Chylomicronemia elicits atherosclerosis in mice—brief report.
Open accessAbstract
OBJECTIVE: The risk of atherosclerosis in the setting of chylomicronemia has been a topic of debate. In this study, we examined susceptibility to atherosclerosis in Gpihbp1-deficient mice (Gpihbp1(-/-)), which manifest severe chylomicronemia as a result of defective lipolysis. METHODS AND RESULTS: Gpihbp1(-/-) mice on a chow diet have plasma triglyceride and cholesterol levels of 2812+/-209 and 319+/-27 mg/dL, respectively. Even though nearly all of the lipids were contained in large lipoproteins (50 to 135 nm), the mice developed progressive aortic atherosclerosis. In other experiments, we found that both Gpihbp1-deficient "apo-B48-only" mice and Gpihbp1-deficient "apo-B100-only" mice manifest severe chylomicronemia. Thus, GPIHBP1 is required for the processing of both apo-B48- and apo-B100-containing lipoproteins. CONCLUSIONS: Chylomicronemia causes atherosclerosis in mice. Also, we found that GPIHBP1 is required for the lipolytic processing of both apo-B48- and apo-B100-containing lipoproteins.
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A variety of animal models produced using dietary or genetic manipulations have confirmed that chylomicron remnants are atherogenic.
“A variety of animal models produced using dietary or genetic manipulations have confirmed that chylomicron remnants are atherogenic (139, 144).”
From Evaluation and Treatment of Hypertriglyceridemia: An Endocrine Society Clinical Practice Guideline (2012) · cites this paper as [139]
The Introduction states that human and mouse studies have shown cholesterol-rich remnants cause atherosclerosis. But the Methods and Discussion describe this paper’s own experiment as a genetic mouse model fed low-fat chow: it found atherosclerosis with severe chylomicronemia, not that a variety of dietary and genetic models confirmed the atherogenicity of chylomicron remnants. Page numbers are unavailable in our copy. (LLM, conf=0.86)
Experimental — accuracy not yet measuredSeverely hypertriglyceridemic animals, especially genetically modified mice, develop only early-stage lesions.
“Although there are a number of severely hypertriglyceridemic animals, especially genetically modified mice, these animals develop only early-stage lesions (138, 139).”
From Evaluation and Treatment of Hypertriglyceridemia: An Endocrine Society Clinical Practice Guideline (2012) · cites this paper as [139]
The Discussion (page unavailable) says lesions in severely hypertriglyceridemic Gpihbp1-deficient mice are small and develop more slowly than those in Apoe- or Ldlr-deficient mice. The Results (page unavailable) report that the lesions become larger with age. The paper does not classify them as only early-stage lesions or establish that this holds for severely hypertriglyceridemic animals generally. (LLM, conf=0.83)
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Cites
Beigneux, A. P., Davies, B. S. J., Gin, P., Weinstein, M. M., Farber, E., Qiao, X., Peale, F. V., Jr., Bunting, S., Walzem, R. L., Wong, J. S., et al. (2007) · Cell Metabolism · doi:10.1016/j.cmet.2007.02.002 · Cited by 470 · see citing works
Self-citationBenlian, P., Gennes, J. L. D., Foubert, L., Zhang, H., Gagné, S., & Hayden, M. R. (1996) · New England Journal of Medicine · doi:10.1056/nejm199609193351203 · Cited by 296 · see citing works
Chylomicronemia With a Mutant GPIHBP1 (Q115P) That Cannot Bind Lipoprotein Lipase
Beigneux, A. P., Franssen, R., Bensadoun, A., Gin, P., Melford, K., Peter, J., Walzem, R. L., Weinstein, M. M., Davies, B. S. J., Kuivenhoven, J. A., et al. (2009) · Arteriosclerosis Thrombosis and Vascular Biology · doi:10.1161/atvbaha.109.186577 · Cited by 160 · see citing works
Self-citationLarge lipoproteins are excluded from the arterial wall in diabetic cholesterol-fed rabbits
Nordestgaard, B. G., & Zilversmit, D. B. (1988) · Journal of Lipid Research · doi:10.1016/s0022-2275(20)38428-5 · Cited by 156 · see citing works
Adenovirus-mediated Rescue of Lipoprotein Lipase-deficient Mice
Bogner‐Strauß, J. G., Frank, S., Kratky, D., Hämmerle, G., Hrzenjak, A., Knipping, G., von Eckardstein, A., Kostner, G. M., & Zechner, R. (2001) · Journal of Biological Chemistry · doi:10.1074/jbc.m104430200 · Cited by 103 · see citing works
Véniant, M. M., Pierotti, V, Newland, D., Cham, C. M., Sanan, D. A., Walzem, R. L., & Young, S. G. (1997) · Journal of Clinical Investigation · doi:10.1172/jci119511 · Cited by 100 · see citing works
Self-citationZhang, X., Qi, R., Xian, X., Yang, F., Blackstein, M., Deng, X., Fan, J., Ross, C., Karasinska, J., Hayden, M. R., et al. (2008) · Circulation Research · doi:10.1161/circresaha.107.156554 · Cited by 98 · see citing works
Why does the gut choose apolipoprotein B48 but not B100 for chylomicron formation?
Lo, C. C., Nordskog, B. K., Nauli, A. M., Zheng, S., vonLehmden, S. B., Yang, Q., Lee, D., Swift, L. L., Davidson, N. O., & Tso, P. (2007) · American Journal of Physiology-Gastrointestinal and Liver Physiology · doi:10.1152/ajpgi.00123.2007 · Cited by 83 · see citing works
Triglycerides and Coronary Heart Disease Revisited (Again)
Criqui, M. H. (2007) · Annals of Internal Medicine · doi:10.7326/0003-4819-147-6-200709180-00014 · Cited by 15 · see citing works
Flagged first, then by citations
Cited by
Sorted by citations
Chapman, M. J., Ginsberg, H. N., Amarenco, P., Andreotti, F., Borén, J., Catapano, A. L., Descamps, O. S., Fisher, E., Kovanen, P. T., Kuivenhoven, J. A., et al. (2011) · European Heart Journal · doi:10.1093/eurheartj/ehr112 · Cited by 1,227 · see citing works
“Others observed the opposite,(95) consistent with experimental data in animal models.(96,97) However, the rarity of this disease prevents firm conclusions to be made.”
ResultEvaluation and Treatment of Hypertriglyceridemia: An Endocrine Society Clinical Practice Guideline
Berglund, L., Brunzell, J. D., Goldberg, A. C., Goldberg, I. J., Sacks, F., Murad, M. H., & Stalenhoef, A. F. H. (2012) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jc.2011-3213 · Cited by 887 · see citing works
Molecular Biology of Atherosclerosis
Hopkins, P. N. (2013) · Physiological Reviews · doi:10.1152/physrev.00004.2012 · Cited by 456 · see citing works
Biochemistry and pathophysiology of intravascular and intracellular lipolysisPreprint
Young, S. G., & Zechner, R. (2013) · Genes & Development · doi:10.1101/gad.209296.112 · Cited by 344 · see citing works
“2008) and GPIHBP1-deficient mice (Weinstein et al. 2010) develop spontaneous atherosclerosis even on a lowfat chow diet.”
BackgroundSelf-citationTriglyceride lpases and atherosclerosis
Olivecrona, G., & Olivecrona, T. (1995) · Current Opinion in Lipidology · doi:10.1097/00041433-199510000-00009 · Cited by 238 · see citing works
Triglycerides and Heart Disease
Goldberg, I. J., Eckel, R. H., & McPherson, R. (2011) · Arteriosclerosis Thrombosis and Vascular Biology · doi:10.1161/atvbaha.111.226100 · Cited by 219 · see citing works
Cardiovascular disease in diabetes, beyond glucose
Eckel, R. H., Bornfeldt, K., & Goldberg, I. J. (2021) · Cell Metabolism · doi:10.1016/j.cmet.2021.07.001 · Cited by 224 · see citing works
The metabolism of triglyceride-rich lipoproteins revisited: New players, new insight
Dallinga‐Thie, G. M., Franssen, R., Mooij, H. L., Visser, M. E., Hassing, H. C., Peelman, F., Kastelein, J. J. P., Péterfy, M., & Nieuwdorp, M. (2009) · Atherosclerosis · doi:10.1016/j.atherosclerosis.2009.12.027 · Cited by 181 · see citing works
“[61] In line with these observation is the identification of atherosclerosis in aged GPIHBP1 deficient mice.[62] It remains an intriguing question whether humans, deficient in LPL or GPIHBP1, develop increased atherosclerosis.”
Drager, L. F., Li, J. P., Shin, M., Reinke, C., Aggarwal, N. R., Jun, J. C., Bevans‐Fonti, S., Sztalryd, C., O’Byrne, S. M., Kroupa, O., et al. (2011) · European Heart Journal · doi:10.1093/eurheartj/ehr097 · Cited by 168 · see citing works
“Mice deficient in glycophosphatidyl-anchored HDL-binding protein 1, which anchors LpL to CM, develop severe chylomicronemia and atherosclerosis.(39,40) LpL activation in the muscle and adipose tissue plays an anti-atherogenic role due to a decrease in plasma triglycerides and increased HDL.”
BackgroundMorita, S. (2015) · Biological and Pharmaceutical Bulletin · doi:10.1248/bpb.b15-00716 · Cited by 156 · see citing works
Addressing dyslipidemic risk beyond LDL-cholesterol
Tall, A. R., Thomas, D. G., Gonzalez-Cabodevilla, A. G., & Goldberg, I. J. (2022) · Journal of Clinical Investigation · doi:10.1172/jci148559 · Cited by 150 · see citing works
GPIHBP1 and Lipoprotein Lipase, Partners in Plasma Triglyceride Metabolism
Young, S. G., Fong, L. G., Beigneux, A. P., Allan, C. M., He, C. H., Jiang, H., Nakajima, K., Muthuraman, M., Birrane, G., & Ploug, M. (2019) · Cell Metabolism · doi:10.1016/j.cmet.2019.05.023 · Cited by 141 · see citing works
“The first clue that GPIHBP1 was important for plasma triglyceride metabolism was finding severe hypertriglyceridemia in Gpihbp1 knockout mice (Gpihbp1–/–) (Beigneux et al., 2007; Weinstein et al., 2010a; Weinstein et al., 2010b).”
Self-citationLipolysis of triglyceride-rich lipoproteins, vascular inflammation, and atherosclerosis
Schwartz, E. A., & Reaven, P. D. (2012) · Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids · doi:10.1016/j.bbalip.2011.09.021 · Cited by 130 · see citing works
GPIHBP1, an endothelial cell transporter for lipoprotein lipase
Young, S. G., Davies, B. S. J., Voss, C. V., Gin, P., Weinstein, M. M., Tontonoz, P., Reue, K., Bensadoun, A., Fong, L. G., & Beigneux, A. P. (2011) · Journal of Lipid Research · doi:10.1194/jlr.r018689 · Cited by 109 · see citing works
Self-citationChapman, M. J., Ginsberg, H. N., Amarenco, P., Andreotti, F., Borén, J., Catapano, A. L., Descamps, O. S., Fisher, E. A. A., Kovanen, P. T., Kuivenhoven, J. A., et al. (2011) · Atherosclerosis Supplements · doi:10.1016/s1567-5688(11)70033-2 · Cited by 105 · see citing works
Recent insights into factors affecting remnant lipoprotein uptake
Williams, K. J., & Chen, K. (2010) · Current Opinion in Lipidology · doi:10.1097/mol.0b013e328338cabc · Cited by 91 · see citing works
GPIHBP1 and Plasma Triglyceride Metabolism
Fong, L. G., Young, S. G., Beigneux, A. P., Bensadoun, A., Oberer, M., Jiang, H., & Ploug, M. (2016) · Trends in Endocrinology and Metabolism · doi:10.1016/j.tem.2016.04.013 · Cited by 87 · see citing works
“On a chow diet, the plasma triglyceride levels in Gpihbp1−/− mice were ~2000–5000 mg/dl, and on a high-fat diet they were as high as 35,000 mg/dl [8, 9].”
Self-citationModulation of plasma TG lipolysis by Angiopoietin-like proteins and GPIHBP1
Lichtenstein, L., & Kersten, S. (2010) · Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids · doi:10.1016/j.bbalip.2009.12.015 · Cited by 78 · see citing works
Apoc2 loss-of-function zebrafish mutant as a genetic model of hyperlipidemia
Liu, C., Gates, K. P., Fang, L., Amar, M. J., Schneider, D. A., Geng, H., Huang, W. G., Kim, J., Pattison, J., Zhang, J., et al. (2015) · Disease Models & Mechanisms · doi:10.1242/dmm.019836 · Cited by 68 · see citing works
“APOC3, coronary disease, and complexities of Mendelian Randomization.”
BackgroundResultInfluentialHe, C. H., Weston, T. A., Jung, R. S., Heizer, P. J., Larsson, M., Hu, X., Allan, C. M., Tontonoz, P., Reue, K., Beigneux, A. P., et al. (2018) · Cell Metabolism · doi:10.1016/j.cmet.2018.03.017 · Cited by 69 · see citing works
“The size of TRLs isolated from Gpihbp1−/− mice is 50–150 nm (Weinstein et al., 2010).”
Self-citationLi, H., Han, Y., Qi, R., Wang, Y., Zhang, X., Yu, M., Tang, Y., Wang, M., Shu, Y.-N., Huang, W. Y., et al. (2015) · Cardiovascular Research · doi:10.1093/cvr/cvv192 · Cited by 64 · see citing works
“to: (i) the use of female mice in their study, and the gender differences in lipid levels and susceptibility to atherosclerosis documented in early investigations; 42 and (ii) the base levels of atherosclerotic lesions in ApoE2/2 mice were too high, which could obscure the effect of HTG caused by the ApoCIII transgene…”
BackgroundResultDrager, L. F., Tavoni, T. M., Silva, V. M., Santos, R. D., Pedrosa, R. P., Bortolotto, L. A., Vinagre, C. G. C., Polotsky, V. Y., Lorenzi‐Filho, G., & Maranhão, R. C. (2018) · Journal of Lipid Research · doi:10.1194/jlr.m083436 · Cited by 63 · see citing works
“Chylomicronemia elicits atherosclerosis in mice (26).”
Triglyceride lipases and atherosclerosis
Olivecrona, G., & Olivecrona, T. (2010) · Current Opinion in Lipidology · doi:10.1097/mol.0b013e32833ded83 · Cited by 62 · see citing works
High-resolution imaging of dietary lipids in cells and tissues by NanoSIMS analysis
Jiang, H., Goulbourne, C. N., Tatar, A., Turlo, K. A., Wu, D. Y., Beigneux, A. P., Grovenor, C. R. M., Fong, L. G., & Young, S. G. (2014) · Journal of Lipid Research · doi:10.1194/jlr.m053363 · Cited by 56 · see citing works
Self-citationLipids and the Endothelium: Bidirectional Interactions
Goldberg, I. J., & Bornfeldt, K. (2013) · Current Atherosclerosis Reports · doi:10.1007/s11883-013-0365-1 · Cited by 55 · see citing works
“Severely hypertriglyceridemic mice develop small amounts of atherosclerosis with aging [10, 11].”
BackgroundBasu, D., & Bornfeldt, K. (2020) · Frontiers in Endocrinology · doi:10.3389/fendo.2020.00504 · Cited by 51 · see citing works
“Nearly all of the cholesterol and TGs in plasma of Gpihbp1 mice are associated with large TRLs 50–135 nm in diameter, leading to plasma TG levels close to 3,000 mg/dL, and both male and female Gpihbp1 mice spontaneously develop small atherosclerotic lesions in the aortic root when fed a chow diet (36), phenocopying th…”
BackgroundAdeyo, O., Goulbourne, C. N., Bensadoun, A., Beigneux, A. P., Fong, L. G., & Young, S. G. (2012) · Journal of Internal Medicine · doi:10.1111/joim.12003 · Cited by 48 · see citing works
Self-citationGin, P., Beigneux, A. P., Voss, C. V., Davies, B. S. J., Beckstead, J. A., Ryan, R. O., Bensadoun, A., Fong, L. G., & Young, S. G. (2010) · Arteriosclerosis Thrombosis and Vascular Biology · doi:10.1161/atvbaha.110.214718 · Cited by 48 · see citing works
Self-citationPalmoplantar Keratoderma along with Neuromuscular and Metabolic Phenotypes in Slurp1-Deficient Mice
Adeyo, O., Allan, B. B., Barnes, R. H., Goulbourne, C. N., Tatar, A., Tu, Y., Young, L. C., Weinstein, M. M., Tontonoz, P., Fong, L. G., et al. (2014) · Journal of Investigative Dermatology · doi:10.1038/jid.2014.19 · Cited by 44 · see citing works
“…is highly unlikely because neuromuscular and body weight phenotypes are absent in chow-fed knockout mice for nearby Ly6 genes (Lynx1 and Gpihbp1) (Beigneux et al., 2007; Ibanez-Tallon et al., 2002; Miwa et al., 2006; Weinstein et al., 2012; Weinstein et al., 2010a; Weinstein et al., 2010b).”
BackgroundMethodSelf-citationOlafsen, T., Young, S. G., Davies, B. S. J., Beigneux, A. P., Kenanova, V. E., Voss, C. V., Young, G. W., Wong, K. P., Barnes, R. H., Tu, Y., et al. (2010) · Journal of Biological Chemistry · doi:10.1074/jbc.m110.171041 · Cited by 42 · see citing works
Self-citation2017 George Lyman Duff Memorial Lecture
Goldberg, I. J. (2018) · Arteriosclerosis Thrombosis and Vascular Biology · doi:10.1161/atvbaha.117.309666 · Cited by 39 · see citing works
“Moreover, while hypercholesterolemia causes atherosclerosis in mice (albeit with levels of cholesterol rarely seen in humans), even marked hypertriglyceridemia caused minimal lesion.(17) Nevertheless, recent genetic analyses have resurrected the triglyceride/atherosclerosis hypothesis.”
BackgroundLipoprotein Lipase and Its Delivery of Fatty Acids to the Heart
Shang, R., & Rodrigues, B. B. (2021) · Biomolecules · doi:10.3390/biom11071016 · Cited by 38 · see citing works
Use of Mouse Models in Atherosclerosis Research.
Getz, G., & Reardon, C. (2015) · Methods in molecular biology · doi:10.1007/978-1-4939-2929-0_1 · Cited by 37 · see citing works
Diabetic Dyslipidemia: From Evolving Pathophysiological Insight to Emerging Therapeutic Targets
Ng, D. S. (2013) · Canadian Journal of Diabetes · doi:10.1016/j.jcjd.2013.07.062 · Cited by 35 · see citing works
Zafrir, B., Jubran, A., Hijazi, R., & Shapira, C. (2018) · Journal of clinical lipidology · doi:10.1016/j.jacl.2018.03.086 · Cited by 32 · see citing works
Novel Combined GPIHBP1 Mutations in a Patient with Hypertriglyceridemia Associated with CAD
Yamamoto, H., Onishi, M., Miyamoto, N., Oki, R., Ueda, H., Ishigami, M., Hiraoka, H., Matsuzawa, Y., & Kihara, S. (2013) · Journal of Atherosclerosis and Thrombosis · doi:10.5551/jat.18861 · Cited by 28 · see citing works
Jenkins, N. T., Padilla, J., Thorne, P. K., Martin, J. S., Rector, R. S., Davis, J. W., & Laughlin, M. H. (2014) · Journal of Applied Physiology · doi:10.1152/japplphysiol.01233.2013 · Cited by 27 · see citing works
“The known functions of selected genes listed in Table 5 suggest that the GFA takes on a more inflamed, proatherogenic phenotype compared with the SFA within the OLETF rat, including Nnat, a novel marker of endothelial inflammation in diabetes (45), Cidec, which is involved in ectopic fat accumulation (47), Gpihbp1, an…”
BackgroundLipoprotein lipase as a target for obesity/diabetes related cardiovascular disease
Shang, R., & Rodrigues, B. B. (2024) · Journal of Pharmacy & Pharmaceutical Sciences · doi:10.3389/jpps.2024.13199 · Cited by 21 · see citing works
Dietary fatty acids linking postprandial metabolic response and chronic diseases
Ortega‐Gómez, A., Varela, L. M., Bermúdez, B., López, S., Abia, R., & Muriana, F. J. G. (2011) · Food & Function · doi:10.1039/c1fo10085h · Cited by 21 · see citing works
Planer, D., Metzger, S., Zcharia, E., Wexler, I. D., Vlodavsky, I., & Chajek‐Shaul, T. (2011) · PLoS ONE · doi:10.1371/journal.pone.0018370 · Cited by 18 · see citing works
“. The association between hypertriglyceridemia and atherosclerosis development has been demonstrated recently in mice that are mutated in chylomicron-processing due to mutations in LPL binding or activity and accumulation of large TG-rich particles”
BackgroundLipoprotein lipase transporter GPIHBP1 and triglyceride-rich lipoprotein metabolism
Liu, C., Li, L., Guo, D., Lv, Y.-C., Zheng, X., Mo, Z., & Xie, W. (2018) · Clinica Chimica Acta · doi:10.1016/j.cca.2018.09.020 · Cited by 18 · see citing works
GPIHBP1 and the processing of triglyceride-rich lipoproteins
Beigneux, A. P. (2010) · Clinical Lipidology · doi:10.2217/clp.10.43 · Cited by 17 · see citing works
Self-citationKurooka, N., Eguchi, J., & Wada, J. (2023) · Journal of Diabetes Investigation · doi:10.1111/jdi.14056 · Cited by 17 · see citing works
Regulating intestinal function to reduce atherogenic lipoproteins
Hussain, M. M., Leung, T. M., Zhou, L., & Abu-Merhi, S. (2013) · Clinical Lipidology · doi:10.2217/clp.13.40 · Cited by 16 · see citing works
Klop, B., & Cabezas, M. C. (2011) · Current Cardiovascular Risk Reports · doi:10.1007/s12170-011-0215-z · Cited by 14 · see citing works
Genetic Predisposition of Human Plasma Triglyceride Concentrations
Schwarzová, L., Hubacek, J. A., & Vrablı́k, M. (2015) · Physiological Research · doi:10.33549/physiolres.933197 · Cited by 14 · see citing works
Cell-mediated lipoprotein transport: A novel anti-atherogenic concept
Bovenberg, S. A., Alipour, A., Elte, J. W. F., Rietveld, A. P., Janssen, J. W., van de Geijn, G. J., Njo, T. N., van Mechelen, R., Martínez‐Hervás, S., & Cabezas, M. C. (2010) · Atherosclerosis Supplements · doi:10.1016/j.atherosclerosissup.2010.04.003 · Cited by 13 · see citing works
Gpihbp1 deficiency accelerates atherosclerosis and plaque instability in diabetic Ldlr-/- mice
Liu, X., Li, J., Liao, J., Wang, H., Huang, X., Zhao, D., Shen, Q., Zhang, L., Wang, Y., Kong, W., et al. (2019) · Atherosclerosis · doi:10.1016/j.atherosclerosis.2019.01.025 · Cited by 13 · see citing works
Research Progress of Hypertriglyceridemia and Coronary Heart Disease
Ji, Y., & Bai, C. (2018) · Heart and Mind · doi:10.4103/hm.hm_2_19 · Cited by 13 · see citing works
Jiang, S., Ren, Z., Yang, Y., Liu, Q., Zhou, S., & Xiao, Y. (2023) · Biomedicine & Pharmacotherapy · doi:10.1016/j.biopha.2023.115874 · Cited by 12 · see citing works
Avis, H. J., Scheffer, H., Kastelein, J. J. P., Dallinga‐Thie, G. M., & Wijburg, F. A. (2010) · Clinical Genetics · doi:10.1111/j.1399-0004.2009.01369.x · Cited by 11 · see citing works
Triglycerides and carotid intima-media thickness in ischemic stroke patients
Batluk, J., Leonards, C. O., Grittner, U., Lange, K. S., Schreiber, S. J., Endres, M., & Ebinger, M. (2015) · Atherosclerosis · doi:10.1016/j.atherosclerosis.2015.09.003 · Cited by 11 · see citing works
Abnormality of hepatic triglyceride metabolism in Apc/+ mice with colon cancer cachexia
Yu, B., Zhang, M., Chen, J., Wang, L., Peng, X., Zhang, X., Wang, H., Wang, A., Zhao, D., Pang, D., et al. (2019) · Life Sciences · doi:10.1016/j.lfs.2019.04.041 · Cited by 7 · see citing works
Wakita, K., Morita, S., Okamoto, N., Takata, E., Handa, T., & Nakano, M. (2015) · Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids · doi:10.1016/j.bbalip.2015.01.015 · Cited by 6 · see citing works
Management of severe hypertriglyceridaemia
Cybulska, B., & Kłosiewicz−Latoszek, L. (2013) · Kardiologia Polska · doi:10.5603/kp.2013.0254 · Cited by 7 · see citing works
Cabodevilla, A. G., Izquierdo, M. C., Basu, D., Younis, W., Tirumalasetty, M. B., Miao, Q. R., Nasias, D., Kanter, J. E., Ho, T. W. W., Gjini, J., et al. (2026) · Nature Communications · doi:10.1038/s41467-025-68193-3 · Cited by 5 · see citing works
“Although both sexes of mice had increased aortic lesions with LpL de fi ciency, BCAs were signi fi cantly ( p = 0.0309) increased only in males (females trended to larger lesions).”
InfluentialFan, R., An, X., Wang, Y., Zhang, J., Liu, S., Bai, J., Li, J., Lin, Q., Xie, Y., Xia, Y., et al. (2023) · Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids · doi:10.1016/j.bbalip.2023.159330 · Cited by 5 · see citing works
Lipolysis Needed for Chylomicron Uptake?
Parthasarathy, S. (2009) · Arteriosclerosis Thrombosis and Vascular Biology · doi:10.1161/atvbaha.109.198317 · Cited by 5 · see citing works
Ortega‐Gómez, A., Lourdes, M., Bermúdez, B., López, S., Francisco, J. G., & Abi, R. (2012) · InTech eBooks · doi:10.5772/26141 · Cited by 4 · see citing works
“In fact, chylomicronemia causes atherosclerosis in mice (Weinstein et al., 2010) and decreasing the TRLs level reduces the progression of coronary artery disease to the same degree as decreasing the LDL-cholesterol level (Hodis et al., 1999).”
BackgroundDing, Y., Zhang, L., Wang, Y., Huang, W. Y., Tang, Y., Bai, L., Ross, C. J., Hayden, M. R., & Liu, C. (2011) · PLoS ONE · doi:10.1371/journal.pone.0025620 · Cited by 4 · see citing works
Guay, S., Gaudet, D., & Brisson, D. (2011) · Nutrition Metabolism and Cardiovascular Diseases · doi:10.1016/j.numecd.2011.08.005 · Cited by 4 · see citing works
Lipoprotein Lipase in the Arterial Wall: Regulation by Dietary Fatty Acids
Chang, C. L. (2011) · doi:10.7916/d81r6xh3 · Cited by 3 · see citing works
Nguyen, L. P., Song, W., Yang, Y., Tran, A. P., Weston, T. A., Jung, H., Tu, Y., Kim, P. H., Kim, J. R., Xie, K., et al. (2024) · JCI Insight · doi:10.1172/jci.insight.184940 · Cited by 2 · see citing works
“The plasma TG levels in chow-fed Gpi-hbp1 –/– mice are 2,500–3,000 mg/dL (11, 15) but can reach 30,000 mg/dL on a high-fat diet (16).”
BackgroundSelf-citationEndogenous and exogenous factors affecting lipoprotein lipase activity
Larsson, M. (2014) · KTH Publication Database DiVA (KTH Royal Institute of Technology) · Cited by 2 · see citing works
Cholesterol metabolism: increasingly complex
Julio Sanhueza, C., Valenzuela, R., & Valenzuela, A. (2012) · Grasas y Aceites · doi:10.3989/gya.035512 · Cited by 1 · see citing works
“La acumulación experimental de colesterol intracelular produce externalización de la fosfatidilserina (transferencia desde la cara interna de la membrana a la externa) y fragmentación del DNA, eventos que evidencian una mayor apoptosis (yao and Tabas, 2000).”
BackgroundVergès, B. L. (2013) · EMC - Endocrinologie - Nutrition · doi:10.1016/s1155-1941(13)51263-7 · Cited by 1 · see citing works
The Acute Regulation of Intestinal Chylomicron Secretion by Glucagon-like Peptides
Hsieh, J. (2012) · TSpace (University of Toronto)
Lambda-cyhalothrin exposure enhances the development of atherosclerosis in ApoE−/− mice
Yu, L., Chen, H., Li, L., Zhang, H., He, F., Fang, Z., Zheng, G., Zhou, B., Chen, X., Liu, M., et al. (2025) · Ecotoxicology and Environmental Safety · doi:10.1016/j.ecoenv.2025.119165
Role of Lipoprotein Lipase in Fatty Acid Delivery to the Heart
Wan, A., & Rodrigues, B. B. (2014) · Springer eBooks · doi:10.1007/978-1-4939-1227-8_3
Wang, B., Meng, Z., Li, J., Wu, F., Song, B., Huang, W., & Liao, J. (2026) · Arteriosclerosis Thrombosis and Vascular Biology · doi:10.1161/atvbaha.126.324300
- Authors
- Weinstein, M. M., Yin, L., Tu, Y., Wang, X., Wu, X., Castellani, L. W., Walzem, R. L., Lusis, A. J., Fong, L. G., Beigneux, A. P., & Young, S. G.
- Affiliations
- University of California, Los Angeles (US)
- ORCID
- Venue
- Arteriosclerosis, Thrombosis, and Vascular Biology
- Published
- 2010-01
- Volume
- 30
- Issue
- 1
- Pages
- 20-23
- ISSN
- 1079-5642 (ISSN-L)
- 1524-4636
- PMC
- PMC2796285
- OpenAlex
- W2116482139
- Cited by
- 71
- References
- 9
- Citations by year
- 2026: 2 · 2025: 1 · 2024: 2 · 2023: 3 · 2022: 1 · 2021: 2 · 2020: 1 · 2019: 3 · 2018: 6 · 2016: 1 · 2015: 7 · 2014: 5 · 2013: 8 · 2012: 6
- FWCI
- 6.04
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Arteriosclerosis Thrombosis and Vascular Biology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Heart, Lung, and Blood Institute (P01HL090553, T32 HL-69766, R01HL087228, HL-087228, HL090553, R01HL094732, T32HL069766)
- Topics
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Lipid metabolism and disorders
- Health Sciences › Medicine › Surgery › Cholesterol and Lipid Metabolism
- Health Sciences › Medicine › Surgery › Lipoproteins and Cardiovascular Health
- Keywords
- chylomicronemia, atherosclerosis, GPIHBP1, lipolysis, lipoprotein processing, plasma triglycerides, aortic atherosclerosis
- MeSH terms
- Animals, Animal Feed, Aortic Diseases, Chylomicrons, Fatty Acids, Female, Lipolysis, Male, Mice, Mutant Strains, Risk Factors, Triglycerides, Receptors, Lipoprotein, Genetic Predisposition to Disease, Atherosclerosis, Mice, Apolipoprotein B-48, Apolipoprotein B-100
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