Relevant bibliographies by topics / Postprandial triglycerides

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  2. Dissertations / Theses
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  5. Conference papers

Academic literature on the topic 'Postprandial triglycerides'

Author: Grafiati
Published: 4 June 2021
Last updated: 26 July 2025

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Journal articles on the topic "Postprandial triglycerides"

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Lomangino, Kevin. "Postprandial Triglycerides." Clinical Nutrition INSIGHT 33, no. 10 (2007): 9. http://dx.doi.org/10.1097/01.nmd.0000294127.80085.c5.

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Folwaczny, Alexander, Elisa Waldmann, Julia Altenhofer, Kerstin Henze, and Klaus G. Parhofer. "Postprandial Lipid Metabolism in Normolipidemic Subjects and Patients with Mild to Moderate Hypertriglyceridemia: Effects of Test Meals Containing Saturated Fatty Acids, Mono-Unsaturated Fatty Acids, or Medium-Chain Fatty Acids." Nutrients 13, no. 5 (2021): 1737. http://dx.doi.org/10.3390/nu13051737.

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Fasting and postprandial hypertriglyceridemia are causal risk factors for atherosclerosis. The prevalence of hypertriglyceridemia is approximately 25–30% and most hypertriglyceridemic patients suffer from mild to moderate hypertriglyceridemia. Data regarding dietary interventions on postprandial triglyceride metabolism of mildly to moderately hypertriglyceridemic patients is, however, sparse. In a randomized controlled trial, eight mildly hypertriglyceridemic patients and five healthy, normolipidemic controls received three separate standardized fat-meals containing either saturated fatty acid
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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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Hansen, John-Bjarne, José A. Fernández, Ann-Trude With Notø, Hiroshi Deguchi, Johan Björkegren, and Ellisiv B. Mathiesen. "The Apolipoprotein C-I Content of Very-Low-Density Lipoproteins Is Associated with Fasting Triglycerides, Postprandial Lipemia, and Carotid Atherosclerosis." Journal of Lipids 2011 (2011): 1–9. http://dx.doi.org/10.1155/2011/271062.

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Background. Experimental studies in animals suggest that apolipoprotein (apo) C-I is an important regulator of triglycerides in fasting and postprandial conditions and associated with carotid atherosclerosis.Methods. A cross-sectional study was conducted with 81 subjects, aged 56–80 years recruited from a population health survey. The participants underwent a fat tolerance test (1 g fat per Kg body weight) and carotid atherosclerosis was determined by ultrasound examination. VLDL particles, Sf 20–400, were isolated and their lipid composition and apoC-I content determined.Results. The carotid
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Georgopoulos, Angeliki, Omer Aras, and Michael Y. Tsai. "Codon-54 Polymorphism of the Fatty Acid-Binding Protein 2 Gene Is Associated with Elevation of Fasting and Postprandial Triglyceride in Type 2 Diabetes*." Journal of Clinical Endocrinology & Metabolism 85, no. 9 (2000): 3155–60. http://dx.doi.org/10.1210/jcem.85.9.6791.

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Abstract Patients with type 2 diabetes are frequently dyslipidemic or hypertriglyceridemic. To assess whether increased intestinal triglyceride input leads to elevated fasting and postprandial triglycerides in type 2 diabetes, we used the codon 54 polymorphism of the fatty acid-binding protein 2 gene, which results in the substitution of threonine (Thr) for alanine and is associated with increased intestinal input of triglyceride. Of the 287 diabetic patients screened, 108 (37.6%) were heterozygous and 31 (10.8%) were homozygous for the Thr-54 allele. Mean (±sem) fasting plasma triglyceride le
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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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Belahsen, Rekia, та Yves Deshaies. "Modulation of lipoprotein lipase activity in the rat by the β2-adrenergic agonist clenbuterol". Canadian Journal of Physiology and Pharmacology 70, № 12 (1992): 1555–62. http://dx.doi.org/10.1139/y92-223.

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This study evaluated the effects of β2-adrenoceptor stimulation on some determinants of triglyceride metabolism. Male Sprague–Dawley rats were injected twice daily with clenbuterol (30 μg∙kg−1) for 7 days, or with an equivalent volume of vehicle. Serum triglycerides, hepatic triglyceride secretion rate, and lipoprotein lipase activity in white and brown adipose tissues as well as in red vastus lateralis muscle and heart were evaluated in the fasting state and following a fat-free, high-sucrose meal, 3 h after the last agonist injection. In rats killed in the fasting and postprandial states, cl
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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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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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Cardona, Fernando, Sonsoles Morcillo, Montserrat Gonzalo-Marín, Lourdes Garrido-Sanchez, Manuel Macias-Gonzalez, and Francisco J. Tinahones. "Pro12Ala Sequence Variant of the PPARG Gene Is Associated with Postprandial Hypertriglyceridemia in Non-E3/E3 Patients with the Metabolic Syndrome." Clinical Chemistry 52, no. 10 (2006): 1920–25. http://dx.doi.org/10.1373/clinchem.2006.069690.

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Abstract Background: Postprandial hypertriglyceridemia, a component of the metabolic syndrome, has varied etiology and involves many genes related to triglyceride metabolism. Variations in these genes may affect postprandial hypertriglyceridemia in the context of the metabolic syndrome. Methods: We orally administered 60 g of fat overload to 74 patients with the metabolic syndrome. We then measured baseline concentrations of cholesterol, triglycerides, HDL cholesterol, apolipoprotein AI, apolipoprotein B, uric acid, and uric acid excretion; we also performed homeostasis model assessments of in
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Dissertations / Theses on the topic "Postprandial triglycerides"

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Mohanlal, Nina. "Modification of postprandial lipid profiles in people with diabetes." Thesis, University of Oxford, 2003. http://ora.ox.ac.uk/objects/uuid:ecb1e165-a53c-430d-aed5-fe855dbb8c2c.

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Background: Abnormalities in postprandial lipid metabolism may explain, in part, the 2 to 4 fold increased risk of coronary heart disease (CHD) in diabetic individuals compared with the general population. Aims: To develop an Oral Triglyceride Tolerance Test (OTTT) to evaluate reliably post challenge metabolism and to determine whether more physiologic insulin profiles can improve lipid responses in diabetic subjects. Methods: Post 50g fat and 50g carbohydrate challenge triglyceride and glucose profiles were measured 2 hourly for 8 hours on 2 occasions to establish test reproducibility and to
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Cohen, Jonathan. "The regulation of postprandial lipemia in man." Doctoral thesis, University of Cape Town, 1989. http://hdl.handle.net/11427/27177.

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The regulation of the serum triglyceride responses to fat ingestion have been examined in normolipidemic men. To evaluate the existing methods for comparing chylomicron-triglyceride clearance, the oral and intravenous fat tolerance tests and a steady state duodenal perfusion method were compared. Good correlations (r > 0.8) were found between each of these methods. Since the intravenous fat tolerance test is independent of fat absorption, these data suggested that the serum triglyceride response to fat feeding was largely determined by the rate of chylomicron-triglyceride clearance. To determi
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Morin, Renée. "The Effect of Acute Intermittent Hypoxia on Postprandial Lipid Metabolism." Thesis, Université d'Ottawa / University of Ottawa, 2020. http://hdl.handle.net/10393/40537.

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Background: Obstructive sleep apnea (OSA) consists of repeated, involuntary breathing suspension during sleep. These events induce rapid depletion/repletion of blood/tissue oxygen content, a phenomenon known as intermittent hypoxia. Aside from causing daytime sleepiness, the most important health consequence of OSA is a 2-fold increase in cardiovascular (CVD) risk. Animal studies provide evidence that intermittent hypoxia, a simulating model of OSA, causes important rise in plasma TG, especially in the postprandial state. However, the underpinning mechanisms linking intermittent hypoxia to alt
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Emerson, Sam R. "Postprandial metabolism and inflammation: novel insights focusing on true-to-life application." Diss., Kansas State University, 2017. http://hdl.handle.net/2097/35605.

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Doctor of Philosophy<br>Department of Human Nutrition<br>Sara Rosenkranz<br>The aims of this dissertation were to provide innovative, applicable insights regarding the impact of single-meal consumption on metabolic and inflammatory responses in the acute post-meal (“postprandial”) period. In Chapter 2, the connection between large postprandial glucose and triglyceride (TG) fluxes and cardiovascular disease (CVD) risk were reviewed. A new marker of metabolic status, Metabolic Load Index (MLI), calculated by adding glucose and TG, was proposed based on several considerations: 1) independent asso
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Wideman, Laurie. "Postprandial lipemia in abdominally obese and non-obese males." Virtual Press, 1993. http://liblink.bsu.edu/uhtbin/catkey/845959.

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Recent research has shown that the combination of high triglyceride (TG) levels and low high density lipoprotein (HDL) levels, significantly increases the incidence of coronary artery disease (CAD). The incidence of CAD is also increased in abdominally obese individuals. To assess differences in postprandial TG clearance patterns between abdominally obese (AO) and controls (C), fourteen healthy, normolipidemic males (seven controls and seven abdominally obese) completed an oral fat loading test (78 grams of fat). Blood samples were collected every hour for eight hours. Abdominally obese indivi
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Bielko, Sylvanna Lauren. "Postprandial effects of three isocaloric high-fat meals with differing lipid loads on triglycerides, oxidative stress, and endothelial function." Thesis, Indiana University, 2015. http://pqdtopen.proquest.com/#viewpdf?dispub=1582853.

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<p> <b>BACKGROUND:</b> There have been numerous studies that compare the relationship of postprandial lipemia, oxidative stress, and endothelial dysfunction, but there is a lack of information as to the dose response nature of isocaloric high-fat meals (HFM). <b>OBJECTIVE:</b> To examine the dose response of lipemia (isocaloric HFM consisting of 25%, 50%, and 75% fat) on plasma triglycerides (TG), oxidative stress, and endothelial function. It was hypothesized that the highest fat load would produce the greatest amount of oxidative stress and endothelial dysfunction; whereas each lipid load wo
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Pezzi, Fernanda. "Efeito agudo do exercício aeróbio na lipemia pós-prandial em adultos obesos de acordo com o polimorfismo -3826 a/g no gene da proteína desacopladora 1 (ucp 1)." reponame:Biblioteca Digital de Teses e Dissertações da UFRGS, 2011. http://hdl.handle.net/10183/103909.

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Introdução: A hipertrigliceridemia é uma das características mais comuns na obesidade e pode ser caracterizada pela elevação dos triglicerídeos nos estados de jejum ou pós-prandial. Objetivo: Identificar os efeitos de uma sessão aguda de exercício aeróbio na lipemia pós-prandial em adultos obesos de acordo com o polimorfismo -3826 A/G no gene da UCP1. Métodos: Trinta e seis adultos jovens de ambos os sexos foram separados para o grupo Eutrófico AA (EAA, n=10), Eutrófico AG (EAG, n=8), Obeso AA (OAA, n=8) e Obeso AG (OAG, n=10). Após sessões de genotipagem e teste máximo, os triglicerídeos fora
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Ahmad, Nazir. "Lipémie postprandiale et lactoferrine : le Lipolysis Stimulated Receptor comme cible potentielle." Thesis, Université de Lorraine, 2012. http://www.theses.fr/2012LORR0167/document.

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La lipémie postprandiale se caractérise par une augmentation des lipoprotéines riches en triglycérides après un repas, et joue un rôle important dans la biodisponibilité des lipides alimentaires pour les tissus périphériques. En effet, une lipémie postprandiale élevée est souvent associée à l'obésité et à une dyslipidémie, deux composantes du syndrome métabolique qui peuvent engendrer des complications médicales, incluant diabète et maladies cardiovasculaires. La lactoferrine (Lf) inhibe l'épuration hépatique des chylomicrons, conduisant à une élévation de la lipémie postprandiale par des méca
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Björkegren, Johan. "Triglyceride-rich lipoproteins : postprandial metabolism and composition in relation to atherosclerosis /." Stockholm, 1998. http://diss.kib.ki.se/search/diss.se.cfm?19980515bjor.

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Kimura, Rino. "Studies on the attenuation effects of intestinal PPARα activation on postprandial hyperlipidemia". Kyoto University, 2014. http://hdl.handle.net/2433/188757.

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Kyoto University (京都大学)<br>0048<br>新制・課程博士<br>博士(農学)<br>甲第18319号<br>農博第2044号<br>新制||農||1021(附属図書館)<br>学位論文||H26||N4826(農学部図書室)<br>31177<br>京都大学大学院農学研究科食品生物科学専攻<br>(主査)教授 河田 照雄, 教授 伏木 亨, 教授 金本 龍平<br>学位規則第4条第1項該当
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Books on the topic "Postprandial triglycerides"

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Lockton, John Andrew. A study of the quantitative and qualitative changes in triglyceride-rich lipoproteins inthe postprandial period and related change in high density lipoprotein cholesterol, preheparin plasma lipase activity, insulin and glucose in insulin dependent diabetis mellitus and controls. University of Manchester, 1993.

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Strausberger, Beate. Ruhe- und postprandialer Energieverbrauch in Abhängigkeit von postprandialer Triglycerid-Antwort und Fettverteilung. 1995.

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Book chapters on the topic "Postprandial triglycerides"

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Weber, P., S. Ausieker, R. Probst, et al. "Postprandial Course of Triglycerides and the Atherogenic Lipoprotein Particle “IDL” in Type 2 Diabetics with Normal Fasting Values." In Recent Developments in Lipid and Lipoprotein Research. Springer Berlin Heidelberg, 1993. http://dx.doi.org/10.1007/978-3-642-84855-1_6.

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Richter, G., S. Schwarz, T. Manthey, K. Ehlenz, H. Kaffarnik, and A. Steinmetz. "Postprandial redistribution of apo E isoforms in triglyceride-rich lipoproteins." In Diätetik und Arteriosklerose. Vieweg+Teubner Verlag, 1993. http://dx.doi.org/10.1007/978-3-663-01942-8_12.

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Koshiyama, Hiroyuki, Satsuki Tanaka, Jun Minamikawa, and Kazuwa Nakao. "Relationship Between Postprandial Triglyceride Level and Intima-Media Thickness of Carotid Artery after Troglitazone Treatment in Type 2 Diabetes." In Lipoprotein Metabolism and Atherogenesis. Springer Japan, 2000. http://dx.doi.org/10.1007/978-4-431-68424-4_34.

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Aras, Turgay. "Dyslipidemia Screening." In Newborn and Childhood Screening Programmes. Nobel Tip Kitabevleri, 2024. http://dx.doi.org/10.69860/nobel.9786053358961.13.

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Dyslipidemia is lipoprotein metabolism disorders characterized by high total cholesterol (TC), LDL-C, non-HDL-C, triglyceride (TG) and low HDL-C.Although lipid and lipoprotein levels vary according to age and gender, acceptable, borderline high and high values ​​have been determined for children.Dyslipidemia can occur for various reasons, such as dietary saturated and trans fats, consumption of refined carbohydrates and sugar, alcohol, medications, endocrine/metabolic/renal problems, infections and genetic factors.The frequency and duration of dyslipidemia screening are planned according to ag
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Le, Ngoc-Anh. "Postprandial Triglycerides, Oxidative Stress, and Inflammation." In Apolipoproteins, Triglycerides and Cholesterol. IntechOpen, 2020. http://dx.doi.org/10.5772/intechopen.91303.

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Le, Ngoc-Anh. "Fat-Soluble Antioxidants: Role of Postprandial Lipoproteins." In The Power of Antioxidants - Unleashing Nature's Defense Against Oxidative Stress [Working Title]. IntechOpen, 2024. http://dx.doi.org/10.5772/intechopen.1004853.

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Many commonly known antioxidants, from probucol to vitamin E, are fat-soluble and have been shown to be most effective when administered with meals. Following meal consumption, these compounds are incorporated into intestinal lipoproteins, known as chylomicrons, and secreted into the circulation. These lipid-carrying particles are responsible for the transport of newly absorbed dietary fat for delivery to peripheral tissues. In the bloodstream, chylomicrons interact with heparin-releasable lipases common known as lipoprotein lipase and hepatic triglyceride lipase. Bothe lipases are anchored al
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"- Consumption of Fructose and High Fructose Corn Syrup Increase Postprandial Triglycerides, LDL-Cholesterol, and Apolipoprotein-B in Young Men and Women." In Nutritional Biochemistry. Apple Academic Press, 2015. http://dx.doi.org/10.1201/b18536-10.

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Stanhope, Kimber, Andrew Bremer, Valentina Medici, et al. "Consumption of Fructose and High Fructose Corn Syrup Increase Postprandial Triglycerides, LDL-Cholesterol, and Apolipoprotein-B in Young Men and Women." In Nutritional Biochemistry. Apple Academic Press, 2015. http://dx.doi.org/10.1201/b18536-6.

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Cabello-Moruno, Rosana, Javier S. Perona, and Valentina Ruiz-Gutiérrez. "Postprandial Triglyceride-rich Lipoprotein Composition and Size after Olive Oil." In Olives and Olive Oil in Health and Disease Prevention. Elsevier, 2010. http://dx.doi.org/10.1016/b978-0-12-374420-3.00094-2.

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ro Gotoh, Naohi, and Hiroyuki Shimasaki. "Suppressive Effects of Diacylglycerol Oil on Postprandial Serum Triglyceride Elevation in Animals." In Diacylglycerol Oil. AOCS Publishing, 2004. http://dx.doi.org/10.1201/9781439822333.ch7.

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Conference papers on the topic "Postprandial triglycerides"

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Thomas, David, Emma Bermingham, Mark Roberts, and Wayne Young. "An investigation into the effect of high fat and carbohydrate diets on a range of biomarkers associated with pancreatitis in dogs." In 2022 AOCS Annual Meeting & Expo. American Oil Chemists' Society (AOCS), 2022. http://dx.doi.org/10.21748/uvdt4784.

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Studies suggest that dogs preferentially choose fat as their major dietary energy source (59-63% of the total metabolisable energy (ME) content of the diet). However, high fat diets have been linked to the development of pancreatitis in dogs. This study investigated several biomarkers associated with pancreatitis in dogs fed either a high fat (HF; Protein: Fat: Carbohydrate content; 35%:63%:2% ME; n= 10 dogs) or high carbohydrate (HC; Protein: Fat: Carbohydrate content; 17%:32%:51% ME) diet.A high fat meal tolerance test (MTT) was undertaken on dogs (n=20) at baseline consuming a commercial dr
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