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Journal articles on the topic 'Postprandial metabolism'

Author: Grafiati

Published: 4 June 2021

Last updated: 10 February 2022

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1

Gill, Jason M. R., Muriel J. Caslake, Craig McAllister, et al. "Effects of Short-Term Detraining on Postprandial Metabolism, Endothelial Function, and Inflammation in Endurance-Trained Men: Dissociation between Changes in Triglyceride Metabolism and Endothelial Function." Journal of Clinical Endocrinology & Metabolism 88, no. 9 (2003): 4328–35. http://dx.doi.org/10.1210/jc.2003-030226.

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Endurance-trained athletes experience a low level of postprandial lipaemia, but this rapidly increases with detraining. We sought to determine whether detraining-induced changes to postprandial metabolism influenced endothelial function and inflammation. Eight endurance-trained men each undertook two oral fat tolerance tests [blood taken fasted and for 6 h following a high-fat test meal (80 g fat, 80 g carbohydrate)]: one during a period of their normal training (trained) and one after 1 wk of no exercise (detrained). Endothelial function in the cutaneous microcirculation was assessed using la

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2

Riccardi, Gabriele, Lutgarda Bozzetto, and Giovanni Annuzzi. "Postprandial lipid metabolism." Scandinavian Journal of Food and Nutrition 50, sup2 (2006): 99–106. http://dx.doi.org/10.1080/17482970601080539.

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3

Sethi, Sunil, M. J. Gibney, and Christine M. Williams. "Postprandial Lipoprotein Metabolism." Nutrition Research Reviews 6, no. 1 (1993): 161–83. http://dx.doi.org/10.1079/nrr19930011.

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4

Cohn, Jeffrey S. "Postprandial lipid metabolism." Current Opinion in Lipidology 5, no. 3 (1994): 185–90. http://dx.doi.org/10.1097/00041433-199405030-00005.

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5

Widdowson, William M., Anne McGowan, James Phelan, Gerard Boran, John Reynolds, and James Gibney. "Vascular Disease Is Associated With the Expression of Genes for Intestinal Cholesterol Transport and Metabolism." Journal of Clinical Endocrinology & Metabolism 102, no. 1 (2016): 326–35. http://dx.doi.org/10.1210/jc.2016-2728.

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Abstract Context: Intestinal cholesterol metabolism is important in influencing postprandial lipoprotein concentrations, and might be important in the development of vascular disease. Objective: This study evaluated associations between expression of intestinal cholesterol metabolism genes, postprandial lipid metabolism, and endothelial function/early vascular disease in human subjects. Design/Patients: One hundred patients undergoing routine oesophago-gastro-duodenoscopy were recruited. mRNA levels of Nieman-Pick C1-like 1 protein (NPC1L1), ABC-G5, ABC-G8, ABC-A1, microsomal tissue transport

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6

Schrauwen-Hinderling, Vera B., and André C. Carpentier. "Molecular imaging of postprandial metabolism." Journal of Applied Physiology 124, no. 2 (2018): 504–11. http://dx.doi.org/10.1152/japplphysiol.00212.2017.

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Disordered postprandial metabolism of energy substrates is one of the main defining features of prediabetes and contributes to the development of several chronic diseases associated with obesity, such as type 2 diabetes and cardiovascular diseases. Postprandial energy metabolism has been studied using classical isotopic tracer approaches that are limited by poor access to splanchnic metabolism and highly dynamic and complex exchanges of energy substrates involving multiple organs and systems. Advances in noninvasive molecular imaging modalities, such as PET and MRI/magnetic resonance spectrosc

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7

Mero, Niina, Mikko Syvänne, and Marja-Riitta Taskinen. "Postprandial lipid metabolism in diabetes." Atherosclerosis 141 (December 1998): S53—S55. http://dx.doi.org/10.1016/s0021-9150(98)00218-4.

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8

Westerveld, H. E. "Estrogens and postprandial lipid metabolism." Atherosclerosis 141 (December 1998): S105—S107. http://dx.doi.org/10.1016/s0021-9150(98)00227-5.

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9

Havel, Richard J. "Postprandial lipid metabolism: an overview." Proceedings of the Nutrition Society 56, no. 2 (1997): 659–66. http://dx.doi.org/10.1079/pns19970065.

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10

Miller, G. J. "Postprandial lipid metabolism and thrombosis." Proceedings of the Nutrition Society 56, no. 2 (1997): 739–44. http://dx.doi.org/10.1079/pns19970074.

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11

Hardman, Adrianne E., and Sara L. Herd. "Exercise and postprandial lipid metabolism." Proceedings of the Nutrition Society 57, no. 01 (1998): 63–72. http://dx.doi.org/10.1079/pns19980011.

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12

Morgan, Linda, Shelagh Hampton, Michelle Gibbs, and Josephine Arendt. "Circadian Aspects of Postprandial Metabolism." Chronobiology International 20, no. 5 (2003): 795–808. http://dx.doi.org/10.1081/cbi-120024218.

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13

Karpe, F. "Postprandial lipoprotein metabolism and atherosclerosis." Journal of Internal Medicine 246, no. 4 (1999): 341–55. http://dx.doi.org/10.1046/j.1365-2796.1999.00548.x.

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14

Karpe, Fredrik, and Anders Hamsten. "Postprandial lipoprotein metabolism and atherosclerosis." Current Opinion in Lipidology 6, no. 3 (1995): 123–29. http://dx.doi.org/10.1097/00041433-199506000-00003.

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15

Westerveld, H. T., E. Meyer, T. W. A. de Bruin, and D. W. Erkelens. "Oestrogens and postprandial lipid metabolism." Biochemical Society Transactions 25, no. 1 (1997): 45–49. http://dx.doi.org/10.1042/bst0250045.

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16

Plaisance, Eric P., and Gordon Fisher. "Exercise and Dietary-Mediated Reductions in Postprandial Lipemia." Journal of Nutrition and Metabolism 2014 (2014): 1–16. http://dx.doi.org/10.1155/2014/902065.

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Postprandial hyperlipemia produces long-term derangements in lipid/lipoprotein metabolism, vascular endothelial dysfunction, hypercoagulability, and sympathetic hyperactivity which are strongly linked to atherogenesis. The purpose of this review is to (1) provide a qualitative analysis of the available literature examining the dysregulation of postprandial lipid metabolism in the presence of obesity, (2) inspect the role of adiposity distribution and sex on postprandial lipid metabolism, and (3) examine the role of energy deficit (exercise- and/or energy restriction-mediated), isoenergetic low

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17

Robertson, M. D. "Food perception and postprandial lipid metabolism." Physiology & Behavior 89, no. 1 (2006): 4–9. http://dx.doi.org/10.1016/j.physbeh.2006.01.030.

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18

Zock, Peter L. "Postprandial lipoprotein metabolism—pivot or puzzle?" American Journal of Clinical Nutrition 85, no. 2 (2007): 331–32. http://dx.doi.org/10.1093/ajcn/85.2.331.

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19

Lefèbvre and Scheen. "Glucose metabolism and the postprandial state." European Journal of Clinical Investigation 29, S2 (1999): 1–6. http://dx.doi.org/10.1046/j.1365-2362.1999.00003.x.

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20

Hooper, Amanda J., Ken Robertson, P. Hugh R. Barrett, Klaus G. Parhofer, Frank M. van Bockxmeer, and John R. Burnett. "Postprandial Lipoprotein Metabolism in Familial Hypobetalipoproteinemia." Journal of Clinical Endocrinology & Metabolism 92, no. 4 (2007): 1474–78. http://dx.doi.org/10.1210/jc.2006-1998.

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21

Erkelens, D. W. "Insulin resistance and postprandial lipid metabolism." Atherosclerosis 151, no. 1 (2000): 79. http://dx.doi.org/10.1016/s0021-9150(00)80357-3.

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22

Georgopoulos, Angeliki. "Postprandial triglyceride metabolism in diabetes mellitus." Clinical Cardiology 22, S2 (1999): II—28—II—33. http://dx.doi.org/10.1002/clc.4960221406.

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23

Lairon, D., J. Lopez-Miranda, and C. Williams. "Methodology for studying postprandial lipid metabolism." European Journal of Clinical Nutrition 61, no. 10 (2007): 1145–61. http://dx.doi.org/10.1038/sj.ejcn.1602749.

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24

Nakajima, Katsuyuki, Takamitsu Nakano, Yoshiharu Tokita, et al. "Postprandial lipoprotein metabolism: VLDL vs chylomicrons." Clinica Chimica Acta 412, no. 15-16 (2011): 1306–18. http://dx.doi.org/10.1016/j.cca.2011.04.018.

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25

Picard, Frédéric, André Boivin, Josée Lalonde, and Yves Deshaies. "Resistance of adipose tissue lipoprotein lipase to insulin action in rats fed an obesity-promoting diet." American Journal of Physiology-Endocrinology and Metabolism 282, no. 2 (2002): E412—E418. http://dx.doi.org/10.1152/ajpendo.00307.2001.

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This study aimed to assess whether adipose lipoprotein lipase (LPL) becomes resistant to insulin in a nutritional model of resistance of glucose metabolism to insulin. Sprague-Dawley rats were fed for 4 wk chow or a purified high-sucrose, high-fat (HSHF) diet that induced overt insulin resistance. Rats were fasted for 24 h and then refed chow for 1, 3, or 6 h. The postprandial rise in insulinemia was similar in both dietary cohorts, whereas glycemia was higher in HSHF-fed than in chow-fed animals, indicating glucose intolerance and insulin resistance. In chow-fed rats, adipose LPL activity inc

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26

Meessen, Emma C. E., Moritz V. Warmbrunn, Max Nieuwdorp, and Maarten R. Soeters. "Human Postprandial Nutrient Metabolism and Low-Grade Inflammation: A Narrative Review." Nutrients 11, no. 12 (2019): 3000. http://dx.doi.org/10.3390/nu11123000.

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The importance of the postprandial state has been acknowledged, since hyperglycemia and hyperlipidemia are linked with several chronic systemic low-grade inflammation conditions. Humans spend more than 16 h per day in the postprandial state and the postprandial state is acknowledged as a complex interplay between nutrients, hormones and diet-derived metabolites. The purpose of this review is to provide insight into the physiology of the postprandial inflammatory response, the role of different nutrients, the pro-inflammatory effects of metabolic endotoxemia and the anti-inflammatory effects of

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27

Sonne, David P., Kristine J. Hare, Pernille Martens, et al. "Postprandial gut hormone responses and glucose metabolism in cholecystectomized patients." American Journal of Physiology-Gastrointestinal and Liver Physiology 304, no. 4 (2013): G413—G419. http://dx.doi.org/10.1152/ajpgi.00435.2012.

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Preclinical studies suggest that gallbladder emptying, via bile acid-induced activation of the G protein-coupled receptor TGR5 in intestinal L cells, may play a significant role in the secretion of the incretin hormone glucagon-like peptide-1 (GLP-1) and, hence, postprandial glucose homeostasis. We examined the secretion of gut hormones in cholecystectomized subjects to test the hypothesis that gallbladder emptying potentiates postprandial release of GLP-1. Ten cholecystectomized subjects and 10 healthy, age-, gender-, and body mass index-matched control subjects received a standardized fat-ri

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28

Lopez-Miranda, José, Christine Williams, and Denis Lairon. "Dietary, physiological, genetic and pathological influences on postprandial lipid metabolism." British Journal of Nutrition 98, no. 3 (2007): 458–73. http://dx.doi.org/10.1017/s000711450774268x.

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Most of diurnal time is spent in a postprandial state due to successive meal intakes during the day. As long as the meals contain enough fat, a transient increase in triacylglycerolaemia and a change in lipoprotein pattern occurs. The extent and kinetics of such postprandial changes are highly variable and are modulated by numerous factors. This review focuses on factors affecting postprandial lipoprotein metabolism and genes, their variability and their relationship with intermediate phenotypes and risk of CHD. Postprandial lipoprotein metabolism is modulated by background dietary pattern as

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29

Perez-Martinez, Pablo, Manfredi Rizzo, Giuseppe Montalto, and Jose Lopez-Miranda. "Postprandial metabolism: from research to clinical practice." Clinical Lipidology 8, no. 4 (2013): 395–98. http://dx.doi.org/10.2217/clp.13.28.

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30

Lairon, D., J. Lopez-Miranda, and C. Williams. "Erratum: Methodology for studying postprandial lipid metabolism." European Journal of Clinical Nutrition 62, no. 9 (2008): 1154. http://dx.doi.org/10.1038/ejcn.2008.42.

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31

Packard, C. J. "Effects of drugs on postprandial lipoprotein metabolism." Proceedings of the Nutrition Society 56, no. 2 (1997): 745–51. http://dx.doi.org/10.1079/pns19970075.

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32

Malkova, Dalia, and Jason MR Gill. "Effects of exercise on postprandial lipoprotein metabolism." Future Lipidology 1, no. 6 (2006): 743–55. http://dx.doi.org/10.2217/17460875.1.6.743.

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33

Lambert, Jennifer E., and Elizabeth J. Parks. "Postprandial metabolism of meal triglyceride in humans." Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids 1821, no. 5 (2012): 721–26. http://dx.doi.org/10.1016/j.bbalip.2012.01.006.

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34

Murase, Takatoshi, Yuka Yokoi, Koichi Misawa, et al. "Coffee polyphenols modulate whole-body substrate oxidation and suppress postprandial hyperglycaemia, hyperinsulinaemia and hyperlipidaemia." British Journal of Nutrition 107, no. 12 (2011): 1757–65. http://dx.doi.org/10.1017/s0007114511005083.

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Postprandial energy metabolism, including postprandial hyperglycaemia, hyperinsulinaemia and hyperlipidaemia, is related to the risk for developing obesity and CVD. In the present study, we examined the effects of polyphenols purified from coffee (coffee polyphenols (CPP)) on postprandial carbohydrate and lipid metabolism, and whole-body substrate oxidation in C57BL/6J mice. In mice that co-ingested CPP with a lipid–carbohydrate (sucrose or starch)-mixed emulsion, the respiratory quotient determined by indirect calorimetry was significantly lower than that in control mice, whereas there was no

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35

Parker, Lewan, Dale J. Morrison, Andrew C. Betik, et al. "High-glucose mixed-nutrient meal ingestion impairs skeletal muscle microvascular blood flow in healthy young men." American Journal of Physiology-Endocrinology and Metabolism 318, no. 6 (2020): E1014—E1021. http://dx.doi.org/10.1152/ajpendo.00540.2019.

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Oral glucose ingestion leads to impaired muscle microvascular blood flow (MBF), which may contribute to acute hyperglycemia-induced insulin resistance. We investigated whether incorporating lipids and protein into a high-glucose load would prevent postprandial MBF dysfunction. Ten healthy young men (age, 27 yr [24, 30], mean with lower and upper bounds of the 95% confidence interval; height, 180 cm [174, 185]; weight, 77 kg [70, 84]) ingested a high-glucose (1.1 g/kg glucose) mixed-nutrient meal (10 kcal/kg; 45% carbohydrate, 20% protein, and 35% fat) in the morning after an overnight fast. Fe

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36

Deshaies, Y., and R. Belahsen. "Postprandial plasma triacylglycerols in rats under alpha 1-adrenergic blockade." American Journal of Physiology-Endocrinology and Metabolism 264, no. 4 (1993): E541—E547. http://dx.doi.org/10.1152/ajpendo.1993.264.4.e541.

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The present studies evaluated the effect of prazosin, a selective alpha 1-adrenergic antagonist, on some metabolic determinants of triacylglycerol-rich lipoproteins. Plasma triacylglycerols (TG), TG secretion rate, TG removal rate, plasma insulin, and glucose were evaluated postprandially in animals fed a high-sucrose meal. In the fasted state plasma TG, glucose, and insulin concentrations were minimally affected by prazosin. There was a significant postprandial elevation in plasma TG levels that was larger after ingestion of a meal containing corn oil than after intake of a fat-free meal. Pra

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37

Hampton, S. M., L. M. Morgan, N. Lawrence, et al. "Postprandial hormone and metabolic responses in simulated shift work." Journal of Endocrinology 151, no. 2 (1996): 259–67. http://dx.doi.org/10.1677/joe.0.1510259.

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Abstract This study was designed to investigate postprandial responses to a mixed meal in simulated shift work conditions. Nine normal healthy subjects (six males and three females) were studied on two occasions at the same clock time (1330 h) after consuming test meals, first in their normal environment and secondly after a 9 h phase advance (body clock time 2230 h). Plasma glucose, insulin, glucose-dependent insulinotropic polypeptide (GIP), glucagon-like peptide-1 (GLP-1), triacylglycerol (TAG) and non-esterified fatty acids (NEFAs) were determined at intervals for 6 h after each test meal.

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38

Katsilambros, N. "Postprandial Triglyceridaemia." Diabetic Medicine 12, no. 5 (1995): 451–52. http://dx.doi.org/10.1111/j.1464-5491.1995.tb00519.x.

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39

Roche, Helen M., Antonis Zampelas, Kim G. Jackson, Christine M. Williams, and Michael J. Gibney. "The effect of test meal monounsaturated fatty acid: saturated fatty acid ratio on postprandial lipid metabolism." British Journal of Nutrition 79, no. 5 (1998): 419–24. http://dx.doi.org/10.1079/bjn19980071.

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Epidemiological evidence shows that a diet high in monounsaturated fatty acids (MUFA) but low in saturated fatty acids (SFA) is associated with reduced risk of CHD. The hypocholesterolaemic effect of MUFA is known but there has been little research on the effect of test meal MUFA and SFA composition on postprandial lipid metabolism. The present study investigated the effect of meals containing different proportions of MUFA and SFA on postprandial triacylglycerol and non-esterified fatty acid (NEFA) metabolism. Thirty healthy male volunteers consumed three meals containing equal amounts of fat

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40

Tremblay-Franco, Marie, Nathalie Poupin, Aurélien Amiel, et al. "Postprandial NMR-Based Metabolic Exchanges Reflect Impaired Phenotypic Flexibility across Splanchnic Organs in the Obese Yucatan Mini-Pig." Nutrients 12, no. 8 (2020): 2442. http://dx.doi.org/10.3390/nu12082442.

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The postprandial period represents one of the most challenging phenomena in whole-body metabolism, and it can be used as a unique window to evaluate the phenotypic flexibility of an individual in response to a given meal, which can be done by measuring the resilience of the metabolome. However, this exploration of the metabolism has never been applied to the arteriovenous (AV) exploration of organs metabolism. Here, we applied an AV metabolomics strategy to evaluate the postprandial flexibility across the liver and the intestine of mini-pigs subjected to a high fat–high sucrose (HFHS) diet for

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41

Bruinstroop, Eveline, Susanne E. la Fleur, Mariette T. Ackermans, et al. "The autonomic nervous system regulates postprandial hepatic lipid metabolism." American Journal of Physiology-Endocrinology and Metabolism 304, no. 10 (2013): E1089—E1096. http://dx.doi.org/10.1152/ajpendo.00614.2012.

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The liver is a key organ in controlling glucose and lipid metabolism during feeding and fasting. In addition to hormones and nutrients, inputs from the autonomic nervous system are also involved in fine-tuning hepatic metabolic regulation. Previously, we have shown in rats that during fasting an intact sympathetic innervation of the liver is essential to maintain the secretion of triglycerides by the liver. In the current study, we hypothesized that in the postprandial condition the parasympathetic input to the liver inhibits hepatic VLDL-TG secretion. To test our hypothesis, we determined the

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42

Greenfield, Jerry R., Katherine Samaras, Chris S. Hayward, Donald J. Chisholm, and Lesley V. Campbell. "Beneficial Postprandial Effect of a Small Amount of Alcohol on Diabetes and Cardiovascular Risk Factors: Modification by Insulin Resistance." Journal of Clinical Endocrinology & Metabolism 90, no. 2 (2005): 661–72. http://dx.doi.org/10.1210/jc.2004-1511.

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Moderate alcohol consumption protects against type 2 diabetes and cardiovascular disease. Because humans spend most of their time in the postprandial state, we examined the effect of 15 g alcohol on postprandial metabolic factors in 20 postmenopausal women over 6 h. We measured 1) glucose, insulin, lipids, C-reactive protein, and adiponectin levels; 2) augmentation index by applanation tonometry; and 3) energy expenditure and substrate oxidation by indirect calorimetry. Subjects received low carbohydrate (LC; visits 1 and 2) and high carbohydrate (HC; visits 3 and 4) high fat meals with and wi

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43

Harrison, Michael, Donal J. O'Gorman, Noel McCaffrey, et al. "Influence of acute exercise with and without carbohydrate replacement on postprandial lipid metabolism." Journal of Applied Physiology 106, no. 3 (2009): 943–49. http://dx.doi.org/10.1152/japplphysiol.91367.2008.

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Acute exercise, undertaken on the day before an oral fat tolerance test (OFTT), typically reduces postprandial triglycerides (TG) and increases high-density lipoprotein-cholesterol (HDL-C). However, the benefits of acute exercise may be overstated when studies do not account for compensatory changes in dietary intake. The objective of this study was to determine the influence of acute exercise, with and without carbohydrate (CHO) replacement, on postprandial lipid metabolism. Eight recreationally active young men underwent an OFTT on the morning after three experimental conditions: no exercise

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44

Klop, B., T. M. van den Berg, A. P. Rietveld, et al. "AT1 Receptor Gene Polymorphisms in relation to Postprandial Lipemia." International Journal of Vascular Medicine 2012 (2012): 1–6. http://dx.doi.org/10.1155/2012/271030.

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Background. Recent data suggest that the renin-angiotensin system may be involved in triglyceride (TG) metabolism. We explored the effect of the common A1166C and C573T polymorphisms of the angiotensin II type 1 receptor (AT1R) gene on postprandial lipemia.Methods. Eighty-two subjects measured daytime capillary TG, and postprandial lipemia was estimated as incremental area under the TG curve. The C573T and A1166C polymorphisms of the AT1R gene were determined.Results. Postprandial lipemia was significantly higher in homozygous carriers of the 1166-C allele (9.39±8.36 mM*h/L) compared to homozy

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45

Parhofer, Klaus G., P. Hugh R. Barrett, and Peter Schwandt. "Atorvastatin Improves Postprandial Lipoprotein Metabolism in Normolipidemic Subjects1." Journal of Clinical Endocrinology & Metabolism 85, no. 11 (2000): 4224–30. http://dx.doi.org/10.1210/jcem.85.11.6978.

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Atorvastatin is a potent HMG-CoA reductase inhibitor that decreases low-density lipoprotein (LDL) cholesterol and fasting triglyceride concentrations. Because of the positive association between elevated postprandial lipoproteins and atherosclerosis, we investigated the effect of atorvastatin on postprandial lipoprotein metabolism. The effect of 4 weeks of atorvastatin therapy (10 mg/day) was evaluated in 10 normolipidemic men (30 ± 2 yr; body mass index, 22 ± 3 kg/m2; cholesterol, 4.84 ± 0.54 mmol/L; triglyceride, 1.47 ± 0.50 mmol/L; high-density lipoprotein cholesterol, 1.17 ± 0.18 mmol/L; L

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46

Rendell, Marc S., and Lois Jovanovic. "Targeting postprandial hyperglycemia." Metabolism 55, no. 9 (2006): 1263–81. http://dx.doi.org/10.1016/j.metabol.2006.05.012.

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47

RAJARATNAM, Radhakrishnan A., Helena GYLLING, and Tatu A. MIETTINEN. "Impaired postprandial clearance of squalene and apolipoprotein B-48 in post-menopausal women with coronary artery disease." Clinical Science 97, no. 2 (1999): 183–92. http://dx.doi.org/10.1042/cs0970183.

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It is not known in detail whether postprandial lipaemia is associated with coronary artery disease (CAD) in women. To investigate this, we administered an oral vitamin A/squalene/fat meal to 24 post-menopausal women with angiographically proven CAD who were not taking hormone replacement therapy, and to 30 healthy controls (18 without and 12 with hormone replacement therapy) to evaluate the effects of CAD on postprandial lipoprotein metabolism. This was done by assessing squalene, triacylglycerols, retinyl palmitate and apolipoprotein B-48 (apoB-48) during the subsequent 24 h. The subjects wit

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48

Lewis, Gary F. "Postprandial Lipoprotein Metabolism in Diabetes Mellitus and Obesity." Journal of Atherosclerosis and Thrombosis 2, Supplement1 (1995): S34—S35. http://dx.doi.org/10.5551/jat1994.2.supplement1_s34.

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49

Beisiegel, U., J. Heeren, and A. Laatsch. "Abstract: 549 NEW ASPECTS OF POSTPRANDIAL LIPID METABOLISM." Atherosclerosis Supplements 10, no. 2 (2009): e1618. http://dx.doi.org/10.1016/s1567-5688(09)71570-3.

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50

Schauren, B. C., V. L. Portal, F. G. Beltrami, T. J. dos Santos, and L. C. Pellanda. "Postprandial metabolism and inflammatory markers in overweight adolescents." Journal of Developmental Origins of Health and Disease 5, no. 4 (2014): 299–306. http://dx.doi.org/10.1017/s2040174414000269.

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Lifestyle changes have an impact on lipid metabolism. The overload of circulating lipids may lead to endothelial dysfunction, oxidative stress and exaggerated inflammatory response, which may be further aggravated in the presence of overweight. This study aims to describe the postprandial metabolism and inflammatory response in overweight and normal-weight adolescents. Sixty-two adolescents aged 11–18 years were divided into two groups: overweight (OW; n=38) and normal weight (NW; n=24). Total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (

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