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Relevant bibliographies by topics / Postprandial hypertriglyceridemia

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Academic literature on the topic 'Postprandial hypertriglyceridemia'

Author: Grafiati

Published: 4 June 2021

Last updated: 2 February 2022

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Journal articles on the topic "Postprandial hypertriglyceridemia"

1

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 acids (SFA), mono-unsaturated fatty acids (MUFA), or medium-chain fatty acids (MCFA) in a randomized order. Fasting and postprandial lipid parameters were determined over a 10 h period and the (incremental) area under the curve (AUC/iAUC) for plasma triglycerides and other parameters were determined. MCFA do not lead to a significant elevation of postprandial total plasma triglycerides and other triglyceride parameters, while both SFA (patients: p = 0.003, controls: p = 0.03 compared to MCFA) and MUFA (patients: p = 0.001; controls: p = 0.14 compared to MCFA) do lead to such an increase. Patients experienced a significantly more pronounced increase of plasma triglycerides than controls (SFA: patients iAUC = 1006 mg*h/dL, controls iAUC = 247 mg*h/dL, p = 0.02; MUFA: patients iAUC = 962 mg*h/dL, controls iAUC = 248 mg*h/dL, p = 0.05). Replacing SFA with MCFA may be a treatment option for mildly to moderately hypertriglyceridemic patients as it prevents postprandial hypertriglyceridemia.

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Vega, Gloria Lena, Fredrick L. Dunn, and Scott M. Grundy. "Impaired Hepatic Ketogenesis in Moderately Obese Men With Hypertriglyceridemia." Journal of Investigative Medicine 57, no. 4 (2009): 590–94. http://dx.doi.org/10.2310/jim.0b013e31819e2f61.

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BackgroundSeveral studies suggest that increased nonesterified fatty acid flux and increased de novo lipogenesis may contribute to hypertriglyceridemia, but few studies have examined fatty acid oxidation as a factor.RationaleEndogenous hypertriglyceridemia (increased very low density lipoprotein triglyceride) could result from (a) re-esterification of excess nonesterified fatty acids entering the liver, (b) activation of hepatic lipogenesis, and/or (c) defective oxidation of hepatic fatty acids leading to greater triglyceride synthesis. Therefore, this study used plasma levels of 3-hydroxybutyrate as a marker for fatty acid oxidation. The study was carried out in hypertriglyceridemic and normotriglyceridemic subjects under 3 conditions: (a) in the fasting state, (b) after a fatty meal that should enhance fatty acid oxidation, and (c) after an oxandrolone challenge, which we recently showed increases fatty acid oxidation.ResultsIn the fasting state, 3-hydroxybutyrate concentrations in hypertriglyceridemic patients were only 53% of levels in normotriglyceridemic subjects. After a fatty meal, moderate increases in 3-hydroxybutyrate were observed, but values for patients with hypertriglceridemia remained 62% of the levels in the normotriglyceridemic group. A similar pattern of response was observed with oxandrolone challenge. There were no significant changes in fasting or postprandial levels of nonesterfified fatty acids, glycerol, or triglycerides before and during the oxandrolone challenge.ConclusionPatients with endogenous hypertriglyceridemia seem to have a defect in fatty acid oxidation as indicated by reduced levels of 3-hydroxybutyrate. This defect was observed during fasting, postprandially, and during oxandrolone challenge. We propose that this defect contributes to the development of hypertriglyceridemia.

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3

Masuda, D., T. Kobayashi, T. Okada, et al. "Eicosapentaenoic acid ameriolates postprandial hypertriglyceridemia." Atherosclerosis 235, no. 2 (2014): e104-e105. http://dx.doi.org/10.1016/j.atherosclerosis.2014.05.281.

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4

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 insulin resistance and insulin sensitivity. At 3 h, we measured triglycerides, cholesterol, apolipoprotein AI, and apolipoprotein B. Patients were considered to have postprandial hypertriglyceridemia if the difference in plasma triglycerides between baseline and 3 h after the test was 1.71 mmol/L or more. We also measured anthropometrical variables and classified the patients according to their peroxisome proliferative activated receptor, gamma (PPARG) gene and apolipoprotein E (APOE) genotype. Results: Postprandial hypertriglyceridemia occurred in 64.7% of patients with the Ala12 allele vs 19.9% of the Pro12Pro patients, (P = 0.00032; odds ratio, 7.6), and in 87.5% of the patients with both the Ala12 allele and the non-E3/E3 APOE genotype (odds ratio, 23.8). Logistic regression analysis showed that PPARG and APOE sequence variants were associated with the presence of postprandial hypertriglyceridemia. Conclusion: The Pro12Ala PPARG sequence variant together with a non-E3/E3 APOE genotype is associated with a high risk for postprandial hypertriglyceridemia in patients with the metabolic syndrome, indicating a close association between these genes and the regulation of lipoproteinase clearance.

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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 increased two- to fourfold postprandially, but only minimally (30%) in HSHF-fed rats. Muscle LPL decreased postprandially in HSHF-fed rats, suggesting intact sensitivity to insulin, but it increased in chow-fed animals. Peak postprandial triglyceridemia was higher (+70%) in insulin-resistant than in control rats. The postprandial rate of appearance of triglycerides in the circulation was similar in control and insulin-resistant rats, indicating that hypertriglyceridemia of the latter was the result of impaired clearance. These results demonstrate that adipose LPL becomes resistant to insulin in diet-induced IR and further suggest that, under certain nutritional conditions, modifications in adipose LPL modulation associated with insulin resistance, along with low muscle LPL, heightens postprandial hypertriglyceridemia through attenuated triglyceride clearance.

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Ooi, T. C. "Postprandial Remnant-like Lipoproteins in Hypertriglyceridemia." Journal of Clinical Endocrinology & Metabolism 86, no. 7 (2001): 3134–42. http://dx.doi.org/10.1210/jc.86.7.3134.

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Kabagambe, Edmond K., Jose M. Ordovas, Michael Y. Tsai, et al. "Smoking, inflammatory patterns and postprandial hypertriglyceridemia." Atherosclerosis 203, no. 2 (2009): 633–39. http://dx.doi.org/10.1016/j.atherosclerosis.2008.08.005.

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Kuntarattanakool, M., N. Isarakul, O. Tangvarasittichai, and Surapon Tangvarasittichai. "Postprandial Dysmetabolism (Postprandial Hyperglycemia and Hypertriglyceridemia) in Type 2 Diabetes Patients." Madridge Journal of Diabetes 2, no. 1 (2018): 47–50. http://dx.doi.org/10.18689/mjd-1000109.

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Matsuda, Hiroko, Kodai Kumazaki, Ryo Otokozawa, Mamiko Tanaka, Eri Udagawa, and Takaaki Shirai. "Resistant starch suppresses postprandial hypertriglyceridemia in rats." Food Research International 89 (November 2016): 838–42. http://dx.doi.org/10.1016/j.foodres.2016.10.022.

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Borén, Jan, Niina Matikainen, Martin Adiels, and Marja-Riitta Taskinen. "Postprandial hypertriglyceridemia as a coronary risk factor." Clinica Chimica Acta 431 (April 2014): 131–42. http://dx.doi.org/10.1016/j.cca.2014.01.015.

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Dissertations / Theses on the topic "Postprandial hypertriglyceridemia"

1

Zhang, Qiang. "Effect of acute exercise on postprandial lipemia and HDL cholesterol subfractions /." free to MU campus, to others for purchase, 1997. http://wwwlib.umi.com/cr/mo/fullcit?p9842578.

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2

Brown, Malcolm. "The acute effects of exercise and postprandial hypertriglyceridemia on physiological and biochemical risk factors for disease." Thesis, Ulster University, 2016. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.701436.

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Oxidative stress is an integral component in the pathology of cardiovascular disease, the leading cause of global mortality. Metabolic disturbances observed during postprandial hypertriglyceridemia have been identified as an independent risk factor within the aetiology of this disease, mainly via oxidative stress and pro-inflammatory mechanisms. Physical exercise has shown promising signs in ameliorating the symptoms of cardiovascular disease, but its role in the generation of oxidative stress, inflammation and associated molecular damage to lipids, protein and DNA is not fully understood. The principal aim of this thesis is to examine the transient effects of differing walking exercise trials on free radical metabolism, inflammation and subsequent molecular damage over time, in conditions of fasting and metabolic disturbance.

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3

Park, Sanghee. "Effects of prolonged sitting and walking for two days on postprandial triglycerides in men : interaction with energy intake." Thesis, 2011. http://hdl.handle.net/2152/ETD-UT-2011-05-2708.

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Postprandial hypertriglyceridemia (PPHT), an independent risk factor for atherosclerosis (Smyth and Heron 2006; Nordestgaard, Benn et al. 2007), is strongly associated with metabolic syndrome and cardiovascular diseases (CVD) (Kolovou, Anagnostopoulou et al. 2005). It has been proposed that elevated triglycerides after a high-fat meal may be a postprandial phenomenon (Zilversmit 1979). PPHT are commonly concurrent with sedentary behaviors, such as extended sitting, which amplify PPHT (Levine, Vander Weg et al. 2006). The purpose of this study was to examine the effects of prolonged sitting with or without a balanced caloric diet and walking with a balanced diet on postprandial triglycerides (PPTG). Seven healthy, young men (age, 25.6 ± 3.7 y; height, 174 ± 5 cm; weight, 71.4 ± 6.2kg; VO2max, 49.3 ± 7.7 ml/kg/min) were recruited from a college and from within the Austin community. After 2 days of food and activity control (D1and D2), subjects performed one of three trials in a randomized, cross-over design for 2 days (D3 and D4); (1) active walking with a balanced diet (WB), (2) prolonged sitting with a hyper-caloric diet (SH), and (3) prolonged sitting with a balanced diet (SB). High fat tolerance tests (HFTT) were conducted on the following day, (D5), after 13 hour over-night fasting. Blood samples were obtained in the fasting state and every hour for 6 hours after subjects had eaten a high fat test meal consisting of 1.2 g fat, 1.1 g CHO, 0.2 g protein/kg body mass. All food was provided during the 5-day duration of the study. Body postures, heart rate, and daily steps were monitored. In both sit trials (SH and SB), subjects sat ~320 minutes longer and took 10 times fewer steps than WB. In WB, the total area under the curves for plasma triglycerides (AUC[subscript T] TG) was lower, compared to SH by 21.3% (p<0.001) and to SB by 19.7% (N.S.; p = 0.055), respectively. In WB, the incremental AUC TG (AUC[subscript I] TG), an index of postprandial response, was lower than both SH by 17.4% (p <0.005) and SB by 20.1% (p <0.05), respectively. Postprandial plasma insulin concentration was lower in WB, compared to SH by 19.4% (p <0.005) in AUC[scubscript T] and 18.8 % (p < 0.05) in AUC[subscript I]. No differences were shown in the metabolic responses between SB and SH despite the diet modifications. These findings indicate that two days of prolonged sitting significantly amplifies PPTG and suppresses insulin action.<br>text

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