INTESTINAL ABSORPTION OF BILIRUBIN*." Annals of the New York Academy of Sciences 111, no. 1 (December 15, 2006): 290–94. http://dx.doi.org/10.1111/j.1749-6632.1963.tb36970.x.

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13

Kotake-Nara, Eiichi. "Intestinal Absorption of Carotenoid." Journal of Lipid Nutrition 21, no. 1 (2012): 35–43. http://dx.doi.org/10.4010/jln.21.35.

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14

Zhao, Yuan H., Michael H. Abraham, Joelle Le, Anne Hersey, Chris N. Luscombe, Gordon Beck, Brad Sherborne, and Ian Cooper. "Evaluation of rat intestinal absorption data and correlation with human intestinal absorption." European Journal of Medicinal Chemistry 38, no. 3 (March 2003): 233–43. http://dx.doi.org/10.1016/s0223-5234(03)00015-1.

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15

Sherwood, RA, JT Marsden, CA Stein, S. Somasundaram, C. Aitken, JS Oxford, IS Menzies, and I. Bjarnason. "Intra-Individual Variation in Serum AZT Concentration is Not Related to Intestinal Absorption or Small Intestinal Inflammatory Changes in Human Immunodeficiency Virus-Infected Subjects." Antiviral Chemistry and Chemotherapy 8, no. 4 (August 1997): 327–32. http://dx.doi.org/10.1177/095632029700800405.

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3′-Azido-3′-deoxythymidine (AZT; zidovudine) either alone or in combination with didanosine or another nucleoside analogue is the first-line treatment for patients with human immunodeficiency virus (HIV) infection, many of whom have concurrent gastrointestinal (GI) disease. This study assessed whether the absorption of AZT was affected by GI disease. The absorption and pharmacokinetics of AZT in 23 HIV-infected individuals was measured after a single dose of AZT and was related in 12 patients to small intestinal function. Levels of AZT and its metabolite 5′-glucopyranuronosylthymidine (G-AZT) were measured by radioimmunoassay. Intestinal permeability was assessed by differential urinary excretion of orally administered lactulose/1-rhamnose; absorptive capacity was measured simultaneously by the urinary excretion of 3-o-methyl-D-glucose, d-xylose and 1-rhamnose. Small intestinal inflammation was assessed by faecal excretion of indium-labelled neutrophils. Peak levels of AZT in serum varied between 170 and 1820 ng mL−1. The metabolite G-AZT was present in serum at peak concentrations varying from 1020 to 9930 ng mL−1. There was up to a sevenfold variation in the area under the curve (AUC). The time to maximum serum concentration for AZT was between 30 and 120 min, with an absorption half-life of between 2 and 38 min. The median elimination half-life was 57 min (range 46–72 min), close to the predicted half-life of 60 min. Intestinal permeability was increased in six of the 12 subjects studied and eight had evidence of reduced absorptive capacity. Ten of the 12 patients had evidence of small intestinal inflammation. We concluded that neither changes in permeability nor absorptive capacity influenced the absorption of AZT. There was no relationship between the presence of intestinal inflammation and AZT absorption. This study showed a significant intra-individual variation of serum AZT levels which cannot be explained on the basis of altered intestinal absorptive capacity or intestinal inflammatory changes.

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16

Inoue, Makoto, Yuichi Tanaka, Sakiko Matsushita, Yuri Shimozaki, Hirohito Ayame, and Hidenori Akutsu. "Xenogeneic-Free Human Intestinal Organoids for Assessing Intestinal Nutrient Absorption." Nutrients 14, no. 3 (January 19, 2022): 438. http://dx.doi.org/10.3390/nu14030438.

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Since many nutrients, including the three major ones of glucose, dipeptides, and cholesterol, are mainly absorbed in the small intestine, the assessment of their effects on intestinal tissue is important for the study of food absorption. However, cultured intestinal cell lines, such as Caco-2 cells, or animal models, which differ from normal human physiological conditions, are generally used for the evaluation of intestinal absorption and digestion. Therefore, it is necessary to develop an alternative in vitro method for more accurate analyses. In this study, we demonstrate inhibitory effects on nutrient absorption through nutrient transporters using three-dimensional xenogeneic-free human intestinal organoids (XF-HIOs), with characteristics of the human intestine, as we previously reported. We first show that the organoids absorbed glucose, dipeptide, and cholesterol in a transporter-dependent manner. Next, we examine the inhibitory effect of natural ingredients on the absorption of glucose and cholesterol. We reveal that glucose absorption was suppressed by epicatechin gallate or nobiletin, normally found in green tea catechin or citrus fruits, respectively. In comparison, cholesterol absorption was not inhibited by luteolin and quercetin, contained in some vegetables. Our findings highlight the usefulness of screening for the absorption of functional food substances using XF-HIOs.

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17

Watanabe, Kazuhiro, Tetsuya Sawano, Toshiya Jinriki, and Juichi Sato. "Studies on Intestinal Absorption of Sulpiride (3): Intestinal Absorption of Sulpiride in Rats." Biological & Pharmaceutical Bulletin 27, no. 1 (2004): 77–81. http://dx.doi.org/10.1248/bpb.27.77.

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18

Thompson, J. "Intestinal flora and nutrient absorption after intestinal resection." Journal of Gastrointestinal Surgery 1, no. 6 (December 1997): 554–60. http://dx.doi.org/10.1016/s1091-255x(97)80072-8.

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19

Benvenga, Salvatore, and Flavia Di Bari. "Intestinal absorption and buccal absorption of liquid levothyroxine." Endocrine 58, no. 3 (March 7, 2017): 591–94. http://dx.doi.org/10.1007/s12020-017-1250-4.

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20

Cottrell, J. J., B. Stoll, R. K. Buddington, J. E. Stephens, L. Cui, X. Chang, and D. G. Burrin. "Glucagon-like peptide-2 protects against TPN-induced intestinal hexose malabsorption in enterally refed piglets." American Journal of Physiology-Gastrointestinal and Liver Physiology 290, no. 2 (February 2006): G293—G300. http://dx.doi.org/10.1152/ajpgi.00275.2005.

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Premature infants receiving chronic total parenteral nutrition (TPN) due to feeding intolerance develop intestinal atrophy and reduced nutrient absorption. Although providing the intestinal trophic hormone glucagon-like peptide-2 (GLP-2) during chronic TPN improves intestinal growth and morphology, it is uncertain whether GLP-2 enhances absorptive function. We placed catheters in the carotid artery, jugular and portal veins, duodenum, and a portal vein flow probe in piglets before providing either enteral formula (ENT), TPN or a coinfusion of TPN plus GLP-2 for 6 days. On postoperative day 7, all piglets were fed enterally and digestive functions were evaluated in vivo using dual infusion of enteral (13C) and intravenous (2H) glucose, in vitro by measuring mucosal lactase activity and rates of apical glucose transport, and by assessing the abundances of sodium glucose transporter-1 (SGLT-1) and glucose transporter-2 (GLUT2). Both ENT and GLP-2 pigs had larger intestine weights, longer villi, and higher lactose digestive capacity and in vivo net glucose and galactose absorption compared with TPN alone. These endpoints were similar in ENT and GLP-2 pigs except for a lower intestinal weight and net glucose absorption in GLP-2 compared with ENT pigs. The enhanced hexose absorption in GLP-2 compared with TPN pigs corresponded with higher lactose digestive and apical glucose transport capacities, increased abundance of SGLT-1, but not GLUT-2, and lower intestinal metabolism of [13C]glucose to [13C]lactate. Our findings indicate that GLP-2 treatment during chronic TPN maintains intestinal structure and lactose digestive and hexose absorptive capacities, reduces intestinal hexose metabolism, and may facilitate the transition to enteral feeding in TPN-fed infants.

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21

Jiang, Cui-Ping, Xin He, Xiao-Lin Yang, Su-Li Zhang, Hui Li, Zi-Jing Song, Chun-Feng Zhang, Zhong-Lin Yang, and Ping Li. "Intestinal Absorptive Transport of Genkwanin from Flos genkwa Using a Single-Pass Intestinal Perfusion Rat Model." American Journal of Chinese Medicine 42, no. 02 (January 2014): 349–59. http://dx.doi.org/10.1142/s0192415x14500232.

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To investigate the absorptive transport behavior of genkwanin and the beneficial effects of monoterpene enhancers with different functional groups, the single-pass intestinal perfusion (SPIP) of rats was used. The results showed that genkwanin was segmentally-dependent and the best absorptive site was the duodenum. The effective permeability coefficient (P eff ) was 1.97 × 10-4 cm/s and the absorption rate constant (Ka) was 0.62 × 10-2 s-1. Transepithelial transportation descended with increasing concentrations of genkwanin. This was a 1.4-fold increase in P eff by probenecid, whereas a 1.4-fold or 1.6-fold decrease was observed by verapamil and pantoprazole, respectively. Furthermore, among the absorption enhancers, the enhancement with carbonyl (camphor and menthone) was higher than that with hydroxyl (borneol and menthol). The concentration-independent permeability and enhancement by coperfusion of probenecid indicated that genkwanin was transported by both passive diffusion and multidrug resistance protein (MDR)-mediated efflux mechanisms.

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22

Holt, P. R., and J. A. Balint. "Effects of aging on intestinal lipid absorption." American Journal of Physiology-Gastrointestinal and Liver Physiology 264, no. 1 (January 1, 1993): G1—G6. http://dx.doi.org/10.1152/ajpgi.1993.264.1.g1.

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Because of the "graying" of the population there is increasing interest in age-related changes in organ physiology. Impairment of lipid absorption, if present, could lead to malnutrition in the elderly while increased uptake of cholesterol could contribute to the rise in serum cholesterol levels seen in older individuals. This review critically analyzes the available information on age-related changes in digestive and absorptive physiology of lipids. Overall, the data suggest that lipid digestion and absorption are, in general, well-preserved in aging. However, intercurrent illness or experimental stress may produce impairment in aging animals and humans that are not seen in younger controls. Areas deserving more detailed study are identified in this review and include intestinal motility, adaptation to stress, and assembly and transport of lipoproteins from enterocytes to lymph.

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23

Burdick, Scott, Ningren Cui, Lonnie R. Empey, and Richard N. Fedorak. "Vitamin E Prevents Cold Wrap Restraint Stress-Induced Intestinal Fluid Transport Alterations in Rats." Canadian Journal of Gastroenterology 8, no. 7 (1994): 417–21. http://dx.doi.org/10.1155/1994/712352.

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Psychological stress may alter gastrointestinal absorptive function by increasing the quantity of intestinal free radicals or by lowering endogenous intestinal free radical scavenging capacity. Vitamin E has been shown to be a potent endogenous antioxidant and free radical scavenger under both physiological and pathological conditions. The purpose of this study was to determine whether cold wrap restraint stress altered in vivo intestinal fluid absorption in rats, and whether vitamin E administration prior to the induction of cold wrap restraint stress could prevent such changes in intestinal secretion. Jejunal, ileal and colonic fluid and electrolyte transport rates were measured in vivo using an isolated loop technique. Cold wrap restraint stress reduced in vivo fluid absorption in the ileum and colon, but not in the jejunum. Administration of vitamin E prior to the cold wrap restraint stress procedure completely prevented this alteration of ileal and colonic fluid absorption.

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24

DONG, Yu. "Drug Transporters of Intestinal Absorption." Chinese Journal of Natural Medicines 6, no. 3 (September 26, 2008): 161–67. http://dx.doi.org/10.3724/sp.j.1009.2008.00161.

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25

YAMAGUCHI, Toshikazu, Makiko YOKOGAWA, Yutaka SEKINE, and Masahisa HASHIMOTO. "Intestinal Absorption Characteristics of Sparfloxacin." Drug Metabolism and Pharmacokinetics 6, no. 1 (1991): 53–59. http://dx.doi.org/10.2133/dmpk.6.53.

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26

Phan, Cam, T. "Intestinal lipid absorption and transport." Frontiers in Bioscience 6, no. 1 (2001): d299. http://dx.doi.org/10.2741/phan.

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27

IKEDA, Ikuo, and Masaki KATO. "Mechanisms of Intestinal Cholesterol Absorption." Oleoscience 12, no. 3 (2012): 107–14. http://dx.doi.org/10.5650/oleoscience.12.107.

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28

WASSEF, RAMSES, ZANE COHEN, SVANTE NORDGREN, and BERNARD LANGER. "CYCLOSPORINE ABSORPTION IN INTESTINAL TRANSPLANTATION." Transplantation 39, no. 5 (May 1985): 496–98. http://dx.doi.org/10.1097/00007890-198505000-00007.

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29

Visentin, Michele, Ndeye Diop-Bove, Rongbao Zhao, and I. David Goldman. "The Intestinal Absorption of Folates." Annual Review of Physiology 76, no. 1 (February 10, 2014): 251–74. http://dx.doi.org/10.1146/annurev-physiol-020911-153251.

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30

Sjaastad, Ottar. "INTESTINAL ABSORPTION IN MYOTONIC DYSTROPHY." Acta Neurologica Scandinavica 51, no. 1 (January 29, 2009): 59–73. http://dx.doi.org/10.1111/j.1600-0404.1975.tb01359.x.

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31

Mansbach, Charles M. "Small intestinal absorption and secretion." Current Opinion in Gastroenterology 8, no. 2 (April 1992): 213–19. http://dx.doi.org/10.1097/00001574-199204000-00003.

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32

Mansbach, Charles M., and Ajay Kumar. "Small intestinal absorption and secretion." Current Opinion in Gastroenterology 9, no. 2 (March 1993): 201–6. http://dx.doi.org/10.1097/00001574-199303000-00003.

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33

Fordtran, J. S. "Measurement of intestinal water absorption." American Journal of Physiology-Gastrointestinal and Liver Physiology 262, no. 2 (February 1, 1992): G377—G378. http://dx.doi.org/10.1152/ajpgi.1992.262.2.g377.

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34

LAHER, J. M., and J. A. BARROWMAN. "Intestinal Absorption of Carcinogenic Hydrocarbons." Annals of the New York Academy of Sciences 534, no. 1 Living in a C (June 1988): 565–74. http://dx.doi.org/10.1111/j.1749-6632.1988.tb30147.x.

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35

Roth, P., A. Guissani, and E. Werner. "Kinetics of Gastro-Intestinal Absorption." Radiation Protection Dosimetry 79, no. 1 (October 1, 1998): 279–82. http://dx.doi.org/10.1093/oxfordjournals.rpd.a032409.

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36

THOMSON, A. B. R. "Intestinal Aspects of Lipid Absorption." Nutrition Today 24, no. 4 (July 1989): 16–20. http://dx.doi.org/10.1097/00017285-198907000-00004.

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37

Dohil, Ranjan, Meredith Fidler, Bruce A. Barshop, Jon Gangoiti, Reena Deutsch, Michael Martin, and Jerry A. Schneider. "Understanding intestinal cysteamine bitartrate absorption." Journal of Pediatrics 148, no. 6 (June 2006): 764–69. http://dx.doi.org/10.1016/j.jpeds.2006.01.050.

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38

BENVENGA, SALVATORE, LUIGI BARTOLONE, STEFANO SQUADRITO, FRANCESCO LO GIUDICE, and FRANCESCO TRIMARCHI. "Delayed Intestinal Absorption of Levothyroxine." Thyroid 5, no. 4 (August 1995): 249–53. http://dx.doi.org/10.1089/thy.1995.5.249.

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39

Inui, Ken-ichi, and Tomohiro Terada. "Intestinal absorption and drug transporters." Japanese Journal of Pharmacology 82 (2000): 8. http://dx.doi.org/10.1016/s0021-5198(19)47509-4.

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40

Wang, David Q. H. "Regulation of Intestinal Cholesterol Absorption." Annual Review of Physiology 69, no. 1 (March 2007): 221–48. http://dx.doi.org/10.1146/annurev.physiol.69.031905.160725.

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41

Phan, Cam T. "Intestinal lipid absorption and transport." Frontiers in Bioscience 6, no. 3 (2001): d299–319. http://dx.doi.org/10.2741/a612.

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42

Kellett, George L. "Stress and intestinal sugar absorption." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 292, no. 2 (February 2007): R860—R861. http://dx.doi.org/10.1152/ajpregu.00741.2006.

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43

Fullmer, Curtis S. "Intestinal Calcium Absorption: Calcium Entry." Journal of Nutrition 122, suppl_3 (March 1, 1992): 644–50. http://dx.doi.org/10.1093/jn/122.suppl_3.644.

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44

Ong, David E. "Retinoid Metabolism During Intestinal Absorption." Journal of Nutrition 123, suppl_2 (February 1, 1993): 351–55. http://dx.doi.org/10.1093/jn/123.suppl_2.351.

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45

Chesner, I. M., N. A. Small, and P. W. Dykes. "Intestinal absorption at high altitude." Postgraduate Medical Journal 63, no. 737 (March 1, 1987): 173–75. http://dx.doi.org/10.1136/pgmj.63.737.173.

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46

Madsen, Karen. "Intestinal Absorption of Bile Salts." Canadian Journal of Gastroenterology 4, no. 2 (1990): 79–84. http://dx.doi.org/10.1155/1990/624985.

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Bile acids are secreted from the liver into the duodenum where they aid in the digestion and absorption of dietary lipids. Absorption of bile acids occurs through both ionic and nonionic diffusion in the jejunum and colon and through an active sodium ion-dependent carrier mechanism in the ileum. The prima, y bile acids synthesized in the liver can be converted by intestinal bacteria into secondary and tertiary bile acids. Bile acids may also be conjugated with glycine or taurine which results in an increase in the hydrophilicity and solubility of these compounds at physiological pH. The amount of passive diffusion of bile acids that occurs across the brush border membrane along the length of the entire intestine depends upon the ratio of ionized to nonionized bile acids coupled with the bile salt concentration and the individual permeability coefficients of monomers. Active transport of both conjugated and nonconjugated species of bile acids depends upon the presence of a single negative charge on the side chain. Maximal transport rates for bile acids are related to the number of hydroxyl groups present while the Michaelis-Menten constant for transport is dependent upon whether or not the bile acid is conjugated. Although active uptake of bile acids from the ileum has been considered the major route for bile salt absorption in the small intestine, the mechanism may actually be responsible for only a small proportion of the total bile acid pool absorbed from the lumen.

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47

Touitou, Elka. "Enhancement of intestinal peptide absorption." Journal of Controlled Release 21, no. 1-3 (July 1992): 139–44. http://dx.doi.org/10.1016/0168-3659(92)90015-j.

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48

Bronner, Felix. "Mechanisms of intestinal calcium absorption." Journal of Cellular Biochemistry 88, no. 2 (November 27, 2002): 387–93. http://dx.doi.org/10.1002/jcb.10330.

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49

Yonekura, Lina, and Akihiko Nagao. "Intestinal absorption of dietary carotenoids." Molecular Nutrition & Food Research 51, no. 1 (January 2007): 107–15. http://dx.doi.org/10.1002/mnfr.200600145.

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50

Hui, David Y., Eric D. Labonté, and Philip N. Howles. "Development and Physiological Regulation of Intestinal Lipid Absorption. III. Intestinal transporters and cholesterol absorption." American Journal of Physiology-Gastrointestinal and Liver Physiology 294, no. 4 (April 2008): G839—G843. http://dx.doi.org/10.1152/ajpgi.00061.2008.

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Intestinal cholesterol absorption is modulated by transport proteins in enterocytes. Cholesterol uptake from intestinal lumen requires several proteins on apical brush-border membranes, including Niemann-Pick C1-like 1 (NPC1L1), scavenger receptor B-I, and CD36, whereas two ATP-binding cassette half transporters, ABCG5 and ABCG8, on apical membranes work together for cholesterol efflux back to the intestinal lumen to limit cholesterol absorption. NPC1L1 is essential for cholesterol absorption, but its function as a cell surface transporter or an intracellular cholesterol transport protein needs clarification. Another ATP transporter, ABCA1, is present in the basolateral membrane to mediate HDL secretion from enterocytes.

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