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Journal articles on the topic 'Postprandial hypertriglyceridemia'

Author: Grafiati

Published: 4 June 2021

Last updated: 2 February 2022

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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 acid

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2

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-hydroxybuty

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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 in

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5

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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6

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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7

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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8

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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9

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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10

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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11

Kassem, Hania S., Mira S. Zantout, and Sami T. Azar. "Gemfibrozil Improves Postprandial Hypertriglyceridemia in Patients with Isolated Low HDL." Lipid Insights 4 (January 2011): LPI.S5722. http://dx.doi.org/10.4137/lpi.s5722.

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Aim To assess the response of postprandial (PP) hypertriglyceridemia to genfibrozil in healthy male subjects with isolated low HDL-Cholesterol but without the metabolic syndrome (MS). Patients and methods 14 male subjects with isolated low HDL (HDL-C ≤ 33), normal fasting triglycerides and LDL-C levels and without any feature of the MS, were studied. 13 male subjects with HDL-C > 38 mg/dl served as controls. They also had normal fasting triglycerides and LDL-C levels and without any feature of the MS. The 2 groups were statistically similar with respect to age, blood pressure, BMI, body fat

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12

Leary, Miriam, and Hirofumi Tanaka. "Role of Fluid Milk in Attenuating Postprandial Hyperglycemia and Hypertriglyceridemia." Nutrients 12, no. 12 (2020): 3806. http://dx.doi.org/10.3390/nu12123806.

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Postprandial plasma glucose and triglyceride concentrations are predictive of relative cardiovascular disease (CVD) risk, and the pathogenesis of both insulin resistance and atherosclerosis has been attributed to acute states of hyperglycemia and hypertriglyceridemia. Postprandial lipemia and hyperglycemia suppress vascular reactivity and induce endothelial dysfunction. Epidemiological studies suggest that chronically-high consumption of milk and milk products is associated with a reduced risk of type 2 diabetes, metabolic syndrome, and CVD. The addition of dairy products to meals high in carb

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13

Oliveira, Paula Lima de, Stéfany Lima Souza, Natália Camila Minucci Bonatto, et al. "Effect of food intake on complete blood count of healthy dogs." Revista Agraria Academica 3, no. 6 (2020): 105–16. http://dx.doi.org/10.32406/v3n62020/105-116/agrariacad.

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The present determined the hematological alterations of healthy dogs at the peak of postprandial hypertriglyceridemia. Twenty-four clinically healthy dogs had blood samples collected to perform complete blood count on three consecutive days at the same time every day: first day after a 12-hour fast; second day three hours after feeding with commercial feed, during the peak of postprandial lipemia; and third day after a 12-hour fast. Feeding led to an increase in MCHC, hemoglobin and white blood cell count due to the increase in segmented neutrophil, monocyte and eosinophil concentrations. A si

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14

Sandoval, José C., Yumiko Nakagawa-Toyama, Daisaku Masuda, et al. "Fenofibrate Reduces Postprandial Hypertriglyceridemia in CD36 Knockout Mice." Journal of Atherosclerosis and Thrombosis 17, no. 6 (2010): 610–18. http://dx.doi.org/10.5551/jat.3988.

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15

ZIOGAS, GEORGE G., TOM R. THOMAS, and WILLIAM S. HARRIS. "Exercise training, postprandial hypertriglyceridemia, and LDL subfraction distribution." Medicine &amp Science in Sports &amp Exercise 29, no. 8 (1997): 986–91. http://dx.doi.org/10.1097/00005768-199708000-00002.

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16

Sairyo, M., D. Masuda, T. Kobayashi, et al. "DPP4 inhibitor, anagliptin, ameliorates fasting and postprandial hypertriglyceridemia." Atherosclerosis 252 (September 2016): e213. http://dx.doi.org/10.1016/j.atherosclerosis.2016.07.159.

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17

Bae, Jang Ho, Kwon Bae Kim, Hee Ja Lee, et al. "Postprandial Hypertriglyceridemia Following a Single High-Fat Meal in Patients with Coronary Artery Disease and Normal Subjects: The Significance of the Postprandial Hypertriglyceridemia and the Effects of Fibrate on the Postprandial Hypertriglyceridemia." Korean Circulation Journal 29, no. 7 (1999): 680. http://dx.doi.org/10.4070/kcj.1999.29.7.680.

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18

Lino, Marsel, Sarah Farr, Chris Baker, Mark Fuller, Bernardo Trigatti, and Khosrow Adeli. "Intestinal scavenger receptor class B type I as a novel regulator of chylomicron production in healthy and diet-induced obese states." American Journal of Physiology-Gastrointestinal and Liver Physiology 309, no. 5 (2015): G350—G359. http://dx.doi.org/10.1152/ajpgi.00086.2015.

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The small intestine contributes to diabetic dyslipidemia through the overproduction of apolipoprotein B48 (apoB48)-containing chylomicron particles. An important regulator of chylomicron generation is dietary lipid absorption, underlining the potential involvement of intestinal lipid transporters for developing dyslipidemia. Intestinal expression of scavenger receptor class B type I (SR-BI) has been found to be upregulated in animal models of insulin resistance. Here we characterized the potential importance of SR-BI in contributing to chylomicron production and postprandial hypertriglyceridem

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19

Ohno, Yuko, Hiroki Oe, Toru Miyoshi, et al. "Bezafibrate Improves Postprandial Hypertriglyceridemia and Postprandial Endothelial Dysfunction in Patients with Metabolic Syndrome." Journal of Cardiac Failure 19, no. 10 (2013): S172. http://dx.doi.org/10.1016/j.cardfail.2013.08.484.

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20

Garcés Da Silva, María, Yamil Guarin, Yenny Carrero, et al. "Postprandial Hypertriglyceridemia Is Associated with the Variant 54 Threonine FABP2 Gene." Journal of Cardiovascular Development and Disease 5, no. 3 (2018): 47. http://dx.doi.org/10.3390/jcdd5030047.

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Purpose: Fasting or postprandial hypertriglyceridemia is considered an independent cardiovascular disease (CVD) risk factor. The intestinal fatty acid binding protein (FABP2) is involved in the intracellular transport and metabolism of fatty acids. The presence of the Ala54Thr polymorphism of the FABP2 gene appears to be involved in postprandial hypertriglyceridemia. We explored the possible association of the Ala54Thr polymorphism with fat intolerance in apparently healthy, fasting, normolipidemic subjects with normal body-mass index and without diabetes. Methodology: A total of 158 apparentl

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21

Van de Wiel, Albert. "The Effect of Alcohol on Postprandial and Fasting Triglycerides." International Journal of Vascular Medicine 2012 (2012): 1–4. http://dx.doi.org/10.1155/2012/862504.

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Alcohol has a significant additive effect on the postprandial triglyceride peak when it accompanies a meal containing fat, especially saturated fat. This results from a decrease in the breakdown of chylomicrons and VLDL remnants due to an acute inhibitory effect of alcohol on lipoprotein lipase activity. Furthermore, alcohol increases the synthesis of large VLDL particles in the liver, which is the main source of triglycerides in the hypertriglyceridemia associated with chronic excessive alcohol intake. In case of chronic consumption, lipoprotein lipase activity seems to adapt itself. The effe

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22

Sandoval, José C., Yumiko Nakagawa-Toyama, Daisaku Masuda, et al. "Molecular Mechanisms of Ezetimibe-Induced Attenuation of Postprandial Hypertriglyceridemia." Journal of Atherosclerosis and Thrombosis 17, no. 9 (2010): 914–24. http://dx.doi.org/10.5551/jat.4929.

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23

Sniderman, A. D. "Postprandial hypertriglyceridemia(s): time to enlarge our pathophysiologic perspective." European Journal of Clinical Investigation 30, no. 11 (2000): 935–37. http://dx.doi.org/10.1046/j.1365-2362.2000.00733.x.

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24

Hotoleanu, C., M. L. Rusu, M. Porojan-Iuga, and D. L. Rusu. "PO21-664 POSTPRANDIAL HYPERTRIGLYCERIDEMIA: RISK FACTOR IN METABOLIC SYNDROME." Atherosclerosis Supplements 8, no. 1 (2007): 178. http://dx.doi.org/10.1016/s1567-5688(07)71674-4.

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25

Bae, Jang-Ho, Eberhard Bassenge, Kwon-Bae Kim, et al. "Postprandial hypertriglyceridemia impairs endothelial function by enhanced oxidant stress." Atherosclerosis 155, no. 2 (2001): 517–23. http://dx.doi.org/10.1016/s0021-9150(00)00601-8.

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26

Kurihara, Hiroshi, Hiroshi Shibata, Yuko Fukui, et al. "Evaluation of the Hypolipemic Property ofCamellia sinensisVar.ptilophyllaon Postprandial Hypertriglyceridemia." Journal of Agricultural and Food Chemistry 54, no. 14 (2006): 4977–81. http://dx.doi.org/10.1021/jf0603681.

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27

Ferreira, Alexandre C., Arley A. Peter, Armando J. Mendez, et al. "Postprandial Hypertriglyceridemia Increases Circulating Levels of Endothelial Cell Microparticles." Circulation 110, no. 23 (2004): 3599–603. http://dx.doi.org/10.1161/01.cir.0000148820.55611.6b.

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28

Leon-Acuña, Ana, Jose D. Torres-Peña, Juan F. Alcala-Diaz, et al. "Lifestyle factors modulate postprandial hypertriglyceridemia: From the CORDIOPREV study." Atherosclerosis 290 (November 2019): 118–24. http://dx.doi.org/10.1016/j.atherosclerosis.2019.09.025.

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29

Egashira, Yukari, Tomoko Kamohara, Wataru Yamaguchi, et al. "Suppression of Postprandial Hypertriglyceridemia in Rats by Benifuuki Tea Extract." Nippon Shokuhin Kagaku Kogaku Kaishi 60, no. 8 (2013): 407–11. http://dx.doi.org/10.3136/nskkk.60.407.

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30

Sandoval, J., Y. Toyama, D. Masuda, et al. "Abstract: P416 FENOFIBRATE REDUCES POSTPRANDIAL HYPERTRIGLYCERIDEMIA IN CD36-DEFICIENT MICE." Atherosclerosis Supplements 10, no. 2 (2009): e726. http://dx.doi.org/10.1016/s1567-5688(09)70711-1.

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31

Cardona, F., S. Morcillo, M. Gonzalo-Marin, and F. J. Tinahones. "W11-O-001 The apolipoprotein E genotype predicts postprandial hypertriglyceridemia." Atherosclerosis Supplements 6, no. 1 (2005): 56. http://dx.doi.org/10.1016/s1567-5688(05)80223-5.

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32

Higashi, K., H. Shige, T. Ito, et al. "Impaired Glucose Tolerance Without Hypertriglyceridemia Does not Enhance Postprandial Lipemia." Hormone and Metabolic Research 33, no. 2 (2001): 101–5. http://dx.doi.org/10.1055/s-2001-12400.

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33

Katsanos, Christos S., and Robert J. Moffatt. "Acute Effects of Premeal Versus Postmeal Exercise on Postprandial Hypertriglyceridemia." Clinical Journal of Sport Medicine 14, no. 1 (2004): 33–39. http://dx.doi.org/10.1097/00042752-200401000-00006.

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34

Saito, Shinichiro, Toru Yamaguchi, Kentaro Shoji, Masanobu Hibi, Toshiro Sugita, and Hideto Takase. "Effect of low concentration of diacylglycerol on mildly postprandial hypertriglyceridemia." Atherosclerosis 213, no. 2 (2010): 539–44. http://dx.doi.org/10.1016/j.atherosclerosis.2010.07.062.

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35

Zhang, John Q., Lisa L. Ji, Vicki S. Fretwell, and Guadalupe Nunez. "Effect of exercise on postprandial lipemia in men with hypertriglyceridemia." European Journal of Applied Physiology 98, no. 6 (2006): 575–82. http://dx.doi.org/10.1007/s00421-006-0304-8.

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36

Zhang, John Q., Lisa L. Ji, Donovan L. Fogt, and Vicki S. Fretwell. "Effect of exercise duration on postprandial hypertriglyceridemia in men with metabolic syndrome." Journal of Applied Physiology 103, no. 4 (2007): 1339–45. http://dx.doi.org/10.1152/japplphysiol.00181.2007.

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We examined the effect of exercise on postprandial hypertriglyceridemia (PHTG) and insulin resistance in individuals with metabolic syndrome. Subjects were 10 hypertriglyceridemic men with insulin resistance [age = 35.0 ± 1.8 yr, body weight = 90.7 ± 3.3 kg, fasting triglyceride (TG) = 2.6 ± 0.4 mmol/l, peak oxygen consumption (V̇o2peak) = 36.0 ± 1.3 ml−1·kg−1·min−1, and homeostatic model assessment of insulin resistance (HOMA-IR)= 3.1 ± 0.3]. Each participant performed a control trial (Ctr; no exercise) and three exercise trials at 60% of their V̇o2peak for 30 min (30 min-Ex), 45 min (45 min-

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37

Sato, Daisuke, Katsutaro Morino, Fumiyuki Nakagawa, et al. "Acute Effect of Metformin on Postprandial Hypertriglyceridemia through Delayed Gastric Emptying." International Journal of Molecular Sciences 18, no. 6 (2017): 1282. http://dx.doi.org/10.3390/ijms18061282.

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38

G. Nordestgaard, Borge, and Jacob J. Freiberg. "Clinical Relevance of Non-Fasting and Postprandial Hypertriglyceridemia and Remnant Cholesterol." Current Vascular Pharmacology 9, no. 3 (2011): 281–86. http://dx.doi.org/10.2174/157016111795495585.

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39

Gudmundsson, G. Steinar, Christine A. Sinkey, Catherine A. Chenard, Phyllis J. Stumbo, and William G. Haynes. "Resistance vessel endothelial function in healthy humans during transient postprandial hypertriglyceridemia." American Journal of Cardiology 85, no. 3 (2000): 381–85. http://dx.doi.org/10.1016/s0002-9149(99)00751-1.

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40

Otto, Carsten, Volkhard Pschierer, Andreas C. Soennichsen, Peter Schwandt, and Werner O. Richter. "Postprandial hemorrheology and apolipoprotein B metabolism in patients with familial hypertriglyceridemia." Metabolism 46, no. 11 (1997): 1299–304. http://dx.doi.org/10.1016/s0026-0495(97)90234-1.

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41

G. Nordestgaard, Borge, and Jacob J. Freiberg. "Clinical Relevance of Non-Fasting and Postprandial Hypertriglyceridemia and Remnant Cholesterol." Current Vascular Pharmacology 999, no. 999 (2011): 1–6. http://dx.doi.org/10.2174/1570211213146301611.

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42

Zhang, J. Q., L. L. Ji, V. Fretwell, et al. "EFFECT OF EXERCISE INTENSITY ON POSTPRANDIAL LIPEMIA IN PATIENTS WITH HYPERTRIGLYCERIDEMIA." Medicine & Science in Sports & Exercise 35, Supplement 1 (2003): S87. http://dx.doi.org/10.1097/00005768-200305001-00476.

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43

Zhang, Tianhua, Xiaoyu Tang, Ling Mao, et al. "HDL-associated apoCIII plays an independent role in predicting postprandial hypertriglyceridemia." Clinical Biochemistry 79 (May 2020): 14–22. http://dx.doi.org/10.1016/j.clinbiochem.2020.02.004.

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44

Simo, I. E., J. A. Yakichuk, M. Cousins, P. V. N. Murthy, and T. C. Ooi. "Metabolism of postprandial VLDL subfractions in the hypoalphalipoproteinemia and hypertriglyceridemia syndrome." Atherosclerosis 109, no. 1-2 (1994): 128–29. http://dx.doi.org/10.1016/0021-9150(94)93525-4.

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45

Desmarchelier, Charles, Patrick Borel, Denis Lairon, Marie Maraninchi, and René Valéro. "Effect of Nutrient and Micronutrient Intake on Chylomicron Production and Postprandial Lipemia." Nutrients 11, no. 6 (2019): 1299. http://dx.doi.org/10.3390/nu11061299.

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Postprandial lipemia, which is one of the main characteristics of the atherogenic dyslipidemia with fasting plasma hypertriglyceridemia, low high-density lipoprotein cholesterol and an increase of small and dense low-density lipoproteins is now considered a causal risk factor for atherosclerotic cardiovascular disease and all-cause mortality. Postprandial lipemia, which is mainly related to the increase in chylomicron production, is frequently elevated in individuals at high cardiovascular risk such as obese or overweight patients, type 2 diabetic patients and subjects with a metabolic syndrom

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46

Zhang, John Q., Lisa L. Ji, Guadalupe Nunez, Scott Feathers, Curtis L. Hart, and Wan Xiang Yao. "Effect of Exercise Timing on Postprandial Lipemia in Hypertriglyceridemic Men." Canadian Journal of Applied Physiology 29, no. 5 (2004): 590–603. http://dx.doi.org/10.1139/h04-038.

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We investigated the effect of exercise timing on attenuation of postprandial hyper-triglyceridemia (PHTG) in individuals with hypertriglyceridemia (HTG). Subjects were 10 males (TG = 290.1 ± 28.5 mg/dl). Each subject performed a control trial (Ctr), 12-hr premeal exercise trial (12-hr Pre), and 24-hr premeal exercise trial (24-hr Pre). In each trial, subjects had a fat-rich meal. In the exercise trials they jogged on a treadmill at 60% of their [Formula: see text] for 1 hr at a designated time. Blood samples were taken at 0 (immediately before the fat meal), and at 2, 4, 6, 8, and 24 hrs after

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47

Hiel, Sophie, Audrey Neyrinck, Julie Rodriguez, et al. "Inulin Improves Postprandial Hypertriglyceridemia by Modulating Gene Expression in the Small Intestine." Nutrients 10, no. 5 (2018): 532. http://dx.doi.org/10.3390/nu10050532.

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48

Geloen, Alain, Lionel Helin, Benjamine Geeraert, Eric Malaud, Paul Holvoet, and Gerard Marguerie. "CD36 Inhibitors Reduce Postprandial Hypertriglyceridemia and Protect against Diabetic Dyslipidemia and Atherosclerosis." PLoS ONE 7, no. 5 (2012): e37633. http://dx.doi.org/10.1371/journal.pone.0037633.

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49

Rosenson, Robert S., and Irene B. Helenowski. "Fenofibrate abrogates postprandial blood viscosity among hypertriglyceridemia subjects with the metabolic syndrome." Diabetes & Metabolic Syndrome: Clinical Research & Reviews 3, no. 1 (2009): 17–23. http://dx.doi.org/10.1016/j.dsx.2008.10.004.

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50

Lambadiari, Vaia, Emmanouil Korakas, and Vasilios Tsimihodimos. "The Impact of Dietary Glycemic Index and Glycemic Load on Postprandial Lipid Kinetics, Dyslipidemia and Cardiovascular Risk." Nutrients 12, no. 8 (2020): 2204. http://dx.doi.org/10.3390/nu12082204.

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Many recent studies have acknowledged postprandial hypetriglyceridemia as a distinct risk factor for cardiovascular disease. This dysmetabolic state is the result of the hepatic overproduction of very low-density lipoproteins (VLDLs) and intestinal secretion of chylomicrons (CMs), which leads to highly atherogenic particles and endothelial inflammation. Postprandial lipid metabolism does not only depend on consumed fat but also on the other classes of nutrients that a meal contains. Various mechanisms through which carbohydrates exacerbate lipidemia have been identified, especially for fructos

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