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  1. Article ; Online: Differential effects of plant and animal fats on obesity-induced dyslipidemia and atherosclerosis in Ldlr-/-.Leiden mice.

    Morrison, Martine C / Egelandsdal, Bjørg / Harvei, Silje / Rocha, Sérgio D C / Pieterman, Elsbet J / Kleemann, Robert / Carlsen, Harald

    FASEB journal : official publication of the Federation of American Societies for Experimental Biology

    2023  Volume 37, Issue 8, Page(s) e23096

    Abstract: Cardiovascular disease (CVD) is closely associated with obesity through risk factors such as dyslipidemia and chronic low-grade inflammation, which may be affected by diet. Dietary fats have been extensively studied in relation to CVD risk, however these ...

    Abstract Cardiovascular disease (CVD) is closely associated with obesity through risk factors such as dyslipidemia and chronic low-grade inflammation, which may be affected by diet. Dietary fats have been extensively studied in relation to CVD risk, however these studies have not always yielded consistent results, most likely due to lack in control of experimental conditions and confounding factors. Here we studied the effects of different plant and animal fats on dyslipidemia, inflammation, and atherosclerosis. Ldlr-/-.Leiden mice were fed isocaloric energy-dense diets with translational macronutrient composition for 28 weeks. The diets were identical apart from the type of fat they contained: either (1) a mixture of olive and rapeseed oil, (2) sunflower oil, (3) pork fat, (4) beef fat, or (5) milk fat. The fatty acid composition of the diets was determined and effects on circulating lipid and inflammatory risk factors and atherosclerosis were examined, complemented by adipose tissue histology and liver transcriptomics. While visceral fat mass, adipocyte size, and adipose tissue inflammation were not differentially affected by the diets, atherosclerotic lesion load and severity was more pronounced with increasing dietary saturated fatty acid content and decreasing monounsaturated and polyunsaturated fatty acid content, and hence most pronounced with beef and milk fat. These differential effects were accompanied by increases in pro-atherogenic plasma lipids/lipoproteins (e.g., triglycerides, apolipoprotein B), activation of pro-atherogenic cytokine/chemokine signaling pathways in liver, and with circulating pro-atherogenic mediators of inflammation altogether providing a rationale for the differential effects of plant and animal fats.
    MeSH term(s) Cattle ; Animals ; Mice ; Dietary Fats/adverse effects ; Atherosclerosis/etiology ; Atherosclerosis/prevention & control ; Fatty Acids ; Obesity/complications ; Obesity/chemically induced ; Inflammation/etiology ; Dyslipidemias/chemically induced
    Chemical Substances Dietary Fats ; Fatty Acids
    Language English
    Publishing date 2023-02-15
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 639186-2
    ISSN 1530-6860 ; 0892-6638
    ISSN (online) 1530-6860
    ISSN 0892-6638
    DOI 10.1096/fj.202300585R
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Atorvastatin Attenuates Diet-Induced Non-Alcoholic Steatohepatitis in APOE*3-Leiden Mice by Reducing Hepatic Inflammation.

    Inia, José A / Stokman, Geurt / Pieterman, Elsbet J / Morrison, Martine C / Menke, Aswin L / Verschuren, Lars / Caspers, Martien P M / Giera, Martin / Jukema, J Wouter / van den Hoek, Anita M / Princen, Hans M G

    International journal of molecular sciences

    2023  Volume 24, Issue 9

    Abstract: Patients with metabolic syndrome are often prescribed statins to prevent the development of cardiovascular disease. Conversely, data on their effects on non-alcoholic steatohepatitis (NASH) are lacking. We evaluated these effects by feeding APOE*3-Leiden ...

    Abstract Patients with metabolic syndrome are often prescribed statins to prevent the development of cardiovascular disease. Conversely, data on their effects on non-alcoholic steatohepatitis (NASH) are lacking. We evaluated these effects by feeding APOE*3-Leiden mice a Western-type diet (WTD) with or without atorvastatin to induce NASH and hepatic fibrosis. Besides the well-known plasma cholesterol lowering (-30%) and anti-atherogenic effects (severe lesion size -48%), atorvastatin significantly reduced hepatic steatosis (-22%), the number of aggregated inflammatory cells in the liver (-80%) and hepatic fibrosis (-92%) compared to WTD-fed mice. Furthermore, atorvastatin-treated mice showed less immunohistochemically stained areas of inflammation markers. Atorvastatin prevented accumulation of free cholesterol in the form of cholesterol crystals (-78%). Cholesterol crystals are potent inducers of the NLRP3 inflammasome pathway and atorvastatin prevented its activation, which resulted in reduced expression of the pro-inflammatory cytokines interleukin (IL)-1β (-61%) and IL-18 (-26%). Transcriptome analysis confirmed strong reducing effects of atorvastatin on inflammatory mediators, including NLRP3, NFκB and TLR4. The present study demonstrates that atorvastatin reduces hepatic steatosis, inflammation and fibrosis and prevents cholesterol crystal formation, thereby precluding NLRP3 inflammasome activation. This may render atorvastatin treatment as an attractive approach to reduce NAFLD and prevent progression into NASH in dyslipidemic patients.
    MeSH term(s) Mice ; Animals ; Non-alcoholic Fatty Liver Disease/etiology ; Non-alcoholic Fatty Liver Disease/chemically induced ; Atorvastatin/adverse effects ; Inflammasomes/metabolism ; NLR Family, Pyrin Domain-Containing 3 Protein/genetics ; NLR Family, Pyrin Domain-Containing 3 Protein/metabolism ; Liver/metabolism ; Liver Cirrhosis/metabolism ; Inflammation/metabolism ; Cholesterol/metabolism ; Diet ; Apolipoproteins E/metabolism ; Mice, Inbred C57BL
    Chemical Substances Atorvastatin (A0JWA85V8F) ; Inflammasomes ; NLR Family, Pyrin Domain-Containing 3 Protein ; Cholesterol (97C5T2UQ7J) ; Apolipoproteins E
    Language English
    Publishing date 2023-04-25
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2019364-6
    ISSN 1422-0067 ; 1422-0067 ; 1661-6596
    ISSN (online) 1422-0067
    ISSN 1422-0067 ; 1661-6596
    DOI 10.3390/ijms24097818
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article: Comment on "Hypercholesterolemia with consumption of PFOA-laced Western diets is dependent on strain and sex of mice" by Rebholz S.L. et al. Toxicol. Rep. 2016 (3) 46-54.

    Princen, Hans M G / Pouwer, Marianne G / Pieterman, Elsbet J

    Toxicology reports

    2016  Volume 3, Page(s) 306–309

    Language English
    Publishing date 2016-02-11
    Publishing country Ireland
    Document type Journal Article
    ZDB-ID 2805786-7
    ISSN 2214-7500
    ISSN 2214-7500
    DOI 10.1016/j.toxrep.2016.02.002
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article: Chronic Oral Administration of Mineral Oil Compared With Corn Oil: Effects on Gut Permeability and Plasma Inflammatory and Lipid Biomarkers.

    Pieterman, Elsbet J / Princen, Hans M G / Jarke, Annica / Nilsson, Ralf / Cavallin, Anders / Bergenholm, Linnéa / Henricsson, Marcus / Gopaul, V Sashi / Agrawal, Rahul / Nissen, Steven E / Hurt-Camejo, Eva

    Frontiers in pharmacology

    2021  Volume 12, Page(s) 681455

    Abstract: We investigated the effects of chronic oral administration of mineral oil, versus corn oil as control, on intestinal permeability, inflammatory markers, and plasma lipids in APOE*3-Leiden.CETP mice. Mice received mineral oil or corn oil 15 or 30 μL/mouse/ ...

    Abstract We investigated the effects of chronic oral administration of mineral oil, versus corn oil as control, on intestinal permeability, inflammatory markers, and plasma lipids in APOE*3-Leiden.CETP mice. Mice received mineral oil or corn oil 15 or 30 μL/mouse/day for 16 weeks (15 mice/group). Intestinal permeability was increased with mineral versus corn oil 30 µL/day, shown by increased mean plasma FITC-dextran concentrations 2 h post-administration (11 weeks: 1.5 versus 1.1 μg/ml,
    Language English
    Publishing date 2021-08-16
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2587355-6
    ISSN 1663-9812
    ISSN 1663-9812
    DOI 10.3389/fphar.2021.681455
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Alirocumab, evinacumab, and atorvastatin triple therapy regresses plaque lesions and improves lesion composition in mice.

    Pouwer, Marianne G / Pieterman, Elsbet J / Worms, Nicole / Keijzer, Nanda / Jukema, J Wouter / Gromada, Jesper / Gusarova, Viktoria / Princen, Hans M G

    Journal of lipid research

    2019  Volume 61, Issue 3, Page(s) 365–375

    Abstract: Atherosclerosis-related CVD causes nearly 20 million deaths annually. Most patients are treated after plaques develop, so therapies must regress existing lesions. Current therapies reduce plaque volume, but targeting all apoB-containing lipoproteins with ...

    Abstract Atherosclerosis-related CVD causes nearly 20 million deaths annually. Most patients are treated after plaques develop, so therapies must regress existing lesions. Current therapies reduce plaque volume, but targeting all apoB-containing lipoproteins with intensive combinations that include alirocumab or evinacumab, monoclonal antibodies against cholesterol-regulating proprotein convertase subtilisin/kexin type 9 and angiopoietin-like protein 3, may provide more benefit. We investigated the effect of such lipid-lowering interventions on atherosclerosis in APOE*3-Leiden.CETP mice, a well-established model for hyperlipidemia. Mice were fed a Western-type diet for 13 weeks and thereafter matched into a baseline group (euthanized at 13 weeks) and five groups that received diet alone (control) or with treatment [atorvastatin; atorvastatin and alirocumab; atorvastatin and evinacumab; or atorvastatin, alirocumab, and evinacumab (triple therapy)] for 25 weeks. We measured effects on cholesterol levels, plaque composition and morphology, monocyte adherence, and macrophage proliferation. All interventions reduced plasma total cholesterol (37% with atorvastatin to 80% with triple treatment; all
    MeSH term(s) Administration, Oral ; Animals ; Antibodies, Monoclonal/administration & dosage ; Antibodies, Monoclonal/therapeutic use ; Antibodies, Monoclonal, Humanized/administration & dosage ; Antibodies, Monoclonal, Humanized/therapeutic use ; Anticholesteremic Agents/administration & dosage ; Anticholesteremic Agents/therapeutic use ; Atorvastatin/administration & dosage ; Atorvastatin/therapeutic use ; Drug Therapy, Combination ; Female ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Plaque, Atherosclerotic/chemically induced ; Plaque, Atherosclerotic/drug therapy ; Plaque, Atherosclerotic/pathology
    Chemical Substances Antibodies, Monoclonal ; Antibodies, Monoclonal, Humanized ; Anticholesteremic Agents ; Atorvastatin (A0JWA85V8F) ; alirocumab (PP0SHH6V16) ; evinacumab (T8B2ORP1DW)
    Language English
    Publishing date 2019-12-16
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 80154-9
    ISSN 1539-7262 ; 0022-2275
    ISSN (online) 1539-7262
    ISSN 0022-2275
    DOI 10.1194/jlr.RA119000419
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: A Novel, Orally Bioavailable, Small-Molecule Inhibitor of PCSK9 With Significant Cholesterol-Lowering Properties In Vivo.

    Suchowerska, Alexandra K / Stokman, Geurt / Palmer, James T / Coghlan, Phillip A / Pieterman, Elsbet J / Keijzer, Nanda / Lambert, Gilles / Chemello, Kevin / Jaafar, Ali K / Parmar, Jasneet / Yan, Liping / Tong, Yingtao / Mu, Lin / Princen, Hans M G / Bonnar, James / Evison, Benny J

    Journal of lipid research

    2022  Volume 63, Issue 11, Page(s) 100293

    Abstract: Proprotein convertase subtilisin kexin type 9 (PCSK9) inhibits the clearance of low-density lipoprotein (LDL) cholesterol (LDL-C) from plasma by directly binding with the LDL receptor (LDLR) and sending the receptor for lysosomal degradation. As the ... ...

    Abstract Proprotein convertase subtilisin kexin type 9 (PCSK9) inhibits the clearance of low-density lipoprotein (LDL) cholesterol (LDL-C) from plasma by directly binding with the LDL receptor (LDLR) and sending the receptor for lysosomal degradation. As the interaction promotes elevated plasma LDL-C levels, and therefore a predisposition to cardiovascular disease, PCSK9 has attracted intense interest as a therapeutic target. Despite this interest, an orally bioavailable small-molecule inhibitor of PCSK9 with extensive lipid-lowering activity is yet to enter the clinic. We report herein the discovery of NYX-PCSK9i, an orally bioavailable small-molecule inhibitor of PCSK9 with significant cholesterol-lowering activity in hyperlipidemic APOE∗3-Leiden.CETP mice. NYX-PCSK9i emerged from a medicinal chemistry campaign demonstrating potent disruption of the PCSK9-LDLR interaction in vitro and functional protection of the LDLR of human lymphocytes from PCSK9-directed degradation ex vivo. APOE∗3-Leiden.CETP mice orally treated with NYX-PCSK9i demonstrated a dose-dependent decrease in plasma total cholesterol of up to 57%, while its combination with atorvastatin additively suppressed plasma total cholesterol levels. Importantly, the majority of cholesterol lowering by NYX-PCSK9i was in non-HDL fractions. A concomitant increase in total plasma PCSK9 levels and significant increase in hepatic LDLR protein expression strongly indicated on-target function by NYX-PCSK9i. Determinations of hepatic lipid and fecal cholesterol content demonstrated depletion of liver cholesteryl esters and promotion of fecal cholesterol elimination with NYX-PCSK9i treatment. All measured in vivo biomarkers of health indicate that NYX-PCSK9i has a good safety profile. NYX-PCSK9i is a potential new therapy for hypercholesterolemia with the capacity to further enhance the lipid-lowering activities of statins.
    MeSH term(s) Animals ; Humans ; Mice ; Apolipoproteins E ; Cholesterol ; Cholesterol, LDL ; Receptors, LDL/genetics ; Receptors, LDL/metabolism ; PCSK9 Inhibitors/pharmacology ; Hyperlipidemias/drug therapy ; Anticholesteremic Agents/pharmacology
    Chemical Substances Apolipoproteins E ; Cholesterol (97C5T2UQ7J) ; Cholesterol, LDL ; Receptors, LDL ; PCSK9 Inhibitors ; Anticholesteremic Agents
    Language English
    Publishing date 2022-10-06
    Publishing country United States
    Document type Journal Article
    ZDB-ID 80154-9
    ISSN 1539-7262 ; 0022-2275
    ISSN (online) 1539-7262
    ISSN 0022-2275
    DOI 10.1016/j.jlr.2022.100293
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: Effects of mineral oil administration on the pharmacokinetics, metabolism and pharmacodynamics of atorvastatin and pravastatin in mice and dogs.

    Gopaul, V Sashi / Pieterman, Elsbet J / Princen, Hans M G / Bergenholm, Linnéa / Lundborg, Eva / Cavallin, Anders / Johansson, Magnus J / Hawthorne, Glen / Björkbom, Anders / Hammarberg, Maria / Li, XueQing / Jarke, Annica / Bright, Jonathan / Svensson, Lena / Jansson-Löfmark, Rasmus / Abrahamsson, Bertil / Agrawal, Rahul / Hurt-Camejo, Eva

    European journal of pharmaceutical sciences : official journal of the European Federation for Pharmaceutical Sciences

    2021  Volume 161, Page(s) 105776

    Abstract: We investigated the effects of mineral oil on statin pharmacokinetics and inflammatory markers in animal models. A new synthesis strategy produced regioisomers that facilitated the characterization of the main metabolite (M1) of atorvastatin, a ... ...

    Abstract We investigated the effects of mineral oil on statin pharmacokinetics and inflammatory markers in animal models. A new synthesis strategy produced regioisomers that facilitated the characterization of the main metabolite (M1) of atorvastatin, a lipophilic statin, in C57BL/6NCrl mice. The chemical structure of M1 in mice was confirmed as ortho-hydroxy β-oxidized atorvastatin. Atorvastatin and M1 pharmacokinetics and inflammatory markers were assessed in C57BL6/J mice given atorvastatin 5 mg/kg/day or 10 mg/kg/day, as a single dose or for 21 days, with or without 10 µL or 30 µL mineral oil. No consistent differences in plasma exposure of atorvastatin or M1 were observed in mice after single or repeat dosing of atorvastatin with or without mineral oil. However, mice administered atorvastatin 10 mg/kg with 30 µL mineral oil for 21 days had significantly increased plasma levels of serum amyloid A (mean 9.6 µg/mL vs 7.9 µg/mL without mineral oil; p < 0.01) and significantly increased proportions of C62L
    MeSH term(s) Animals ; Atorvastatin ; Dogs ; Heptanoic Acids ; Hydroxymethylglutaryl-CoA Reductase Inhibitors ; Mice ; Mice, Inbred C57BL ; Mineral Oil ; Pravastatin ; Pyrroles
    Chemical Substances Heptanoic Acids ; Hydroxymethylglutaryl-CoA Reductase Inhibitors ; Pyrroles ; Mineral Oil (8020-83-5) ; Atorvastatin (A0JWA85V8F) ; Pravastatin (KXO2KT9N0G)
    Language English
    Publishing date 2021-03-02
    Publishing country Netherlands
    Document type Journal Article
    ZDB-ID 1154366-8
    ISSN 1879-0720 ; 0928-0987
    ISSN (online) 1879-0720
    ISSN 0928-0987
    DOI 10.1016/j.ejps.2021.105776
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article ; Online: Dose Effects of Ammonium Perfluorooctanoate on Lipoprotein Metabolism in APOE*3-Leiden.CETP Mice.

    Pouwer, Marianne G / Pieterman, Elsbet J / Chang, Shu-Ching / Olsen, Geary W / Caspers, Martien P M / Verschuren, Lars / Jukema, J Wouter / Princen, Hans M G

    Toxicological sciences : an official journal of the Society of Toxicology

    2019  Volume 168, Issue 2, Page(s) 519–534

    Abstract: Epidemiological studies have reported positive associations between serum perfluorooctanoic acid (PFOA) and total and non-high-density lipoprotein cholesterol (non-HDL-C) although the magnitude of effect of PFOA on cholesterol lacks consistency. The ... ...

    Abstract Epidemiological studies have reported positive associations between serum perfluorooctanoic acid (PFOA) and total and non-high-density lipoprotein cholesterol (non-HDL-C) although the magnitude of effect of PFOA on cholesterol lacks consistency. The objectives of this study were to evaluate the effect of PFOA on plasma cholesterol and triglyceride metabolism at various plasma PFOA concentrations relevant to humans, and to elucidate the mechanisms using APOE*3-Leiden.CETP mice, a model with a human-like lipoprotein metabolism. APOE*3-Leiden.CETP mice were fed a Western-type diet with PFOA (10, 300, 30 000 ng/g/d) for 4-6 weeks. PFOA exposure did not alter plasma lipids in the 10 and 300 ng/g/d dietary PFOA dose groups. At 30 000 ng/g/d, PFOA decreased plasma triglycerides (TG), total cholesterol (TC), and non-HDL-C, whereas HDL-C was increased. The plasma lipid alterations could be explained by decreased very low-density lipoprotein (VLDL) production and increased VLDL clearance by the liver through increased lipoprotein lipase activity. The concomitant increase in HDL-C was mediated by decreased cholesteryl ester transfer activity and changes in gene expression of proteins involved in HDL metabolism. Hepatic gene expression and pathway analysis confirmed the changes in lipoprotein metabolism that were mediated for a major part through activation of the peroxisome proliferator-activated receptor (PPAR)α. Our data confirmed the findings from a phase 1 clinical trial in humans that demonstrated high serum or plasma PFOA levels resulted in lower cholesterol levels. The study findings do not show an increase in cholesterol at environmental or occupational levels of PFOA exposure, thereby indicating these findings are associative rather than causal.
    MeSH term(s) Animals ; Apolipoprotein E3/genetics ; Caprylates/blood ; Caprylates/toxicity ; Cholesterol, HDL/blood ; Cholesterol, VLDL/blood ; Dose-Response Relationship, Drug ; Fluorocarbons/blood ; Fluorocarbons/toxicity ; Humans ; Lipoproteins/blood ; Liver/drug effects ; Liver/metabolism ; Liver/pathology ; Male ; Mice, Transgenic ; PPAR alpha/blood ; Triglycerides/blood ; Water Pollutants, Chemical/blood ; Water Pollutants, Chemical/toxicity
    Chemical Substances Apolipoprotein E3 ; Caprylates ; Cholesterol, HDL ; Cholesterol, VLDL ; Fluorocarbons ; Lipoproteins ; PPAR alpha ; Triglycerides ; Water Pollutants, Chemical ; perfluorooctanoic acid (947VD76D3L)
    Language English
    Publishing date 2019-01-15
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1420885-4
    ISSN 1096-0929 ; 1096-6080
    ISSN (online) 1096-0929
    ISSN 1096-6080
    DOI 10.1093/toxsci/kfz015
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  9. Article ; Online: Icosabutate Exerts Beneficial Effects Upon Insulin Sensitivity, Hepatic Inflammation, Lipotoxicity, and Fibrosis in Mice.

    van den Hoek, Anita M / Pieterman, Elsbet J / van der Hoorn, José W / Iruarrizaga-Lejarreta, Marta / Alonso, Cristina / Verschuren, Lars / Skjæret, Tore / Princen, Hans M G / Fraser, David A

    Hepatology communications

    2019  Volume 4, Issue 2, Page(s) 193–207

    Abstract: Icosabutate is a structurally engineered eicosapentaenoic acid derivative under development for nonalcoholic steatohepatitis (NASH). In this study, we investigated the absorption and distribution properties of icosabutate in relation to liver targeting ... ...

    Abstract Icosabutate is a structurally engineered eicosapentaenoic acid derivative under development for nonalcoholic steatohepatitis (NASH). In this study, we investigated the absorption and distribution properties of icosabutate in relation to liver targeting and used rodents to evaluate the effects of icosabutate on glucose metabolism, insulin resistance, as well as hepatic steatosis, inflammation, lipotoxicity, and fibrosis. The absorption, tissue distribution, and excretion of icosabutate was investigated in rats along with its effects in mouse models of insulin resistance (
    Language English
    Publishing date 2019-12-24
    Publishing country United States
    Document type Journal Article
    ISSN 2471-254X
    ISSN (online) 2471-254X
    DOI 10.1002/hep4.1453
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  10. Article ; Online: In Vivo Magnetic Resonance Imaging-Based Detection of Heterogeneous Endothelial Response in Thoracic and Abdominal Aorta to Short-Term High-Fat Diet Ascribed to Differences in Perivascular Adipose Tissue in Mice.

    Bar, Anna / Kieronska-Rudek, Anna / Proniewski, Bartosz / Suraj-Prażmowska, Joanna / Czamara, Krzysztof / Marczyk, Brygida / Matyjaszczyk-Gwarda, Karolina / Jasztal, Agnieszka / Kuś, Edyta / Majka, Zuzanna / Kaczor, Agnieszka / Kurpińska, Anna / Walczak, Maria / Pieterman, Elsbet J / Princen, Hans M G / Chlopicki, Stefan

    Journal of the American Heart Association

    2020  Volume 9, Issue 21, Page(s) e016929

    Abstract: Background Long-term feeding with a high-fat diet (HFD) induces endothelial dysfunction in mice, but early HFD-induced effects on endothelium have not been well characterized. Methods and Results Using an magnetic resonance imaging-based methodology that ...

    Abstract Background Long-term feeding with a high-fat diet (HFD) induces endothelial dysfunction in mice, but early HFD-induced effects on endothelium have not been well characterized. Methods and Results Using an magnetic resonance imaging-based methodology that allows characterization of endothelial function in vivo, we demonstrated that short-term (2 weeks) feeding with a HFD to
    MeSH term(s) Adipose Tissue/metabolism ; Adipose Tissue/pathology ; Animals ; Aorta, Abdominal/diagnostic imaging ; Aorta, Abdominal/pathology ; Aorta, Abdominal/physiopathology ; Aorta, Thoracic/diagnostic imaging ; Aorta, Thoracic/pathology ; Aorta, Thoracic/physiopathology ; Diet, High-Fat ; Endothelium, Vascular/diagnostic imaging ; Endothelium, Vascular/pathology ; Endothelium, Vascular/physiopathology ; Magnetic Resonance Imaging ; Male ; Mice ; Mice, Inbred C57BL
    Language English
    Publishing date 2020-10-19
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2653953-6
    ISSN 2047-9980 ; 2047-9980
    ISSN (online) 2047-9980
    ISSN 2047-9980
    DOI 10.1161/JAHA.120.016929
    Database MEDical Literature Analysis and Retrieval System OnLINE

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