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Article ; Online: CardioPulse: The European Medicines Agency's approval of proprotein convertase subtilisin/kexin type 9 inhibitors..

Blind, Eberhard / de Graeff, Pieter A / Meurs, Illiana / Holtkamp, Frank / Baczynska, Ania / Janssen, Heidi

2016 Volume 37, Issue 6, Page(s) 502–503

MeSH term(s)	Antibodies, Monoclonal/therapeutic use ; Anticholesteremic Agents/therapeutic use ; Cholesterol, LDL/drug effects ; Drug Approval ; Europe ; Humans ; Hyperlipoproteinemia Type II/drug therapy ; Proprotein Convertase 9/antagonists & inhibitors
Chemical Substances	Antibodies, Monoclonal ; Anticholesteremic Agents ; Cholesterol, LDL ; PCSK9 protein, human (EC 3.4.21.-) ; Proprotein Convertase 9 (EC 3.4.21.-) ; evolocumab (LKC0U3A8NJ) ; alirocumab (PP0SHH6V16)
Language	English
Publishing date	2016-02-07
Publishing country	England
Document type	Journal Article
ZDB-ID	603098-1
ISSN	1522-9645 ; 0195-668X
ISSN (online)	1522-9645
ISSN	0195-668X
DOI	10.1093/eurheartj/ehv685
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Zs.A 1563: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MO 640: Show issues

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Article ; Online: The European Medicines Agency's approval of proprotein convertase subtilisin/kexin type 9 inhibitors.

Blind, Eberhard / de Graeff, Pieter A / Meurs, Illiana / Holtkamp, Frank / Baczynska, Ania / Janssen, Heidi

European heart journal

2015

Language	English
Publishing date	2015-12-27
Publishing country	England
Document type	Journal Article
ZDB-ID	603098-1
ISSN	1522-9645 ; 0195-668X
ISSN (online)	1522-9645
ISSN	0195-668X
DOI	10.1093/eurheartj/ehv673
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Zs.A 1563: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MO 640: Show issues

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Article: Peptide Antagonists for P-selectin Discriminate between Sulfatide-Dependent Platelet Aggregation and PSGL-1-Mediated Cell Adhesion.

Korporaal, Suzanne J A / Molenaar, Tom J M / Lutters, Bianca C H / Meurs, Illiana / Drost-Verhoef, Sandra / Kuiper, Johan / van Berkel, Theo J C / Biessen, Erik A L

Journal of clinical medicine

2019 Volume 8, Issue 8

Abstract: Background: Membrane-exposed sulfatides are proposed to contribute to P-selectin-dependent platelet aggregation. Here, we demonstrated that P-selectin-mediated platelet aggregation on a collagen-coated surface under flow indeed depended on sulfatides ... ...

Abstract	Background: Membrane-exposed sulfatides are proposed to contribute to P-selectin-dependent platelet aggregation. Here, we demonstrated that P-selectin-mediated platelet aggregation on a collagen-coated surface under flow indeed depended on sulfatides and that this interaction differed considerably from the interaction of P-selectin with P-selectin Glycoprotein Ligand-1 (PSGL-1), which underlies leukocyte-endothelium adhesion. Methods and results: Upon platelet activation, sulfatides were translocated to the platelet surface to form focal hot-spots. Interestingly, P-selectin was observed to exclusively interact with liposomes with a sulfatide density higher than 21% ( Conclusions: Our data suggest that the sulfatide/P-selectin interaction implicates multiple binding pockets, which only partly overlap with that of PSGL-1. These observations open ways to selectively interfere with sulfatide/P-selectin-dependent platelet aggregation without affecting PSGL-1-dependent cell adhesion.
Language	English
Publishing date	2019-08-20
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2662592-1
ISSN	2077-0383
ISSN	2077-0383
DOI	10.3390/jcm8081266
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Article ; Online: High-density lipoprotein: key molecule in cholesterol efflux and the prevention of atherosclerosis.

Meurs, Illiana / Van Eck, Miranda / Van Berkel, Theo J C

Current pharmaceutical design

2009 Volume 16, Issue 13, Page(s) 1445–1467

Abstract: Accumulation of cholesterol by macrophages, leading to their transformation into foam cells is a key event in the initiation of atherosclerosis. As maintenance of cholesterol homeostasis in macrophages is essential to prevent foam cell formation, ... ...

Abstract	Accumulation of cholesterol by macrophages, leading to their transformation into foam cells is a key event in the initiation of atherosclerosis. As maintenance of cholesterol homeostasis in macrophages is essential to prevent foam cell formation, mechanisms by which macrophages export cellular cholesterol have been intensively investigated in recent years. Several epidemiological studies have shown that plasma levels of high-density lipoprotein (HDL) cholesterol are inversely correlated with the risk of atherosclerosis. The protective effect of HDL against macrophage foam cell formation and atherosclerosis is primarily attributed to its role in reverse cholesterol transport (RCT), a process by which excess cholesterol in peripheral tissues is transported to the liver for excretion. The present review discusses current knowledge on the biological activities of the major apolipoproteins, enzymes, lipid transfer proteins, receptors, and lipid transporters associated with HDL function and levels. In addition, current views on the molecular mechanisms underlying the atheroprotective functions of HDL beyond promotion of RCT, including the anti-oxidant, anti-thrombotic, anti-inflammatory and anti-apoptotic properties of HDL are summarized.
MeSH term(s)	Atherosclerosis/prevention & control ; Biological Transport ; Cholesterol/metabolism ; Humans ; Lipoproteins, HDL/physiology ; Macrophages/metabolism
Chemical Substances	Lipoproteins, HDL ; Cholesterol (97C5T2UQ7J)
Language	English
Publishing date	2009-10-20
Publishing country	United Arab Emirates
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1304236-1
ISSN	1873-4286 ; 1381-6128
ISSN (online)	1873-4286
ISSN	1381-6128
DOI	10.2174/138161210791051022
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Zs.A 4714: Show issues

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Article: Structure-affinity relationships of adenosine A2B receptor ligands.

Beukers, Margot W / Meurs, Illiana / Ijzerman, Adriaan P

Medicinal research reviews

2006 Volume 26, Issue 5, Page(s) 667–698

Abstract: Many selective and high affinity agonists and antagonists have been developed for the adenosine A(1), A(2A), and A(3) receptors. Very recently such compounds have been identified for the adenosine A(2B) receptors. This review presents an overview of the ... ...

Abstract	Many selective and high affinity agonists and antagonists have been developed for the adenosine A(1), A(2A), and A(3) receptors. Very recently such compounds have been identified for the adenosine A(2B) receptors. This review presents an overview of the structure-affinity relationships of antagonists and agonists for this receptor subtype as published in the scientific and patent literature. To date the most selective >370-fold, high affinity adenosine A(2B) receptor antagonist is the xanthine analog, compound 16 (8-(1-(3-phenyl-1,2,4-oxadiazol-5-yl)methyl)-1H-pyrazol-4-yl)-1,3-dipropyl-1H-purine-2,6(3H,7H)-dione). The pyrrolopyrimidine analog OSIP339391 (73) is slightly less selective, 70-fold, but has a higher affinity 0.41 nM compared to 1 nM for compound 16. Other promising classes of compounds with selectivities ranging from 10- to 160-fold and affinities ranging from 3 to 112 nM include triazolo, aminothiazole, quinazoline, and pyrimidin-2-amine analogs. Progress has also been achieved concerning the development of selective high affinity agonists for the adenosine A(2B) receptor. For years the most potent, albeit non-selective adenosine A(2B) receptor agonist was (S)PHPNECA (88). Last year, a new class of non-ribose ligands was reported. Several compounds displayed selectivity with respect to adenosine A(2A) and A(3) receptors. In addition, full and partial agonists for the adenosine A(2B) receptor were identified with EC(50) values of 10 nM (LUF5835, 103) and 9 nM (LUF5845, 105), respectively.
MeSH term(s)	Adenosine A2 Receptor Agonists ; Adenosine A2 Receptor Antagonists ; Animals ; Humans ; Ligands ; Receptor, Adenosine A2B/chemistry ; Receptor, Adenosine A2B/metabolism ; Structure-Activity Relationship
Chemical Substances	Adenosine A2 Receptor Agonists ; Adenosine A2 Receptor Antagonists ; Ligands ; Receptor, Adenosine A2B
Language	English
Publishing date	2006-09
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	603210-2
ISSN	0198-6325
ISSN	0198-6325
DOI	10.1002/med.20069
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Zs.A 1764: Show issues

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Article ; Online: Sympathetic nervous system control of triglyceride metabolism: novel concepts derived from recent studies.

Geerling, Janine J / Boon, Mariëtte R / Kooijman, Sander / Parlevliet, Edwin T / Havekes, Louis M / Romijn, Johannes A / Meurs, Illiana M / Rensen, Patrick C N

Journal of lipid research

2013 Volume 55, Issue 2, Page(s) 180–189

Abstract: Important players in triglyceride (TG) metabolism include the liver (production), white adipose tissue (WAT) (storage), heart and skeletal muscle (combustion to generate ATP), and brown adipose tissue (BAT) (combustion toward heat), the collective action ...

Abstract	Important players in triglyceride (TG) metabolism include the liver (production), white adipose tissue (WAT) (storage), heart and skeletal muscle (combustion to generate ATP), and brown adipose tissue (BAT) (combustion toward heat), the collective action of which determine plasma TG levels. Interestingly, recent evidence points to a prominent role of the hypothalamus in TG metabolism through innervating the liver, WAT, and BAT mainly via sympathetic branches of the autonomic nervous system. Here, we review the recent findings in the area of sympathetic control of TG metabolism. Various neuronal populations, such as neuropeptide Y (NPY)-expressing neurons and melanocortin-expressing neurons, as well as peripherally produced hormones (i.e., GLP-1, leptin, and insulin), modulate sympathetic outflow from the hypothalamus toward target organs and thereby influence peripheral TG metabolism. We conclude that sympathetic stimulation in general increases lipolysis in WAT, enhances VLDL-TG production by the liver, and increases the activity of BAT with respect to lipolysis of TG, followed by combustion of fatty acids toward heat. Moreover, the increased knowledge about the involvement of the neuroendocrine system in TG metabolism presented in this review offers new therapeutic options to fight hypertriglyceridemia by specifically modulating sympathetic nervous system outflow toward liver, BAT, or WAT.
MeSH term(s)	Adipose Tissue, Brown/metabolism ; Adipose Tissue, White/metabolism ; Animals ; Humans ; Lipoproteins/metabolism ; Liver/metabolism ; Sympathetic Nervous System/physiology ; Triglycerides/metabolism
Chemical Substances	Lipoproteins ; Triglycerides
Language	English
Publishing date	2013-11-27
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	80154-9
ISSN	1539-7262 ; 0022-2275
ISSN (online)	1539-7262
ISSN	0022-2275
DOI	10.1194/jlr.R045013
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Zs.A 175: Show issues

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Article ; Online: The effect of ABCG1 deficiency on atherosclerotic lesion development in LDL receptor knockout mice depends on the stage of atherogenesis.

Meurs, Illiana / Lammers, Bart / Zhao, Ying / Out, Ruud / Hildebrand, Reeni B / Hoekstra, Menno / Van Berkel, Theo J C / Van Eck, Miranda

Atherosclerosis

2012 Volume 221, Issue 1, Page(s) 41–47

Abstract: Objective: As ABCG1 plays a role in cholesterol efflux, macrophage ABCG1 expression has been suggested to protect against atherosclerosis. However, we and others observed varying effects of ABCG1 deficiency on atherosclerotic lesion size. The objective ... ...

Abstract	Objective: As ABCG1 plays a role in cholesterol efflux, macrophage ABCG1 expression has been suggested to protect against atherosclerosis. However, we and others observed varying effects of ABCG1 deficiency on atherosclerotic lesion size. The objective of this study was to define the effect of ABCG1 deficiency during atherosclerotic lesion progression in LDL receptor knockout (LDLr(-/-)) mice. Methods and results: ABCG1(-/-)/LDLr(-/-) and ABCG1(+/+)/LDLr(-/-) littermates were fed a Western-type diet for 10 and 12 weeks in order to study the effect of ABCG1 deficiency in the exponential phase of atherosclerotic lesion formation. At 10 weeks of diet feeding, a significant 1.5-fold increase in early atherosclerotic lesion size (130±12×10(3) μm(2)) was observed in ABCG1(-/-)/LDLr(-/-) mice compared to ABCG1(+/+)/LDLr(-/-) mice (88±11×10(3) μm(2); p<0.05). Interestingly, in more advanced lesions, induced by 12 weeks of WTD feeding, ABCG1(-/-)/LDLr(-/-) mice showed a significant 1.7-fold decrease in atherosclerotic lesion size (160±20×10(3) μm(2) vs 273±19×10(3) μm(2) in control mice; p<0.01), indicating that in the ABCG1(-/-)/LDLr(-/-) mice progression of lesion formation is retarded as compared to ABCG1(+/+)/LDLr(-/-) mice. In addition, correlation analysis performed on 7 independent published studies and the current study confirmed that ABCG1 is atheroprotective in early lesions, while the development of advanced lesions is stimulated. Conclusions: It appears that the effect of ABCG1 deficiency on lesion development in LDLr(-/-) mice depends on the stage of atherogenesis, whereby the absence of ABCG1 leads to increased lesions at sizes<167×10(3) μm(2) while in more advanced stages of atherosclerosis enhanced apoptosis and/or compensatory mechanisms lead to retarded lesion progression.
MeSH term(s)	ATP Binding Cassette Transporter, Sub-Family G, Member 1 ; ATP-Binding Cassette Transporters/genetics ; Animals ; Apoptosis ; Atherosclerosis/genetics ; Atherosclerosis/metabolism ; Atherosclerosis/pathology ; Atherosclerosis/prevention & control ; Cholesterol/blood ; Disease Models, Animal ; Disease Progression ; Lipoproteins/blood ; Lipoproteins/deficiency ; Lipoproteins/genetics ; Macrophages/metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Necrosis ; Receptors, LDL/deficiency ; Receptors, LDL/genetics ; Time Factors
Chemical Substances	ABCG1 protein, mouse ; ATP Binding Cassette Transporter, Sub-Family G, Member 1 ; Lipoproteins ; Receptors, LDL ; Cholesterol (97C5T2UQ7J)
Language	English
Publishing date	2012-03
Publishing country	Ireland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80061-2
ISSN	1879-1484 ; 0021-9150
ISSN (online)	1879-1484
ISSN	0021-9150
DOI	10.1016/j.atherosclerosis.2011.11.024
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Zs.A 226: Show issues

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Article ; Online: Augmented atherogenesis in LDL receptor deficient mice lacking both macrophage ABCA1 and ApoE.

Lammers, Bart / Zhao, Ying / Hoekstra, Menno / Hildebrand, Reeni B / Ye, Dan / Meurs, Illiana / Van Berkel, Theo J C / Van Eck, Miranda

PloS one

2011 Volume 6, Issue 10, Page(s) e26095

Abstract: Aim: ABCA1 protects against atherosclerosis by facilitating cholesterol efflux from macrophage foam cells in the arterial wall to extracellular apolipoprotein (apo) A-I. In contrast to apoA-I, apoE is secreted by macrophages and can, like apoA-I, induce ...

Abstract	Aim: ABCA1 protects against atherosclerosis by facilitating cholesterol efflux from macrophage foam cells in the arterial wall to extracellular apolipoprotein (apo) A-I. In contrast to apoA-I, apoE is secreted by macrophages and can, like apoA-I, induce ABCA1-mediated cholesterol efflux. Yet, the combined effect of macrophage ABCA1 and apoE on lesion development is unexplored. Methods and results: LDL receptor knockout (KO) mice were transplanted with bone marrow from ABCA1/apoE double KO (dKO) mice, their respective single KO's, and wild-type (WT) controls and were challenged with a high-fat/high-cholesterol diet for 9 weeks. In vitro cholesterol efflux experiments showed no differences between ABCA1 KO and dKO macrophages. The serum non-HDL/HDL ratio in dKO transplanted mice was 1.7-fold and 2.4-fold (p<0.01) increased compared to WT and ABCA1 KO transplanted mice, respectively. The atherosclerotic lesion area in dKO transplanted animals (650±94×10(3) µm(2)), however, was 1.9-fold (p<0.01) and 1.6-fold (p<0.01) increased compared to single knockouts (ABCA1 KO: 341±20×10(3) µm(2); apoE KO: 402±78×10(3) µm(2), respectively) and 3.1-fold increased (p<0.001) compared to WT (211±20×10(3) µm(2)). When normalized for serum cholesterol exposure, macrophage ABCA1 and apoE independently protected against atherosclerotic lesion development (p<0.001). Moreover, hepatic expression levels of TNFα and IL-6 were highly induced in dKO transplanted animals (3.0-fold; p<0.05, and 4.3-fold; p<0.001, respectively). In agreement, serum IL-6 levels were also enhanced in ABCA1 KO transplanted mice (p<0.05) and even further enhanced in dKO transplanted animals (3.1-fold as compared to ABCA1 KO transplanted animals; p<0.05). Conclusions: Combined deletion of macrophage ABCA1 and apoE results in a defect in cholesterol efflux and, compared to ABCA1 KO transplanted mice, elevated serum total cholesterol levels. Importantly, these mice also suffer from enhanced systemic and hepatic inflammation, together resulting in the observed augmented atherosclerotic lesion development.
MeSH term(s)	ATP Binding Cassette Transporter 1 ; ATP-Binding Cassette Transporters/metabolism ; Animals ; Apolipoproteins E/blood ; Apolipoproteins E/deficiency ; Atherosclerosis/blood ; Atherosclerosis/metabolism ; Atherosclerosis/pathology ; Bone Marrow Transplantation ; Cholesterol Esters/metabolism ; Cytokines/metabolism ; Dietary Fats/administration & dosage ; Dietary Fats/pharmacology ; Feeding Behavior/drug effects ; Female ; Gene Expression Regulation, Enzymologic/drug effects ; Inflammation Mediators/metabolism ; Lipoprotein Lipase/genetics ; Lipoprotein Lipase/metabolism ; Lipoproteins/blood ; Liver/drug effects ; Liver/enzymology ; Macrophages/drug effects ; Macrophages/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; RNA, Messenger/genetics ; RNA, Messenger/metabolism ; Receptors, LDL/deficiency ; Receptors, LDL/metabolism ; Spleen/metabolism ; Spleen/pathology
Chemical Substances	ATP Binding Cassette Transporter 1 ; ATP-Binding Cassette Transporters ; Apolipoproteins E ; Cholesterol Esters ; Cytokines ; Dietary Fats ; Inflammation Mediators ; Lipoproteins ; RNA, Messenger ; Receptors, LDL ; Lipoprotein Lipase (EC 3.1.1.34)
Language	English
Publishing date	2011-10-11
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1932-6203
ISSN (online)	1932-6203
DOI	10.1371/journal.pone.0026095
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: The effect of ABCG1 deficiency on atherosclerotic lesion development in LDL receptor knockout mice depends on the stage of atherogenesis

Meurs, Illiana / Lammers, Bart / Zhao, Ying / Out, Ruud / Hildebrand, Reeni B / Hoekstra, Menno / Van Berkel, Theo J.C / Van Eck, Miranda

Atherosclerosis. 2012 Mar., v. 221, no. 1

2012

Abstract: OBJECTIVE: As ABCG1 plays a role in cholesterol efflux, macrophage ABCG1 expression has been suggested to protect against atherosclerosis. However, we and others observed varying effects of ABCG1 deficiency on atherosclerotic lesion size. The objective ... ...

Abstract	OBJECTIVE: As ABCG1 plays a role in cholesterol efflux, macrophage ABCG1 expression has been suggested to protect against atherosclerosis. However, we and others observed varying effects of ABCG1 deficiency on atherosclerotic lesion size. The objective of this study was to define the effect of ABCG1 deficiency during atherosclerotic lesion progression in LDL receptor knockout (LDLr⁻/⁻) mice. METHODS AND RESULTS: ABCG1⁻/⁻/LDLr⁻/⁻ and ABCG1⁺/⁺/LDLr⁻/⁻ littermates were fed a Western-type diet for 10 and 12 weeks in order to study the effect of ABCG1 deficiency in the exponential phase of atherosclerotic lesion formation. At 10 weeks of diet feeding, a significant 1.5-fold increase in early atherosclerotic lesion size (130±12×10³μm²) was observed in ABCG1⁻/⁻/LDLr⁻/⁻ mice compared to ABCG1⁺/⁺/LDLr⁻/⁻ mice (88±11×10³μm²; p<0.05). Interestingly, in more advanced lesions, induced by 12 weeks of WTD feeding, ABCG1⁻/⁻/LDLr⁻/⁻ mice showed a significant 1.7-fold decrease in atherosclerotic lesion size (160±20×10³μm² vs 273±19×10³μm² in control mice; p<0.01), indicating that in the ABCG1⁻/⁻/LDLr⁻/⁻ mice progression of lesion formation is retarded as compared to ABCG1⁺/⁺/LDLr⁻/⁻ mice. In addition, correlation analysis performed on 7 independent published studies and the current study confirmed that ABCG1 is atheroprotective in early lesions, while the development of advanced lesions is stimulated. CONCLUSIONS: It appears that the effect of ABCG1 deficiency on lesion development in LDLr⁻/⁻ mice depends on the stage of atherogenesis, whereby the absence of ABCG1 leads to increased lesions at sizes<167×10³μm² while in more advanced stages of atherosclerosis enhanced apoptosis and/or compensatory mechanisms lead to retarded lesion progression.
Keywords	apoptosis ; arsenic ; atherogenesis ; atherosclerosis ; cholesterol ; diet ; low density lipoprotein ; macrophages ; mice
Language	English
Dates of publication	2012-03
Size	p. 41-47.
Publishing place	Elsevier Ireland Ltd
Document type	Article
ZDB-ID	80061-2
ISSN	1879-1484 ; 0021-9150
ISSN (online)	1879-1484
ISSN	0021-9150
DOI	10.1016/j.atherosclerosis.2011.11.024
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Inhibition of the central melanocortin system decreases brown adipose tissue activity.

Kooijman, Sander / Boon, Mariëtte R / Parlevliet, Edwin T / Geerling, Janine J / van de Pol, Vera / Romijn, Johannes A / Havekes, Louis M / Meurs, Illiana / Rensen, Patrick C N

Journal of lipid research

2014 Volume 55, Issue 10, Page(s) 2022–2032

Abstract: The melanocortin system is an important regulator of energy balance, and melanocortin 4 receptor (MC4R) deficiency is the most common monogenic cause of obesity. We investigated whether the relationship between melanocortin system activity and energy ... ...

Abstract	The melanocortin system is an important regulator of energy balance, and melanocortin 4 receptor (MC4R) deficiency is the most common monogenic cause of obesity. We investigated whether the relationship between melanocortin system activity and energy expenditure (EE) is mediated by brown adipose tissue (BAT) activity. Therefore, female APOE3-Leiden.CETP transgenic mice were fed a Western-type diet for 4 weeks and infused intracerebroventricularly with the melanocortin 3/4 receptor (MC3/4R) antagonist SHU9119 or vehicle for 2 weeks. SHU9119 increased food intake (+30%) and body fat (+50%) and decreased EE by reduction in fat oxidation (-42%). In addition, SHU9119 impaired the uptake of VLDL-TG by BAT. In line with this, SHU9119 decreased uncoupling protein-1 levels in BAT (-60%) and induced large intracellular lipid droplets, indicative of severely disturbed BAT activity. Finally, SHU9119-treated mice pair-fed to the vehicle-treated group still exhibited these effects, indicating that MC4R inhibition impairs BAT activity independent of food intake. These effects were not specific to the APOE3-Leiden.CETP background as SHU9119 also inhibited BAT activity in wild-type mice. We conclude that inhibition of central MC3/4R signaling impairs BAT function, which is accompanied by reduced EE, thereby promoting adiposity. We anticipate that activation of MC4R is a promising strategy to combat obesity by increasing BAT activity.
MeSH term(s)	Adipose Tissue, Brown/metabolism ; Animals ; Apolipoprotein E3/genetics ; Apolipoprotein E3/metabolism ; Female ; Melanocyte-Stimulating Hormones/pharmacology ; Mice ; Mice, Transgenic ; Oxidation-Reduction/drug effects ; Receptor, Melanocortin, Type 3/antagonists & inhibitors ; Receptor, Melanocortin, Type 3/genetics ; Receptor, Melanocortin, Type 3/metabolism ; Receptor, Melanocortin, Type 4/antagonists & inhibitors ; Receptor, Melanocortin, Type 4/genetics ; Receptor, Melanocortin, Type 4/metabolism ; Signal Transduction/drug effects
Chemical Substances	Apolipoprotein E3 ; MC4R protein, mouse ; Mc3r protein, mouse ; Receptor, Melanocortin, Type 3 ; Receptor, Melanocortin, Type 4 ; SHU 9119 (168482-23-3) ; Melanocyte-Stimulating Hormones (9002-79-3)
Language	English
Publishing date	2014-07-12
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.M045989
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