| CETP as a Target in HDL-Raising Therapy: Lessons from APOE*3-Leiden.CETP Transgenic Mice |
| | CETP as a target in HDL-raising therapy lessons from APOE*3-Leiden.CETP mice |
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| Outline of Presentation |
| | Outline of Presentation |
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| Lipoprotein metabolism |
| | Lipoprotein metabolism |
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| Role of CETP in lipoprotein metabolism |
| | Therapy of CVD-associated dyslipidemiamoney spent on drugs to treat dyslipidemia |
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| CVD-associated dyslipidemiamainly treated with statins |
| | Novel therapeutic strategiescurrently in development |
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| Outline of Presentation |
| | HDL-C is a strong inverse predictorof CHD risk at all levels of LDL-C |
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| Antiatherogenic properties of HDL |
| | First HDL-raising strategy: CETP inhibition |
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| CETP inhibitor: Torcetrapib |
| | Torcetrapib strongly increases HDL-C levelsPhase I studies in normolipidemic healthy volunteers |
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| Torcetrapib strongly increases HDL but does not reduce atherosclerosis! |
| | Elucidation of (adverse) effects of torcetrapib in mice through translational research |
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| Wild-type mice:low (V)LDL and high HDL |
| | Mouse model for human-like lipoprotein metabolism |
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| Structure apoE |
| | APOE*3-Leiden.CETP transgenic mice:human-like lipoprotein metabolism |
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| APOE*3-Leiden.CETP transgenic mice: human-like lipoprotein metabolism |
| | APOE*3-Leiden.CETP mice:human-like lipoprotein metabolism |
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| Effect CETP expression on atherosclerosisstudy design |
| | CETP expression in APOE*3-Leiden mice aggravates diet-induced atherosclerosis |
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| Atherosclerosis development in E3L.CETP miceis not simply predicted from cholesterol exposure |
| | APOE*3-Leiden.CETP mouse:model for human-like lipoprotein metabolism |
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| Torcetrapib in E3L.CETP mice |
| | Torcetrapib decreases CETP activityOral gavage in solutol:ethanol:saline (10:10:80) |
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| Torcetrapib decreases CETP activityOral gavage in solutol:ethanol:saline (10:10:80) (10 mg/kg) |
| | Torcetrapib tends to decreases cholesterolDiet + 0.1% cholesterol + torcetrapib |
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| Torcetrapib increases HDL in E3L.CETP miceDiet + 0.1% cholesterol + 0.01% torcetrapib |
| | Effect of torcetrapib on atherosclerosis development in APOE*3-Leiden.CETP mice |
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| Torcetrapib reduces CETP activityand increases CETP mass |
| | Torcetrapib reduces CETP activity |
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| Torcetrapib reduces plasma total cholesteroland increases HDL-cholesterol |
| | Torcetrapib reduces atherosclerotic lesion area, but does not add to the effect of atorvastatin |
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| Torcetrapib reduces atherosclerotic plaque severity,but not beyond atorvastatin |
| | Torcetrapib increases MCP-1 content, monocyte adherence, and macrophage content of the plaque |
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| Torcetrapib decreases collagen content of the plaque, independent of smooth muscle cell content |
| | Torcetrapib induces an unstable lesion phenotype as compared to atorvastatin |
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| Torcetrapib tends to increasegeneral inflammatory status |
| | Torcetrapib increases generalinflammatory status and plasma aldosterone |
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| Torcetrapib increases plasma aldosterone viaclass-specific effect independent of CETP inhibition |
| | Outline of Presentation |
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| Current drugs that increase HDL-C levels |
| | Fenofibrate and atorvastatin in E3L.CETP mice |
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| Fenofibrate |
| | Fenofibrate decreases TG in E3L.CETP miceDiet + 0.25% cholesterol + 0-0.04% fenofibrate (males) |
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| Fenofibrate increases HDL in E3L.CETP miceDiet + 0.25% cholesterol + fenofibrate (males) |
| | Fenofibrate increases HDL in E3L.CETP miceDiet + 0.25% cholesterol + 0.04% fenofibrate (males) |
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| Fenofibrate increases HDL in E3L.CETP miceDiet + 0.25% cholesterol + 0.04% fenofibrate (males) |
| | FF does not differentially affect HDL genesDiet + 0.25% cholesterol + 0.04% fenofibrate (males) |
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| Fenofibrate increases HDL in E3L.CETP miceDiet + 0.25% cholesterol + 0.04% fenofibrate (males) |
| | Atorvastatin in E3L.CETP mice |
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| Atorvastatin |
| | Atorvastatin decreases TC in E3L.CETP miceDiet + 0.1% cholesterol + atorvastatin (females) |
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| Atorvastatin increases HDL in E3L.CETP miceDiet + 0.25% cholesterol + 0.01% atorvastatin (males) |
| | Atorvastatin increases HDL in E3L.CETP miceDiet + 0.25% cholesterol + 0.01% atorvastatin (males) |
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| Atorva does not differentially affect HDL genesDiet + 0.25% cholesterol + 0.01% atorvastatin (males) |
| | Atorvastatin reduces CETP expressionDiet + 0.25% cholesterol + 0.01% atorvastatin (males) |
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| Atorvastatin reduces CETP mass and activityDiet + 0.25% cholesterol + atorvastatin (females) |
| | Mechanism underlying HDL-raising effectof statins and fibrates |
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| Niacin |
| | Niacin strongly reduces cardiac events |
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| Atheroprotective effect of niacin is accompanied by a large increase in HDL level |
| | Niacin potently increases plasma HDL levels |
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| Niacin does not affect HDL in E3L miceDiet + 0.1% cholesterol + 0.3% niacin (female mice) |
| | Niacin decreases TG and TC in E3L.CETPDiet + 0.1% cholesterol + niacin (female mice) |
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| Niacin decreases TG and TC in E3L.CETPDiet + 0.1% cholesterol + niacin (female mice) |
| | Niacin increases HDL in E3L.CETP miceDiet + 0.1% cholesterol + niacin (female mice) |
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| Niacin increases HDL in E3L.CETP miceDiet + 0.1% cholesterol + niacin (female mice) |
| | Niacin decreases clearance of 125I-apoAI-HDLDiet + 0.1% cholesterol + niacin (female mice) |
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| Niacin decreases liver lipidsDiet + 0.1% cholesterol + niacin (female mice) |
| | Niacin decreases plasma CETP activityDiet + 0.1% cholesterol + niacin (female mice) |
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| Niacin increases HDL particle sizeDiet + 0.1% cholesterol + niacin (female mice) |
| | Mechanism underlying HDL-raising effectof niacin |
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| Niacin causes regression of atherosclerosis |
| | Translational research: relation betweenliver lipid, CETP and HDL-C in humans |
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| Determination of liver TG byproton MR spectroscopy of the liver |
| | Pioglitazone and metforminequally reduce plasma apoB100 and TG |
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| Pioglitazone raises HDL-C,reduces CETP and reduces liver lipid |
| | Outline of Presentation |
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| Conclusions |
| | APOE*3-Leiden.CETP mouse |
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| APOE*3-Leiden.CETP mice |
| | Acknowledgments |
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| Thank you! |
| | The atherogenicity of CETP depends on TGProspective data from the Epic-Norfolk study |
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| CETP mutation Ile405Val increases HDL… |
| | … but increases CVD risk! |
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| Effect of CETP on VLDL levels seem to largely explain increased atherosclerosis |
| | Slide 94 |
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| Effect of CETP expression on atherosclerosis in APOE*3-Leiden mice |
| | APOE*3-Leiden.CETP micealtered lipoprotein profile (female, chow diet) |
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| Effect CETP expression on atherosclerosisstudy design |
| | CETP expression increases plasma cholesterol and shifts cholesterol distribution |
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| Quantification of atherosclerosis development in heart valve area in aortic root |
| | CETP aggravates lesion severity in aortic rootWestern-type diet (19 weeks); HPS staining |
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| CETP increases atherosclerotic lesion areaWestern-type diet (19 weeks); HPS staining |
| | LXR agonist in E3L.CETP mice |
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| LXR agonist decreases HDL in E3L.CETPDiet + 0.25% cholesterol + 0.01% T0901317 (male mice) |
| | LXR agonist decreases HDL in E3L.CETPDiet + 0.25% cholesterol + 0.01% T0901317 (male mice) |
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| LXR agonist decreases HDL in E3L.CETPDiet + 0.25% cholesterol + 0.01% T0901317 (male mice) |
| | Torcetrapib |
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| Torcetrapib increases HDL in E3L.CETP miceOral gavage in solutol:ethanol:saline (10:10:80) (females) |
| | Torcetrapib tends to decreases cholesterolDiet + 0.1% cholesterol + torcetrapib (females) |
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| Torcetrapib increases HDL in E3L.CETP miceDiet + 0.1% cholesterol + 0.01% torcetrapib (females) |
| | CETP inhibitor Merck in CETP mice |
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| CETP-I increases HDL-C in CETP miceChow diet + 0.05% CETP inhibitor (~50 mg/kg) |
| | CETP-I increases HDL-C in CETP miceChow diet + 0.05% CETP inhibitor (male mice) |
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| CETP-I increases HDL-C in CETP miceDiet + 0….% cholesterol + …% CETP-I (male mice) |
| | Bile acids in E3L.CETP mice |
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| Bile acids decrease HDL-C in E3L.CETP miceChow diet + 0.5% TCA (male mice) |
| | Bile acids increase CETP in E3L.CETP miceChow diet + 0.5% TCA (male mice) |
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| Conclusions |
| | Human Lipoprotein Metabolism |
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| Lipoprotein metabolism – back to basics! |
| | Reduction of LDL cholesterol by statins (II) |
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| Lipoproteins - Composition |
| | Lipoproteins - Size |
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| Lipoproteins differ in size and density |
| | Lipoproteins differ in size and density |
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| Lipoprotein Metabolism |
| | Dyslipidemia |
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| Statins reduce LDL-cholesterol by inhibiting HMG-CoA reductase |
| | Factors known to reduce HDL-C levels (I) |
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| Factors known to reduce HDL-C levels (II) |
| | Anti-atherogenic activities of HDL particles (II) |
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| Anti-atherogenic activities of HDL particles (I) |
| | HDL is an anti-inflammatory agent |
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| Torcetrapib strongly increases HDL-C levelsPhase I studies in normolipidemic healthy volunteers (II) |
| | Torcetrapib: large phase III trial in patients |
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| Torcetrapib lacks anti-atherosclerotic efficacy! |
| | Potential explanations for failure of torcetrapib |
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| Lipoprotein Metabolism - mouse |
| | Lipoprotein Metabolism |
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| APOE*3-Leiden mouse |
| | Atherosclerosis development in APOE*3-Leiden mice depends on cholesterol exposure |
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| Rosuvastatin reduces plasma cholesterolin APOE*3-Leiden mice |
| | Rosuvastatin reduces atherosclerosis comparedto high and low cholesterol groups |
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| Rosuvastatin reduces expression ofmonocyte chemotactic protein-1 (MCP-1) |
| | Rosuvastatin reduces expression of MCP-1 compared to high and low cholesterol groups |
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| Rosuvastatin reduces serum amyloid A (SAA) compared to high and low cholesterol groups |
| | Regression of atherosclerosisin APOE*3-Leiden mice |
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| Introduction of CETP in APOE*3-Leiden mice |
| | Introduction of CETP in APOE*3-Leiden mice |
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| Overview of Presentation |
| | raising HDL: novel therapeutic targets |
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| raising HDL: novel therapeutic targets |
| | Experimental HDL-directed drugs |
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| ApoAIMilano (I) |
| | ApoAIMilano (II) |
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| D4F |
| | Niacin decreases plasma lipase activityDiet + 0.1% cholesterol + niacin (female mice) |
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| Therapy of CVD-associated dyslipidemiamarket for drugs to treat dyslipidemia |
| | Anti-atherogenic activities of HDL particles |
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| HDL plays role in reverse cholesterol transport |
| | Anti-atherogenic activities of HDL particles |
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