Triglyceride:High-Density Lipoprotein Cholesterol Effects in Healthy Subjects Administered a Peroxisome Proliferator Activated Receptor δ Agonist
OBJECTIVES—Exercise increases fatty acid oxidation (FAO), improves serum high density lipoprotein cholesterol (HDLc) and triglycerides (TG), and upregulates skeletal muscle peroxisome proliferator activated receptor (PPAR)δ expression. In parallel, PPARδ agonist-upregulated FAO would induce fatty-ac...
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| Published in | Arteriosclerosis, thrombosis, and vascular biology Vol. 27; no. 2; pp. 359 - 365 |
|---|---|
| Main Authors | , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
Philadelphia, PA
American Heart Association, Inc
01.02.2007
Hagerstown, MD Lippincott |
| Subjects | |
| Online Access | Get full text |
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| Abstract | OBJECTIVES—Exercise increases fatty acid oxidation (FAO), improves serum high density lipoprotein cholesterol (HDLc) and triglycerides (TG), and upregulates skeletal muscle peroxisome proliferator activated receptor (PPAR)δ expression. In parallel, PPARδ agonist-upregulated FAO would induce fatty-acid uptake (via peripheral lipolysis), and influence HDLc and TG-rich lipoprotein particle metabolism, as suggested in preclinical models.
METHODS AND RESULTS—Healthy volunteers were allocated placebo (n=6) or PPARδ agonist (GW501516) at 2.5 mg (n=9) or 10 mg (n=9), orally, once-daily for 2 weeks while hospitalized and sedentary. Standard lipid/lipoproteins were measured and in vivo fat feeding studies were conducted. Human skeletal muscle cells were treated with GW501516 in vitro and evaluated for lipid-related gene expression and FAO. Serum TG trended downwards (P=0.08, 10 mg), whereas TG clearance post fat-feeding improved with drug (P=0.02). HDLc was enhanced in both treatment groups (2.5 mg P=0.004, 10 mg P<0.001) when compared with the decrease in the placebo group (−11.5±1.6%, P=0.002). These findings complimented in vitro cell culture results whereby GW501516 induced FAO and upregulated CPT1 and CD36 expression, in addition to a 2-fold increase in ABCA1 (P=0.002). However, LpL expression remained unchanged.
CONCLUSIONS—This is the first report of a PPARδ agonist administered to man. In this small study, GW501516 significantly influenced HDLc and TGs in healthy volunteers. Enhanced in vivo serum fat clearance, and the first demonstrated in vitro upregulation in human skeletal muscle fat utilization and ABCA1 expression, suggests peripheral fat utilization and lipidation as potential mechanisms toward these HDL:TG effects. |
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| AbstractList | Exercise increases fatty acid oxidation (FAO), improves serum high density lipoprotein cholesterol (HDLc) and triglycerides (TG), and upregulates skeletal muscle peroxisome proliferator activated receptor (PPAR)delta expression. In parallel, PPARdelta agonist-upregulated FAO would induce fatty-acid uptake (via peripheral lipolysis), and influence HDLc and TG-rich lipoprotein particle metabolism, as suggested in preclinical models.
Healthy volunteers were allocated placebo (n=6) or PPARdelta agonist (GW501516) at 2.5 mg (n=9) or 10 mg (n=9), orally, once-daily for 2 weeks while hospitalized and sedentary. Standard lipid/lipoproteins were measured and in vivo fat feeding studies were conducted. Human skeletal muscle cells were treated with GW501516 in vitro and evaluated for lipid-related gene expression and FAO. Serum TG trended downwards (P=0.08, 10 mg), whereas TG clearance post fat-feeding improved with drug (P=0.02). HDLc was enhanced in both treatment groups (2.5 mg P=0.004, 10 mg P<0.001) when compared with the decrease in the placebo group (-11.5+/-1.6%, P=0.002). These findings complimented in vitro cell culture results whereby GW501516 induced FAO and upregulated CPT1 and CD36 expression, in addition to a 2-fold increase in ABCA1 (P=0.002). However, LpL expression remained unchanged.
This is the first report of a PPARdelta agonist administered to man. In this small study, GW501516 significantly influenced HDLc and TGs in healthy volunteers. Enhanced in vivo serum fat clearance, and the first demonstrated in vitro upregulation in human skeletal muscle fat utilization and ABCA1 expression, suggests peripheral fat utilization and lipidation as potential mechanisms toward these HDL:TG effects. OBJECTIVES—Exercise increases fatty acid oxidation (FAO), improves serum high density lipoprotein cholesterol (HDLc) and triglycerides (TG), and upregulates skeletal muscle peroxisome proliferator activated receptor (PPAR)δ expression. In parallel, PPARδ agonist-upregulated FAO would induce fatty-acid uptake (via peripheral lipolysis), and influence HDLc and TG-rich lipoprotein particle metabolism, as suggested in preclinical models. METHODS AND RESULTS—Healthy volunteers were allocated placebo (n=6) or PPARδ agonist (GW501516) at 2.5 mg (n=9) or 10 mg (n=9), orally, once-daily for 2 weeks while hospitalized and sedentary. Standard lipid/lipoproteins were measured and in vivo fat feeding studies were conducted. Human skeletal muscle cells were treated with GW501516 in vitro and evaluated for lipid-related gene expression and FAO. Serum TG trended downwards (P=0.08, 10 mg), whereas TG clearance post fat-feeding improved with drug (P=0.02). HDLc was enhanced in both treatment groups (2.5 mg P=0.004, 10 mg P<0.001) when compared with the decrease in the placebo group (−11.5±1.6%, P=0.002). These findings complimented in vitro cell culture results whereby GW501516 induced FAO and upregulated CPT1 and CD36 expression, in addition to a 2-fold increase in ABCA1 (P=0.002). However, LpL expression remained unchanged. CONCLUSIONS—This is the first report of a PPARδ agonist administered to man. In this small study, GW501516 significantly influenced HDLc and TGs in healthy volunteers. Enhanced in vivo serum fat clearance, and the first demonstrated in vitro upregulation in human skeletal muscle fat utilization and ABCA1 expression, suggests peripheral fat utilization and lipidation as potential mechanisms toward these HDL:TG effects. Exercise increases fatty acid oxidation (FAO), improves serum high density lipoprotein cholesterol (HDLc) and triglycerides (TG), and upregulates skeletal muscle peroxisome proliferator activated receptor (PPAR)delta expression. In parallel, PPARdelta agonist-upregulated FAO would induce fatty-acid uptake (via peripheral lipolysis), and influence HDLc and TG-rich lipoprotein particle metabolism, as suggested in preclinical models.OBJECTIVEExercise increases fatty acid oxidation (FAO), improves serum high density lipoprotein cholesterol (HDLc) and triglycerides (TG), and upregulates skeletal muscle peroxisome proliferator activated receptor (PPAR)delta expression. In parallel, PPARdelta agonist-upregulated FAO would induce fatty-acid uptake (via peripheral lipolysis), and influence HDLc and TG-rich lipoprotein particle metabolism, as suggested in preclinical models.Healthy volunteers were allocated placebo (n=6) or PPARdelta agonist (GW501516) at 2.5 mg (n=9) or 10 mg (n=9), orally, once-daily for 2 weeks while hospitalized and sedentary. Standard lipid/lipoproteins were measured and in vivo fat feeding studies were conducted. Human skeletal muscle cells were treated with GW501516 in vitro and evaluated for lipid-related gene expression and FAO. Serum TG trended downwards (P=0.08, 10 mg), whereas TG clearance post fat-feeding improved with drug (P=0.02). HDLc was enhanced in both treatment groups (2.5 mg P=0.004, 10 mg P<0.001) when compared with the decrease in the placebo group (-11.5+/-1.6%, P=0.002). These findings complimented in vitro cell culture results whereby GW501516 induced FAO and upregulated CPT1 and CD36 expression, in addition to a 2-fold increase in ABCA1 (P=0.002). However, LpL expression remained unchanged.METHODS AND RESULTSHealthy volunteers were allocated placebo (n=6) or PPARdelta agonist (GW501516) at 2.5 mg (n=9) or 10 mg (n=9), orally, once-daily for 2 weeks while hospitalized and sedentary. Standard lipid/lipoproteins were measured and in vivo fat feeding studies were conducted. Human skeletal muscle cells were treated with GW501516 in vitro and evaluated for lipid-related gene expression and FAO. Serum TG trended downwards (P=0.08, 10 mg), whereas TG clearance post fat-feeding improved with drug (P=0.02). HDLc was enhanced in both treatment groups (2.5 mg P=0.004, 10 mg P<0.001) when compared with the decrease in the placebo group (-11.5+/-1.6%, P=0.002). These findings complimented in vitro cell culture results whereby GW501516 induced FAO and upregulated CPT1 and CD36 expression, in addition to a 2-fold increase in ABCA1 (P=0.002). However, LpL expression remained unchanged.This is the first report of a PPARdelta agonist administered to man. In this small study, GW501516 significantly influenced HDLc and TGs in healthy volunteers. Enhanced in vivo serum fat clearance, and the first demonstrated in vitro upregulation in human skeletal muscle fat utilization and ABCA1 expression, suggests peripheral fat utilization and lipidation as potential mechanisms toward these HDL:TG effects.CONCLUSIONSThis is the first report of a PPARdelta agonist administered to man. In this small study, GW501516 significantly influenced HDLc and TGs in healthy volunteers. Enhanced in vivo serum fat clearance, and the first demonstrated in vitro upregulation in human skeletal muscle fat utilization and ABCA1 expression, suggests peripheral fat utilization and lipidation as potential mechanisms toward these HDL:TG effects. Objectives— Exercise increases fatty acid oxidation (FAO), improves serum high density lipoprotein cholesterol (HDLc) and triglycerides (TG), and upregulates skeletal muscle peroxisome proliferator activated receptor (PPAR)δ expression. In parallel, PPARδ agonist-upregulated FAO would induce fatty-acid uptake (via peripheral lipolysis), and influence HDLc and TG-rich lipoprotein particle metabolism, as suggested in preclinical models. Methods and Results— Healthy volunteers were allocated placebo (n=6) or PPARδ agonist (GW501516) at 2.5 mg (n=9) or 10 mg (n=9), orally, once-daily for 2 weeks while hospitalized and sedentary. Standard lipid/lipoproteins were measured and in vivo fat feeding studies were conducted. Human skeletal muscle cells were treated with GW501516 in vitro and evaluated for lipid-related gene expression and FAO. Serum TG trended downwards ( P =0.08, 10 mg), whereas TG clearance post fat-feeding improved with drug ( P =0.02). HDLc was enhanced in both treatment groups (2.5 mg P =0.004, 10 mg P <0.001) when compared with the decrease in the placebo group (−11.5±1.6%, P =0.002). These findings complimented in vitro cell culture results whereby GW501516 induced FAO and upregulated CPT1 and CD36 expression, in addition to a 2-fold increase in ABCA1 ( P =0.002). However, LpL expression remained unchanged. Conclusions— This is the first report of a PPARδ agonist administered to man. In this small study, GW501516 significantly influenced HDLc and TGs in healthy volunteers. Enhanced in vivo serum fat clearance, and the first demonstrated in vitro upregulation in human skeletal muscle fat utilization and ABCA1 expression, suggests peripheral fat utilization and lipidation as potential mechanisms toward these HDL:TG effects. A specific PPARδ agonist was administered to human volunteers for the first time, revealing a decline in serum TG, an improvement in TG-clearance post-fat feeding, and an elevation in HDLc compared with placebo. Consistent with these findings, in vitro PPARδ-treated human skeletal muscle cells induced fatty acid oxidation, and upregulated ABCA1 expression. |
| Author | Sprecher, Dennis L. Perlstein, Itay Massien, Christine Hassall, David G. Pearce, Greg Johnson, Tony G. Billin, Andrew N. Willson, Timothy M. Ancellin, Nicolas Patterson, Scott D. Lobe, David C. |
| AuthorAffiliation | From the Department of Discovery Medicine (D.L.S., C.M., G.P., T.G.J.), Cardiovascular and Urogenital Center of Excellence in Drug Discovery, GlaxoSmithKline, King of Prussia, Pa; the Department of High-throughput Biology (A.N.B.), GlaxoSmithKline, Research Triangle Park, NC; the Department of Clinical Pharmacokinetics (I.P.), Modeling and Simulations, GlaxoSmithKline, King of Prussia, Pa; the Department of High Throughput Chemistry (T.M.W.), GlaxoSmithKline, Research Triangle Park, NC; the Department of Safety Assessment (D.G.H.), GlaxoSmithKline, Ware, UK; the Cardiovascular and Urogenital Center of Excellence in Drug Discovery (N.A.), GlaxoSmithKline, Les Ulis, France; the Department of Biomedical Data Sciences (S.D.P.), GlaxoSmithKline, Upper Providence, Pa; and the Department of Metabolic Diseases (D.C.L.), Metabolic and Viral Diseases Center of Excellence in Drug Discovery, GlaxoSmithKline, Research Triangle Park, NC |
| AuthorAffiliation_xml | – name: From the Department of Discovery Medicine (D.L.S., C.M., G.P., T.G.J.), Cardiovascular and Urogenital Center of Excellence in Drug Discovery, GlaxoSmithKline, King of Prussia, Pa; the Department of High-throughput Biology (A.N.B.), GlaxoSmithKline, Research Triangle Park, NC; the Department of Clinical Pharmacokinetics (I.P.), Modeling and Simulations, GlaxoSmithKline, King of Prussia, Pa; the Department of High Throughput Chemistry (T.M.W.), GlaxoSmithKline, Research Triangle Park, NC; the Department of Safety Assessment (D.G.H.), GlaxoSmithKline, Ware, UK; the Cardiovascular and Urogenital Center of Excellence in Drug Discovery (N.A.), GlaxoSmithKline, Les Ulis, France; the Department of Biomedical Data Sciences (S.D.P.), GlaxoSmithKline, Upper Providence, Pa; and the Department of Metabolic Diseases (D.C.L.), Metabolic and Viral Diseases Center of Excellence in Drug Discovery, GlaxoSmithKline, Research Triangle Park, NC |
| Author_xml | – sequence: 1 givenname: Dennis surname: Sprecher middlename: L. fullname: Sprecher, Dennis L. organization: From the Department of Discovery Medicine (D.L.S., C.M., G.P., T.G.J.), Cardiovascular and Urogenital Center of Excellence in Drug Discovery, GlaxoSmithKline, King of Prussia, Pa; the Department of High-throughput Biology (A.N.B.), GlaxoSmithKline, Research Triangle Park, NC; the Department of Clinical Pharmacokinetics (I.P.), Modeling and Simulations, GlaxoSmithKline, King of Prussia, Pa; the Department of High Throughput Chemistry (T.M.W.), GlaxoSmithKline, Research Triangle Park, NC; the Department of Safety Assessment (D.G.H.), GlaxoSmithKline, Ware, UK; the Cardiovascular and Urogenital Center of Excellence in Drug Discovery (N.A.), GlaxoSmithKline, Les Ulis, France; the Department of Biomedical Data Sciences (S.D.P.), GlaxoSmithKline, Upper Providence, Pa; and the Department of Metabolic Diseases (D.C.L.), Metabolic and Viral Diseases Center of Excellence in Drug Discovery, GlaxoSmithKline, Research Triangle Park, NC – sequence: 2 givenname: Christine surname: Massien fullname: Massien, Christine – sequence: 3 givenname: Greg surname: Pearce fullname: Pearce, Greg – sequence: 4 givenname: Andrew surname: Billin middlename: N. fullname: Billin, Andrew N. – sequence: 5 givenname: Itay surname: Perlstein fullname: Perlstein, Itay – sequence: 6 givenname: Timothy surname: Willson middlename: M. fullname: Willson, Timothy M. – sequence: 7 givenname: David surname: Hassall middlename: G. fullname: Hassall, David G. – sequence: 8 givenname: Nicolas surname: Ancellin fullname: Ancellin, Nicolas – sequence: 9 givenname: Scott surname: Patterson middlename: D. fullname: Patterson, Scott D. – sequence: 10 givenname: David surname: Lobe middlename: C. fullname: Lobe, David C. – sequence: 11 givenname: Tony surname: Johnson middlename: G. fullname: Johnson, Tony G. |
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| Copyright | 2007 American Heart Association, Inc. 2007 INIST-CNRS |
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| Keywords | Vascular disease Human PPAR Atherosclerosis Lipids Cardiovascular disease Lipoprotein Triglyceride lipid Cholesterol Peroxisome proliferator |
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| PublicationTitle | Arteriosclerosis, thrombosis, and vascular biology |
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| References | (e_1_3_3_32_2) 2001; 42 e_1_3_3_17_2 e_1_3_3_16_2 e_1_3_3_38_2 e_1_3_3_39_2 e_1_3_3_13_2 e_1_3_3_36_2 e_1_3_3_12_2 e_1_3_3_37_2 e_1_3_3_15_2 e_1_3_3_34_2 e_1_3_3_14_2 e_1_3_3_35_2 e_1_3_3_33_2 e_1_3_3_11_2 e_1_3_3_30_2 (e_1_3_3_41_2) 2000; 28 e_1_3_3_10_2 e_1_3_3_31_2 e_1_3_3_40_2 (e_1_3_3_9_2) 1993; 36 (e_1_3_3_19_2) 1976; 17 e_1_3_3_6_2 e_1_3_3_5_2 e_1_3_3_8_2 e_1_3_3_7_2 e_1_3_3_28_2 e_1_3_3_27_2 e_1_3_3_29_2 e_1_3_3_24_2 e_1_3_3_47_2 e_1_3_3_23_2 (e_1_3_3_26_2) 1996; 50 e_1_3_3_45_2 (e_1_3_3_18_2) 1995; 31 e_1_3_3_25_2 e_1_3_3_46_2 e_1_3_3_2_2 e_1_3_3_20_2 e_1_3_3_43_2 e_1_3_3_1_2 e_1_3_3_44_2 e_1_3_3_4_2 e_1_3_3_22_2 e_1_3_3_3_2 e_1_3_3_21_2 e_1_3_3_42_2 |
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| SubjectTerms | Adult Atherosclerosis (general aspects, experimental research) ATP Binding Cassette Transporter 1 ATP-Binding Cassette Transporters - genetics ATP-Binding Cassette Transporters - metabolism Biological and medical sciences Blood and lymphatic vessels Blood coagulation. Blood cells Cardiology. Vascular system Cardiovascular system CD36 Antigens - genetics CD36 Antigens - metabolism Cells, Cultured Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous Fatty Acids - metabolism Fundamental and applied biological sciences. Psychology Humans Lipoproteins, HDL - metabolism Male Medical sciences Molecular and cellular biology Muscle, Skeletal - cytology Muscle, Skeletal - drug effects Muscle, Skeletal - metabolism Oxidation-Reduction - drug effects Pharmacology. Drug treatments Platelet PPAR delta - agonists PPAR delta - genetics PPAR delta - metabolism Thiazoles - pharmacology Triglycerides - metabolism Up-Regulation - drug effects Vasodilator agents. Cerebral vasodilators |
| Title | Triglyceride:High-Density Lipoprotein Cholesterol Effects in Healthy Subjects Administered a Peroxisome Proliferator Activated Receptor δ Agonist |
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