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Dietary proteins improve endothelial function under fasting conditions but not in the postprandial state, with no effects on markers of low-grade inflammation
- Karianna F. M. Teunissen-Beekman, Janneke Dopheide, Johanna M. Geleijnse, Stephan J. L. Bakker, Elizabeth J. Brink, Peter W. de Leeuw, Casper G. Schalkwijk, Marleen A. van Baak
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- Journal:
- British Journal of Nutrition / Volume 114 / Issue 11 / 14 December 2015
- Published online by Cambridge University Press:
- 24 September 2015, pp. 1819-1828
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- 14 December 2015
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Endothelial dysfunction (ED) and low-grade inflammation (LGI) have a role in the development of CVD. The two studies reported here explored the effects of dietary proteins and carbohydrates on markers of ED and LGI in overweight/obese individuals with untreated elevated blood pressure. In the first study, fifty-two participants consumed a protein mix or maltodextrin (3×20 g/d) for 4 weeks. Fasting levels and 12 h postprandial responses of markers of ED (soluble intercellular adhesion molecule 1 (sICAM), soluble vascular cell adhesion molecule 1 (sVCAM), soluble endothelial selectin and von Willebrand factor) and markers of LGI (serum amyloid A, C-reactive protein and sICAM) were evaluated before and after intervention. Biomarkers were also combined into mean Z-scores of ED and LGI. The second study compared 4 h postprandial responses of ED and LGI markers in forty-eight participants after ingestion of 0·6 g/kg pea protein, milk protein and egg-white protein. In addition, postprandial responses after maltodextrin intake were compared with a protein mix and sucrose. The first study showed significantly lower fasting ED Z-scores and sICAM after 4 weeks on the high-protein diet (P≤0·02). The postprandial studies found no clear differences of ED and LGI between test meals. However, postprandial sVCAM decreased more after the protein mix compared with maltodextrin in both studies (P≤0·04). In conclusion, dietary protein is beneficial for fasting ED, but not for fasting LGI, after 4 weeks of supplementation. On the basis of Z-scores, postprandial ED and LGI were not differentially affected by protein sources or carbohydrates.
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- By Mitchell Aboulafia, Frederick Adams, Marilyn McCord Adams, Robert M. Adams, Laird Addis, James W. Allard, David Allison, William P. Alston, Karl Ameriks, C. Anthony Anderson, David Leech Anderson, Lanier Anderson, Roger Ariew, David Armstrong, Denis G. Arnold, E. J. Ashworth, Margaret Atherton, Robin Attfield, Bruce Aune, Edward Wilson Averill, Jody Azzouni, Kent Bach, Andrew Bailey, Lynne Rudder Baker, Thomas R. Baldwin, Jon Barwise, George Bealer, William Bechtel, Lawrence C. Becker, Mark A. Bedau, Ernst Behler, José A. Benardete, Ermanno Bencivenga, Jan Berg, Michael Bergmann, Robert L. Bernasconi, Sven Bernecker, Bernard Berofsky, Rod Bertolet, Charles J. Beyer, Christian Beyer, Joseph Bien, Joseph Bien, Peg Birmingham, Ivan Boh, James Bohman, Daniel Bonevac, Laurence BonJour, William J. Bouwsma, Raymond D. Bradley, Myles Brand, Richard B. Brandt, Michael E. Bratman, Stephen E. Braude, Daniel Breazeale, Angela Breitenbach, Jason Bridges, David O. Brink, Gordon G. Brittan, Justin Broackes, Dan W. Brock, Aaron Bronfman, Jeffrey E. Brower, Bartosz Brozek, Anthony Brueckner, Jeffrey Bub, Lara Buchak, Otavio Bueno, Ann E. Bumpus, Robert W. Burch, John Burgess, Arthur W. Burks, Panayot Butchvarov, Robert E. Butts, Marina Bykova, Patrick Byrne, David Carr, Noël Carroll, Edward S. Casey, Victor Caston, Victor Caston, Albert Casullo, Robert L. Causey, Alan K. L. Chan, Ruth Chang, Deen K. Chatterjee, Andrew Chignell, Roderick M. Chisholm, Kelly J. Clark, E. J. Coffman, Robin Collins, Brian P. Copenhaver, John Corcoran, John Cottingham, Roger Crisp, Frederick J. Crosson, Antonio S. Cua, Phillip D. Cummins, Martin Curd, Adam Cureton, Andrew Cutrofello, Stephen Darwall, Paul Sheldon Davies, Wayne A. Davis, Timothy Joseph Day, Claudio de Almeida, Mario De Caro, Mario De Caro, John Deigh, C. F. Delaney, Daniel C. Dennett, Michael R. DePaul, Michael Detlefsen, Daniel Trent Devereux, Philip E. Devine, John M. Dillon, Martin C. Dillon, Robert DiSalle, Mary Domski, Alan Donagan, Paul Draper, Fred Dretske, Mircea Dumitru, Wilhelm Dupré, Gerald Dworkin, John Earman, Ellery Eells, Catherine Z. Elgin, Berent Enç, Ronald P. Endicott, Edward Erwin, John Etchemendy, C. Stephen Evans, Susan L. Feagin, Solomon Feferman, Richard Feldman, Arthur Fine, Maurice A. Finocchiaro, William FitzPatrick, Richard E. Flathman, Gvozden Flego, Richard Foley, Graeme Forbes, Rainer Forst, Malcolm R. Forster, Daniel Fouke, Patrick Francken, Samuel Freeman, Elizabeth Fricker, Miranda Fricker, Michael Friedman, Michael Fuerstein, Richard A. Fumerton, Alan Gabbey, Pieranna Garavaso, Daniel Garber, Jorge L. A. Garcia, Robert K. Garcia, Don Garrett, Philip Gasper, Gerald Gaus, Berys Gaut, Bernard Gert, Roger F. Gibson, Cody Gilmore, Carl Ginet, Alan H. Goldman, Alvin I. Goldman, Alfonso Gömez-Lobo, Lenn E. Goodman, Robert M. Gordon, Stefan Gosepath, Jorge J. E. Gracia, Daniel W. Graham, George A. Graham, Peter J. Graham, Richard E. Grandy, I. Grattan-Guinness, John Greco, Philip T. Grier, Nicholas Griffin, Nicholas Griffin, David A. Griffiths, Paul J. Griffiths, Stephen R. Grimm, Charles L. Griswold, Charles B. Guignon, Pete A. Y. Gunter, Dimitri Gutas, Gary Gutting, Paul Guyer, Kwame Gyekye, Oscar A. Haac, Raul Hakli, Raul Hakli, Michael Hallett, Edward C. Halper, Jean Hampton, R. James Hankinson, K. R. Hanley, Russell Hardin, Robert M. Harnish, William Harper, David Harrah, Kevin Hart, Ali Hasan, William Hasker, John Haugeland, Roger Hausheer, William Heald, Peter Heath, Richard Heck, John F. Heil, Vincent F. Hendricks, Stephen Hetherington, Francis Heylighen, Kathleen Marie Higgins, Risto Hilpinen, Harold T. Hodes, Joshua Hoffman, Alan Holland, Robert L. Holmes, Richard Holton, Brad W. Hooker, Terence E. Horgan, Tamara Horowitz, Paul Horwich, Vittorio Hösle, Paul Hoβfeld, Daniel Howard-Snyder, Frances Howard-Snyder, Anne Hudson, Deal W. Hudson, Carl A. Huffman, David L. Hull, Patricia Huntington, Thomas Hurka, Paul Hurley, Rosalind Hursthouse, Guillermo Hurtado, Ronald E. Hustwit, Sarah Hutton, Jonathan Jenkins Ichikawa, Harry A. Ide, David Ingram, Philip J. Ivanhoe, Alfred L. Ivry, Frank Jackson, Dale Jacquette, Joseph Jedwab, Richard Jeffrey, David Alan Johnson, Edward Johnson, Mark D. Jordan, Richard Joyce, Hwa Yol Jung, Robert Hillary Kane, Tomis Kapitan, Jacquelyn Ann K. Kegley, James A. Keller, Ralph Kennedy, Sergei Khoruzhii, Jaegwon Kim, Yersu Kim, Nathan L. King, Patricia Kitcher, Peter D. Klein, E. D. Klemke, Virginia Klenk, George L. Kline, Christian Klotz, Simo Knuuttila, Joseph J. Kockelmans, Konstantin Kolenda, Sebastian Tomasz Kołodziejczyk, Isaac Kramnick, Richard Kraut, Fred Kroon, Manfred Kuehn, Steven T. Kuhn, Henry E. Kyburg, John Lachs, Jennifer Lackey, Stephen E. Lahey, Andrea Lavazza, Thomas H. Leahey, Joo Heung Lee, Keith Lehrer, Dorothy Leland, Noah M. Lemos, Ernest LePore, Sarah-Jane Leslie, Isaac Levi, Andrew Levine, Alan E. Lewis, Daniel E. Little, Shu-hsien Liu, Shu-hsien Liu, Alan K. L. Chan, Brian Loar, Lawrence B. Lombard, John Longeway, Dominic McIver Lopes, Michael J. Loux, E. J. Lowe, Steven Luper, Eugene C. Luschei, William G. Lycan, David Lyons, David Macarthur, Danielle Macbeth, Scott MacDonald, Jacob L. Mackey, Louis H. Mackey, Penelope Mackie, Edward H. Madden, Penelope Maddy, G. B. Madison, Bernd Magnus, Pekka Mäkelä, Rudolf A. Makkreel, David Manley, William E. Mann (W.E.M.), Vladimir Marchenkov, Peter Markie, Jean-Pierre Marquis, Ausonio Marras, Mike W. Martin, A. P. Martinich, William L. McBride, David McCabe, Storrs McCall, Hugh J. McCann, Robert N. McCauley, John J. McDermott, Sarah McGrath, Ralph McInerny, Daniel J. McKaughan, Thomas McKay, Michael McKinsey, Brian P. McLaughlin, Ernan McMullin, Anthonie Meijers, Jack W. Meiland, William Jason Melanson, Alfred R. Mele, Joseph R. Mendola, Christopher Menzel, Michael J. Meyer, Christian B. Miller, David W. Miller, Peter Millican, Robert N. Minor, Phillip Mitsis, James A. Montmarquet, Michael S. Moore, Tim Moore, Benjamin Morison, Donald R. Morrison, Stephen J. Morse, Paul K. Moser, Alexander P. D. Mourelatos, Ian Mueller, James Bernard Murphy, Mark C. Murphy, Steven Nadler, Jan Narveson, Alan Nelson, Jerome Neu, Samuel Newlands, Kai Nielsen, Ilkka Niiniluoto, Carlos G. Noreña, Calvin G. Normore, David Fate Norton, Nikolaj Nottelmann, Donald Nute, David S. Oderberg, Steve Odin, Michael O’Rourke, Willard G. Oxtoby, Heinz Paetzold, George S. Pappas, Anthony J. Parel, Lydia Patton, R. P. Peerenboom, Francis Jeffry Pelletier, Adriaan T. Peperzak, Derk Pereboom, Jaroslav Peregrin, Glen Pettigrove, Philip Pettit, Edmund L. Pincoffs, Andrew Pinsent, Robert B. Pippin, Alvin Plantinga, Louis P. Pojman, Richard H. Popkin, John F. Post, Carl J. Posy, William J. Prior, Richard Purtill, Michael Quante, Philip L. Quinn, Philip L. Quinn, Elizabeth S. Radcliffe, Diana Raffman, Gerard Raulet, Stephen L. Read, Andrews Reath, Andrew Reisner, Nicholas Rescher, Henry S. Richardson, Robert C. Richardson, Thomas Ricketts, Wayne D. Riggs, Mark Roberts, Robert C. Roberts, Luke Robinson, Alexander Rosenberg, Gary Rosenkranz, Bernice Glatzer Rosenthal, Adina L. Roskies, William L. Rowe, T. M. Rudavsky, Michael Ruse, Bruce Russell, Lilly-Marlene Russow, Dan Ryder, R. M. Sainsbury, Joseph Salerno, Nathan Salmon, Wesley C. Salmon, Constantine Sandis, David H. Sanford, Marco Santambrogio, David Sapire, Ruth A. Saunders, Geoffrey Sayre-McCord, Charles Sayward, James P. Scanlan, Richard Schacht, Tamar Schapiro, Frederick F. Schmitt, Jerome B. Schneewind, Calvin O. Schrag, Alan D. Schrift, George F. Schumm, Jean-Loup Seban, David N. Sedley, Kenneth Seeskin, Krister Segerberg, Charlene Haddock Seigfried, Dennis M. Senchuk, James F. Sennett, William Lad Sessions, Stewart Shapiro, Tommie Shelby, Donald W. Sherburne, Christopher Shields, Roger A. Shiner, Sydney Shoemaker, Robert K. Shope, Kwong-loi Shun, Wilfried Sieg, A. John Simmons, Robert L. Simon, Marcus G. Singer, Georgette Sinkler, Walter Sinnott-Armstrong, Matti T. Sintonen, Lawrence Sklar, Brian Skyrms, Robert C. Sleigh, Michael Anthony Slote, Hans Sluga, Barry Smith, Michael Smith, Robin Smith, Robert Sokolowski, Robert C. Solomon, Marta Soniewicka, Philip Soper, Ernest Sosa, Nicholas Southwood, Paul Vincent Spade, T. L. S. Sprigge, Eric O. Springsted, George J. Stack, Rebecca Stangl, Jason Stanley, Florian Steinberger, Sören Stenlund, Christopher Stephens, James P. Sterba, Josef Stern, Matthias Steup, M. A. Stewart, Leopold Stubenberg, Edith Dudley Sulla, Frederick Suppe, Jere Paul Surber, David George Sussman, Sigrún Svavarsdóttir, Zeno G. Swijtink, Richard Swinburne, Charles C. Taliaferro, Robert B. Talisse, John Tasioulas, Paul Teller, Larry S. Temkin, Mark Textor, H. S. Thayer, Peter Thielke, Alan Thomas, Amie L. Thomasson, Katherine Thomson-Jones, Joshua C. Thurow, Vzalerie Tiberius, Terrence N. Tice, Paul Tidman, Mark C. Timmons, William Tolhurst, James E. Tomberlin, Rosemarie Tong, Lawrence Torcello, Kelly Trogdon, J. D. Trout, Robert E. Tully, Raimo Tuomela, John Turri, Martin M. Tweedale, Thomas Uebel, Jennifer Uleman, James Van Cleve, Harry van der Linden, Peter van Inwagen, Bryan W. Van Norden, René van Woudenberg, Donald Phillip Verene, Samantha Vice, Thomas Vinci, Donald Wayne Viney, Barbara Von Eckardt, Peter B. M. Vranas, Steven J. Wagner, William J. Wainwright, Paul E. Walker, Robert E. Wall, Craig Walton, Douglas Walton, Eric Watkins, Richard A. Watson, Michael V. Wedin, Rudolph H. Weingartner, Paul Weirich, Paul J. Weithman, Carl Wellman, Howard Wettstein, Samuel C. Wheeler, Stephen A. White, Jennifer Whiting, Edward R. Wierenga, Michael Williams, Fred Wilson, W. Kent Wilson, Kenneth P. Winkler, John F. Wippel, Jan Woleński, Allan B. Wolter, Nicholas P. Wolterstorff, Rega Wood, W. Jay Wood, Paul Woodruff, Alison Wylie, Gideon Yaffe, Takashi Yagisawa, Yutaka Yamamoto, Keith E. Yandell, Xiaomei Yang, Dean Zimmerman, Günter Zoller, Catherine Zuckert, Michael Zuckert, Jack A. Zupko (J.A.Z.)
- Edited by Robert Audi, University of Notre Dame, Indiana
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- The Cambridge Dictionary of Philosophy
- Published online:
- 05 August 2015
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- 27 April 2015, pp ix-xxx
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Differential effects of proteins and carbohydrates on postprandial blood pressure-related responses
- Karianna F. M. Teunissen-Beekman, Janneke Dopheide, Johanna M. Geleijnse, Stephan J. L. Bakker, Elizabeth J. Brink, Peter W. de Leeuw, Jan Serroyen, Marleen A. van Baak
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- Journal:
- British Journal of Nutrition / Volume 112 / Issue 4 / 28 August 2014
- Published online by Cambridge University Press:
- 03 June 2014, pp. 600-608
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- 28 August 2014
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Diet composition may affect blood pressure (BP), but the mechanisms are unclear. The aim of the present study was to compare postprandial BP-related responses to the ingestion of pea protein, milk protein and egg-white protein. In addition, postprandial BP-related responses to the ingestion of maltodextrin were compared with those to the ingestion of sucrose and a protein mix. We hypothesised that lower postprandial total peripheral resistance (TPR) and BP levels would be accompanied by higher plasma concentrations of nitric oxide, insulin, glucagon-like peptide 1 (GLP-1) and glucagon. On separate occasions, six meals were tested in a randomised order in forty-eight overweight or obese adults with untreated elevated BP. Postprandial responses of TPR, BP and plasma concentrations of insulin, glucagon, GLP-1 and nitrite, nitroso compounds (RXNO) and S-nitrosothiols (NOx) were measured for 4 h. No differences were observed in TPR responses. Postprandial BP levels were higher after the ingestion of the egg-white-protein meal than after that of meals containing the other two proteins (P≤ 0·01). The ingestion of the pea-protein meal induced the highest NOx response (P≤ 0·006). Insulin and glucagon concentrations were lowest after the ingestion of the egg-white-protein meal (P≤ 0·009). Postprandial BP levels were lower after the ingestion of the maltodextrin meal than after that of the protein mix and sucrose meals (P≤ 0·004), while postprandial insulin concentrations were higher after the ingestion of the maltodextrin meal than after that of the sucrose and protein mix meals after 1–2 h (P≤ 0·0001). Postprandial NOx, GLP-1 and glucagon concentrations were lower after the ingestion of the maltodextrin meal than after that of the protein mix meal (P≤ 0·008). In conclusion, different protein and carbohydrate sources induce different postprandial BP-related responses, which may be important for BP management. Lower postprandial BP levels are not necessarily accompanied by higher NOx, insulin, glucagon or GLP-1 responses.
Identification of biomarkers for intake of protein from meat, dairy products and grains: a controlled dietary intervention study
- Wieke Altorf-van der Kuil, Elizabeth J. Brink, Martine Boetje, Els Siebelink, Sabina Bijlsma, Marielle F. Engberink, Pieter van 't Veer, Daniel Tomé, Stephan J. L. Bakker, Marleen A. van Baak, Johanna M. Geleijnse
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- Journal:
- British Journal of Nutrition / Volume 110 / Issue 5 / 14 September 2013
- Published online by Cambridge University Press:
- 04 March 2013, pp. 810-822
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- 14 September 2013
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In the present controlled, randomised, multiple cross-over dietary intervention study, we aimed to identify potential biomarkers for dietary protein from dairy products, meat and grain, which could be useful to estimate intake of these protein types in epidemiological studies. After 9 d run-in, thirty men and seventeen women (22 (sd 4) years) received three high-protein diets (aimed at approximately 18 % of energy (en%)) in random order for 1 week each, with approximately 14 en% originating from either meat, dairy products or grain. We used a two-step approach to identify biomarkers in urine and plasma. With principal component discriminant analysis, we identified amino acids (AA) from the plasma or urinary AA profile that were distinctive between diets. Subsequently, after pooling total study data, we applied mixed models to estimate the predictive value of those AA for intake of protein types. A very good prediction could be made for the intake of meat protein by a regression model that included urinary carnosine, 1-methylhistidine and 3-methylhistidine (98 % of variation in intake explained). Furthermore, for dietary grain protein, a model that included seven AA (plasma lysine, valine, threonine, α-aminobutyric acid, proline, ornithine and arginine) made a good prediction (75 % of variation explained). We could not identify biomarkers for dairy protein intake. In conclusion, specific combinations of urinary and plasma AA may be potentially useful biomarkers for meat and grain protein intake, respectively. These findings need to be cross-validated in other dietary intervention studies.
Dietary protein, blood pressure and renal function in renal transplant recipients
- Else van den Berg, Mariëlle F. Engberink, Elizabeth J. Brink, Marleen A. van Baak, Rijk O. B. Gans, Gerjan Navis, Stephan J. L. Bakker
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- British Journal of Nutrition / Volume 109 / Issue 8 / 28 April 2013
- Published online by Cambridge University Press:
- 21 August 2012, pp. 1463-1470
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- 28 April 2013
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Hypertension is highly prevalent among renal transplant recipients (RTR) and a risk factor for graft failure and cardiovascular events. Protein intake has been claimed to affect blood pressure (BP) in the general population and may affect renal function. We examined the association of dietary protein with BP and renal function in RTR. We included 625 RTR (age 53 (sd 13) years; 57 % male). Protein intake was assessed with a FFQ, differentiating between animal and plant protein. BP was measured according to a strict protocol. Creatinine clearance and albuminuria were measured as renal parameters. Protein intake was 83 (sd 12) g/d, of which 63 % derived from animal sources. BP was 136 (sd 17) mmHg systolic (SBP) and 83 (sd 11) mmHg diastolic (DBP). Creatinine clearance was 66 (sd 26) ml/min; albuminuria 41 (10–178) mg/24 h. An inverse, though statistically insignificant, association was found between the total protein intake and both SBP (β = − 2·22 mmHg per sd, P= 0·07) and DBP (β = − 0·48 mmHg per sd, P= 0·5). Protein intake was not associated with creatinine clearance. Although albuminuria was slightly higher in the highest tertile of animal protein intake compared with the lowest tertile (66 v. 33 mg/d, respectively, P= 0·03), linear regression analyses did not reveal significant associations between dietary protein and albuminuria. Protein intake exceeded the current recommendations. Nevertheless, within the range of protein intake in our RTR population, we found no evidence for an association of dietary protein with BP and renal function. Intervention studies focusing on different protein types are warranted to clarify their effect on BP and renal function in RTR.
Dietary linoleic acid at high and reduced dietary fat level decreases the faecal excretion of vitamin E in young rats
- Lilian B. M. Tuburg, Edward Haddeman, Gerard A. A. Kivits, Jan A. Weststrate, Elizabeth J. Brink
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- British Journal of Nutrition / Volume 77 / Issue 2 / February 1997
- Published online by Cambridge University Press:
- 09 March 2007, pp. 327-336
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- February 1997
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Vitamin E is the major lipid-soluble antioxidant in human subjects and is crucial in protecting polyunsaturated fatty acids (PUFA) against lipid peroxidation. Dietary PUFA have been suggested to inhibit the absorption of vitamin E. The present study in young male rats was designed to investigate the effect of increasing concentrations of dietary linoleic acid on the faecal excretion of vitamin E. The rats were fed on semi-synthetic diets containing two concentrations of fat (59 g/kg diet, 15 energy % (en%) or 131 g/kg, 30 en%) for 3 weeks. Triacylglycerol rich in linoleic acid was added at the expense of triacylglycerol rich in saturated fatty acids to obtain dietary concentrations of 13,39 or 66 g linoleic acid/kg diet for the high-fat diet (131 g fat/kg) and 12, 24 or 36 g linoleic acid/kg diet for the reduced-fat diet (59 g fat/kg). The results from the present study demonstrate that the faecal excretion of vitamin E was significantly lower in rats fed on diets with high levels of linoleic acid compared with rats fed on lower levels of linoleic acid irrespective of the dietary fat content. The concentration of vitamin E in liver and plasma was significantly lower in animals fed on the highest concentration of linoleic acid compared with those fed on the lowest level. Results from the present study also demonstrate that at the same concentration of linoleic acid, the faecal excretion of vitamin E in rats fed on reduced-fat diets was significantly lower than in rats fed on high-fat diets. Our findings indicate that the apparent absorption of vitamin E is not inhibited by dietary PUFA. Results from the present study also demonstrate that a reduction of dietary fat content from 30 en% to 15 en% does not lower the apparent absorption of vitamin E
Vitamin E incorporated into a very-low-fat meal is absorbed from the intestine of young rats
- Elizabeth J. Brink, Edward Haddeman, Lilian B. M. Tijburg
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- Journal:
- British Journal of Nutrition / Volume 75 / Issue 6 / June 1996
- Published online by Cambridge University Press:
- 09 March 2007, pp. 939-948
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- June 1996
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Vegetable fats and oils are major sources of dietary vitamin E. Consequently the current trend to reduce fat consumption is accompanied by a reduction of the intake of vitamin E. In addition, the absorption of vitamin E is thought to be dependent on the hydroiysis of dietary lipids in the small intestine. It is therefore conceivable that a lower dietary fat intake also diminishes the intestinal absorption of vitamin E. The present 3-week feeding study in young male rats was designed to investigate whether different concentrations of vitamin E added to a very-low-fat product (0, 330 or 1350mg dl-α-tocopheryl acetate/kg product) were absorbed. We therefore incorporated these products into a very-low-fat meal (final fat concentration: 7 g/kg) or a low-fat meal containing 52 g fat/kg. The magnitude of vitamin E absorption from these meals was compared with that from meals containing similar amounts of vitamin E, but a high fat concentration of 190 g/kg. Apparent vitamin E absorption was defined as intake of α- tocopherol equivalents (αTE) minus faecal αTE excretion over 4 d during week 3 of the experimental period. The results of this study showed that apparent absorption of vitamin E from a very-low-fat meal varied, depending on the vitamin E concentration, from 73 to 83%. The magnitude of this vitamin E absorption was not significantly different from that from meals containing a high amount of fat. Liver vitamin E status was equal in rats fed on the very-low-fat meals compared with those fed on the high- fat meals. We conclude that, when very-low-fat or low-fat products are used as a replacement for full- fat products, addition of vitamin E to these products, as dl-α-tocopheryl acetate, might be useful in meeting the vitamin E requirements.
Ileal pH and apparent absorption of magnesium in rats fed on diets containing either lactose or lactulose
- Astrid M. P. Heijnen, Elizabeth J. Brink, Arnoldina G. Lemmens, Anton C. Beynen
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- Journal:
- British Journal of Nutrition / Volume 70 / Issue 3 / November 1993
- Published online by Cambridge University Press:
- 02 April 2007, pp. 747-756
- Print publication:
- November 1993
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The hypothesis was tested that dietary lactose v. glucose stimulates Mg absorption in rats because lactose lowers pH of the ileal lumen, which improves Mg solubility which in turn enhances Mg availability for transport across the ileal epithelium. For comparison, the effects of lactulose were studied because it shares with lactose the characteristic of being poorly digestible. Replacement of glucose by lactose (100 g/Kg) significantly stimulated apparent absorption of Mg. Apart from Mg absorption, lactulose also significantly enhanced absorption of Ca and phosphate. Lactose v. glucose lowered the pH of the ileal lumen from 7·5 to 7·2, whereas lactulose significantly reduced it to 7·0. In in vitro incubations a decrease in pH within the range of fluctuation in vivo was found to cause an improved solubility of Mg, and to a lesser extent also of Ca and phosphate. The smaller fall of ileal pH induced by feeding lactose instead of lactulose may explain why lactose improved Mg absorption only. For all individual rats combined there were negative relationships between ileal pH and apparent absorption of minerals, the relationship being strongest for Mg. Neither lactose nor lactulose was found to raise ileal solubility of minerals, which could relate to the possibility that the time of sampling was not appropriate. It is suggested that lactose-induced stimulation of Mg absorption in rats is caused by a lowering of ileal pH.
Urinary excretion of magnesium and calcium as an index of absorption is not affected by lactose intake in healthy adults
- Elizabeth J. Brink, Emerentia C. H. van Beresteijn, Pieter R. Dekker, Anton C. Beynen
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- Journal:
- British Journal of Nutrition / Volume 69 / Issue 3 / May 1993
- Published online by Cambridge University Press:
- 09 March 2007, pp. 863-870
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- May 1993
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The effect of lactose on the urinary excretion of Mg and Ca, as an index of absorption, was studied in a double-blind, crossover study during three 1-week periods. Twenty-four healthy, lactose-tolerant, adult volunteers maintained their habitual diets with the exception that all lactose-containing dairy products in the diet were replaced by 600 g/d of three specially prepared dairy products. These products were based on either lactose-enriched cow's milk or lactose-enriched, lactase (EC 3.2.1.23)-treated cow's milk, with or without added Mg, and were given in turn during 1 week. Lactose intake was increased by 127 mmol/d (46 g/d) while taking the lactose-enriched products. While taking the Mg-enriched products, Mg intake was increased by 2.8 mmol/d (69 mg/d) which was equivalent to 17% of the habitual Mg intake. Apart from the lactose and Mg intake, nutrient intake was comparable during the three dietary periods. Urinary excretions of Mg and Ca were used as indicators for their absorption. Mg supplementation significantly increased urinary Mg excretion by 0.97 mmol/d (equivalent to an increase of 18%, P < 0.001), indicating that urinary Mg excretion is a valid indicator for intestinal Mg absorption. Hydrolysis of lactose did not affect urinary excretion of Mg and Ca, which implies that lactose intake does not affect the absorption of Mg and Ca in healthy adults.
Bioavailability of magnesium and calcium from cow's milk and soya-bean beverage in rats
- Elizabeth J. Brink, Pieter R. Dekker, Emerentia C. H. Van Beresteijn, Anton C. Beynen
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- Journal:
- British Journal of Nutrition / Volume 68 / Issue 1 / July 1992
- Published online by Cambridge University Press:
- 09 March 2007, pp. 271-282
- Print publication:
- July 1992
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The milk components lactose and casein enhance the apparent absorption of magnesium and possibly also of calcium, whereas phytate, which occurs in soya-bean products, has an inhibitory effect. This implies that soya-bean beverage v. cow's milk could lower bioavailability of Mg and Ca. This hypothesis was tested in two experiments with growing rats. Feeding soya-bean beverage v. cow's milk consistently lowered body-weight gain, enhanced bone turnover, as measured by increased plasma alkaline phosphatase (EC 3.1.3.1) activity and increased urinary hydroxyproline excretion, and decreased Mg and Ca concentrations in the femur. Because the mineral compositions of the soya-bean beverage and the cow's milk were different, the intake of Mg was higher in rats fed on soya-bean beverage, whereas that of Ca was higher in rats fed on cow's milk. Supplementation of the soya-bean beverage either with phosphorus and Ca or with P, Ca and methionine, to concentrations identical to those in milk, restored growth and bone mineralization. When using diets carefully balanced for Mg, Ca, P, sodium, potassium and methionine, soya-bean beverage v. cow's milk in the diets decreased apparent absorption and urinary excretion of Mg and Ca. Hydrolysis of lactose in milk decreased absorption and urinary excretion of Mg; it did not significantly affect Ca absorption but lowered urinary Ca excretion. The present study shows that soya-bean beverage v. milk depresses Mg and Ca bioavailability, as would be predicted on the basis of reported effects of their purified components.