Activation of Peroxisome Proliferator–Activated Receptor (PPAR)δ Promotes Reversal of Multiple Metabolic Abnormalities, Reduces Oxidative Stress, and Increases Fatty Acid Oxidation in Moderately Obese Men
Activation of Peroxisome Proliferator–Activated Receptor (PPAR)δ Promotes Reversal of Multiple Metabolic Abnormalities, Reduces Oxidative Stress, and Increases Fatty Acid Oxidation in Moderately Obese Men Ulf Risérus 1 , Dennis Sprecher 2 , Tony Johnson 2 , Eric Olson 2 , Sandra Hirschberg 2 , Aixue...
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| Published in | Diabetes (New York, N.Y.) Vol. 57; no. 2; pp. 332 - 339 |
|---|---|
| Main Authors | , , , , , , , , , , , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
Alexandria, VA
American Diabetes Association
01.02.2008
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| Subjects | |
| Online Access | Get full text |
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| Abstract | Activation of Peroxisome Proliferator–Activated Receptor (PPAR)δ Promotes Reversal of Multiple Metabolic Abnormalities, Reduces
Oxidative Stress, and Increases Fatty Acid Oxidation in Moderately Obese Men
Ulf Risérus 1 ,
Dennis Sprecher 2 ,
Tony Johnson 2 ,
Eric Olson 2 ,
Sandra Hirschberg 2 ,
Aixue Liu 3 ,
Zeke Fang 4 ,
Priti Hegde 5 ,
Duncan Richards 6 ,
Leli Sarov-Blat 5 ,
Jay C. Strum 5 ,
Samar Basu 7 ,
Jane Cheeseman 1 ,
Barbara A. Fielding 1 ,
Sandy M. Humphreys 1 ,
Theodore Danoff 3 ,
Niall R. Moore 8 ,
Peter Murgatroyd 9 ,
Stephen O'Rahilly 10 ,
Pauline Sutton 1 ,
Tim Willson 11 ,
David Hassall 12 ,
Keith N. Frayn 1 and
Fredrik Karpe 1
1 Oxford Centre for Diabetes, Endocrinology and Metabolism, University of Oxford, Oxford, U.K
2 Cardiovascular and Urogenital Center for Excellence in Drug Discovery, GlaxoSmithKline, King of Prussia, Pennsylvania
3 Human Target Validation, Cardiovascular and Urogenital Center for Excellence in Drug Discovery, GlaxoSmithKline, King of Prussia,
Pennsylvania
4 Statistics, GlaxoSmithKline, King of Prussia, Pennsylvania
5 Clinical Pharmacology and Discovery Medicine/Cardiovascular and Urogenital (CPDM CVU) Unit, GlaxoSmithKline, King of Prussia,
Pennsylvania
6 Addenbrooke's Centre for Clinical Investigation (ACCI) Unit, GlaxoSmithKline, Cambridge, U.K
7 Department of Public Health, University of Uppsala, Uppsala, Sweden
8 Department of Radiology, Churchill Hospital, University of Oxford, Oxford, U.K
9 Wellcome Trust Clinical Research Facility, Addenbrooke's Hospital, Cambridge, U.K
10 Department of Clinical Biochemistry and Medicine, University of Cambridge, Cambridge, U.K
11 GlaxoSmithKline, Research Triangle Park, North Carolina
12 GlaxoSmithKline, Stevenage, U.K
Address correspondence and reprint requests to Dr. F. Karpe, Churchill Hospital, Oxford OX3 7LJ, U.K. E-mail: fredrik.karpe{at}ocdem.ox.ac.uk
Abstract
OBJECTIVE— Pharmacological use of peroxisome proliferator–activated receptor (PPAR)δ agonists and transgenic overexpression of PPARδ
in mice suggest amelioration of features of the metabolic syndrome through enhanced fat oxidation in skeletal muscle. We hypothesize
a similar mechanism operates in humans.
RESEARCH DESIGN AND METHODS— The PPARδ agonist (10 mg o.d. GW501516), a comparator PPARα agonist (20 μg o.d. GW590735), and placebo were given in a double-blind,
randomized, three-parallel group, 2-week study to six healthy moderately overweight subjects in each group. Metabolic evaluation
was made before and after treatment including liver fat quantification, fasting blood samples, a 6-h meal tolerance test with
stable isotope fatty acids, skeletal muscle biopsy for gene expression, and urinary isoprostanes for global oxidative stress.
RESULTS— Treatment with GW501516 showed statistically significant reductions in fasting plasma triglycerides (−30%), apolipoprotein
B (−26%), LDL cholesterol (−23%), and insulin (−11%), whereas HDL cholesterol was unchanged. A 20% reduction in liver fat
content ( P < 0.05) and 30% reduction in urinary isoprostanes ( P = 0.01) were also observed. Except for a lowering of triglycerides (−30%, P < 0.05), none of these changes were observed in response to GW590735. The relative proportion of exhaled CO 2 directly originating from the fat content of the meal was increased ( P < 0.05) in response to GW501516, and skeletal muscle expression of carnitine palmitoyl-transferase 1b ( CPT1b ) was also significantly increased.
CONCLUSIONS— The PPARδ agonist GW501516 reverses multiple abnormalities associated with the metabolic syndrome without increasing oxidative
stress. The effect is probably caused by increased fat oxidation in skeletal muscle.
Apo, apolipoprotein
AST, aspartate aminotransferase
AUC, area under the curve
γGT, γ-glutamyltransferase
LCM, laser capture microdissection
LPL, lipoprotein lipase
MRI, magnetic resonance imaging
NEFA, nonesterified fatty acid
TTR, tracer-to-tracee ratio
Footnotes
Published ahead of print at http://diabetes.diabetesjournals.org on 16 November 2007. DOI: 10.2337/db07-1318.
U.R. and D.S. contributed equally to this work.
Additional information for this article can be found in an online appendix at http://dx.doi.org/10.2337/db07-1318 .
The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore
be hereby marked “advertisement” in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
Accepted November 10, 2007.
Received September 14, 2007.
DIABETES |
|---|---|
| AbstractList | Pharmacological use of peroxisome proliferator-activated receptor (PPAR)delta agonists and transgenic overexpression of PPARdelta in mice suggest amelioration of features of the metabolic syndrome through enhanced fat oxidation in skeletal muscle. We hypothesize a similar mechanism operates in humans.
The PPARdelta agonist (10 mg o.d. GW501516), a comparator PPARalpha agonist (20 mug o.d. GW590735), and placebo were given in a double-blind, randomized, three-parallel group, 2-week study to six healthy moderately overweight subjects in each group. Metabolic evaluation was made before and after treatment including liver fat quantification, fasting blood samples, a 6-h meal tolerance test with stable isotope fatty acids, skeletal muscle biopsy for gene expression, and urinary isoprostanes for global oxidative stress.
Treatment with GW501516 showed statistically significant reductions in fasting plasma triglycerides (-30%), apolipoprotein B (-26%), LDL cholesterol (-23%), and insulin (-11%), whereas HDL cholesterol was unchanged. A 20% reduction in liver fat content (P < 0.05) and 30% reduction in urinary isoprostanes (P = 0.01) were also observed. Except for a lowering of triglycerides (-30%, P < 0.05), none of these changes were observed in response to GW590735. The relative proportion of exhaled CO(2) directly originating from the fat content of the meal was increased (P < 0.05) in response to GW501516, and skeletal muscle expression of carnitine palmitoyl-transferase 1b (CPT1b) was also significantly increased.
The PPARdelta agonist GW501516 reverses multiple abnormalities associated with the metabolic syndrome without increasing oxidative stress. The effect is probably caused by increased fat oxidation in skeletal muscle. Activation of Peroxisome Proliferator–Activated Receptor (PPAR)δ Promotes Reversal of Multiple Metabolic Abnormalities, Reduces Oxidative Stress, and Increases Fatty Acid Oxidation in Moderately Obese Men Ulf Risérus 1 , Dennis Sprecher 2 , Tony Johnson 2 , Eric Olson 2 , Sandra Hirschberg 2 , Aixue Liu 3 , Zeke Fang 4 , Priti Hegde 5 , Duncan Richards 6 , Leli Sarov-Blat 5 , Jay C. Strum 5 , Samar Basu 7 , Jane Cheeseman 1 , Barbara A. Fielding 1 , Sandy M. Humphreys 1 , Theodore Danoff 3 , Niall R. Moore 8 , Peter Murgatroyd 9 , Stephen O'Rahilly 10 , Pauline Sutton 1 , Tim Willson 11 , David Hassall 12 , Keith N. Frayn 1 and Fredrik Karpe 1 1 Oxford Centre for Diabetes, Endocrinology and Metabolism, University of Oxford, Oxford, U.K 2 Cardiovascular and Urogenital Center for Excellence in Drug Discovery, GlaxoSmithKline, King of Prussia, Pennsylvania 3 Human Target Validation, Cardiovascular and Urogenital Center for Excellence in Drug Discovery, GlaxoSmithKline, King of Prussia, Pennsylvania 4 Statistics, GlaxoSmithKline, King of Prussia, Pennsylvania 5 Clinical Pharmacology and Discovery Medicine/Cardiovascular and Urogenital (CPDM CVU) Unit, GlaxoSmithKline, King of Prussia, Pennsylvania 6 Addenbrooke's Centre for Clinical Investigation (ACCI) Unit, GlaxoSmithKline, Cambridge, U.K 7 Department of Public Health, University of Uppsala, Uppsala, Sweden 8 Department of Radiology, Churchill Hospital, University of Oxford, Oxford, U.K 9 Wellcome Trust Clinical Research Facility, Addenbrooke's Hospital, Cambridge, U.K 10 Department of Clinical Biochemistry and Medicine, University of Cambridge, Cambridge, U.K 11 GlaxoSmithKline, Research Triangle Park, North Carolina 12 GlaxoSmithKline, Stevenage, U.K Address correspondence and reprint requests to Dr. F. Karpe, Churchill Hospital, Oxford OX3 7LJ, U.K. E-mail: fredrik.karpe{at}ocdem.ox.ac.uk Abstract OBJECTIVE— Pharmacological use of peroxisome proliferator–activated receptor (PPAR)δ agonists and transgenic overexpression of PPARδ in mice suggest amelioration of features of the metabolic syndrome through enhanced fat oxidation in skeletal muscle. We hypothesize a similar mechanism operates in humans. RESEARCH DESIGN AND METHODS— The PPARδ agonist (10 mg o.d. GW501516), a comparator PPARα agonist (20 μg o.d. GW590735), and placebo were given in a double-blind, randomized, three-parallel group, 2-week study to six healthy moderately overweight subjects in each group. Metabolic evaluation was made before and after treatment including liver fat quantification, fasting blood samples, a 6-h meal tolerance test with stable isotope fatty acids, skeletal muscle biopsy for gene expression, and urinary isoprostanes for global oxidative stress. RESULTS— Treatment with GW501516 showed statistically significant reductions in fasting plasma triglycerides (−30%), apolipoprotein B (−26%), LDL cholesterol (−23%), and insulin (−11%), whereas HDL cholesterol was unchanged. A 20% reduction in liver fat content ( P < 0.05) and 30% reduction in urinary isoprostanes ( P = 0.01) were also observed. Except for a lowering of triglycerides (−30%, P < 0.05), none of these changes were observed in response to GW590735. The relative proportion of exhaled CO 2 directly originating from the fat content of the meal was increased ( P < 0.05) in response to GW501516, and skeletal muscle expression of carnitine palmitoyl-transferase 1b ( CPT1b ) was also significantly increased. CONCLUSIONS— The PPARδ agonist GW501516 reverses multiple abnormalities associated with the metabolic syndrome without increasing oxidative stress. The effect is probably caused by increased fat oxidation in skeletal muscle. Apo, apolipoprotein AST, aspartate aminotransferase AUC, area under the curve γGT, γ-glutamyltransferase LCM, laser capture microdissection LPL, lipoprotein lipase MRI, magnetic resonance imaging NEFA, nonesterified fatty acid TTR, tracer-to-tracee ratio Footnotes Published ahead of print at http://diabetes.diabetesjournals.org on 16 November 2007. DOI: 10.2337/db07-1318. U.R. and D.S. contributed equally to this work. Additional information for this article can be found in an online appendix at http://dx.doi.org/10.2337/db07-1318 . The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked “advertisement” in accordance with 18 U.S.C. Section 1734 solely to indicate this fact. Accepted November 10, 2007. Received September 14, 2007. DIABETES Pharmacological use of peroxisome proliferator-activated receptor (PPAR)delta agonists and transgenic overexpression of PPARdelta in mice suggest amelioration of features of the metabolic syndrome through enhanced fat oxidation in skeletal muscle. We hypothesize a similar mechanism operates in humans.OBJECTIVEPharmacological use of peroxisome proliferator-activated receptor (PPAR)delta agonists and transgenic overexpression of PPARdelta in mice suggest amelioration of features of the metabolic syndrome through enhanced fat oxidation in skeletal muscle. We hypothesize a similar mechanism operates in humans.The PPARdelta agonist (10 mg o.d. GW501516), a comparator PPARalpha agonist (20 mug o.d. GW590735), and placebo were given in a double-blind, randomized, three-parallel group, 2-week study to six healthy moderately overweight subjects in each group. Metabolic evaluation was made before and after treatment including liver fat quantification, fasting blood samples, a 6-h meal tolerance test with stable isotope fatty acids, skeletal muscle biopsy for gene expression, and urinary isoprostanes for global oxidative stress.RESEARCH DESIGN AND METHODSThe PPARdelta agonist (10 mg o.d. GW501516), a comparator PPARalpha agonist (20 mug o.d. GW590735), and placebo were given in a double-blind, randomized, three-parallel group, 2-week study to six healthy moderately overweight subjects in each group. Metabolic evaluation was made before and after treatment including liver fat quantification, fasting blood samples, a 6-h meal tolerance test with stable isotope fatty acids, skeletal muscle biopsy for gene expression, and urinary isoprostanes for global oxidative stress.Treatment with GW501516 showed statistically significant reductions in fasting plasma triglycerides (-30%), apolipoprotein B (-26%), LDL cholesterol (-23%), and insulin (-11%), whereas HDL cholesterol was unchanged. A 20% reduction in liver fat content (P < 0.05) and 30% reduction in urinary isoprostanes (P = 0.01) were also observed. Except for a lowering of triglycerides (-30%, P < 0.05), none of these changes were observed in response to GW590735. The relative proportion of exhaled CO(2) directly originating from the fat content of the meal was increased (P < 0.05) in response to GW501516, and skeletal muscle expression of carnitine palmitoyl-transferase 1b (CPT1b) was also significantly increased.RESULTSTreatment with GW501516 showed statistically significant reductions in fasting plasma triglycerides (-30%), apolipoprotein B (-26%), LDL cholesterol (-23%), and insulin (-11%), whereas HDL cholesterol was unchanged. A 20% reduction in liver fat content (P < 0.05) and 30% reduction in urinary isoprostanes (P = 0.01) were also observed. Except for a lowering of triglycerides (-30%, P < 0.05), none of these changes were observed in response to GW590735. The relative proportion of exhaled CO(2) directly originating from the fat content of the meal was increased (P < 0.05) in response to GW501516, and skeletal muscle expression of carnitine palmitoyl-transferase 1b (CPT1b) was also significantly increased.The PPARdelta agonist GW501516 reverses multiple abnormalities associated with the metabolic syndrome without increasing oxidative stress. The effect is probably caused by increased fat oxidation in skeletal muscle.CONCLUSIONSThe PPARdelta agonist GW501516 reverses multiple abnormalities associated with the metabolic syndrome without increasing oxidative stress. The effect is probably caused by increased fat oxidation in skeletal muscle. OBJECTIVE— Pharmacological use of peroxisome proliferator–activated receptor (PPAR)δ agonists and transgenic overexpression of PPARδ in mice suggest amelioration of features of the metabolic syndrome through enhanced fat oxidation in skeletal muscle. We hypothesize a similar mechanism operates in humans. RESEARCH DESIGN AND METHODS— The PPARδ agonist (10 mg o.d. GW501516), a comparator PPARα agonist (20 μg o.d. GW590735), and placebo were given in a double-blind, randomized, three-parallel group, 2-week study to six healthy moderately overweight subjects in each group. Metabolic evaluation was made before and after treatment including liver fat quantification, fasting blood samples, a 6-h meal tolerance test with stable isotope fatty acids, skeletal muscle biopsy for gene expression, and urinary isoprostanes for global oxidative stress. RESULTS— Treatment with GW501516 showed statistically significant reductions in fasting plasma triglycerides (−30%), apolipoprotein B (−26%), LDL cholesterol (−23%), and insulin (−11%), whereas HDL cholesterol was unchanged. A 20% reduction in liver fat content (P < 0.05) and 30% reduction in urinary isoprostanes (P = 0.01) were also observed. Except for a lowering of triglycerides (−30%, P < 0.05), none of these changes were observed in response to GW590735. The relative proportion of exhaled CO2 directly originating from the fat content of the meal was increased (P < 0.05) in response to GW501516, and skeletal muscle expression of carnitine palmitoyl-transferase 1b (CPT1b) was also significantly increased. CONCLUSIONS— The PPARδ agonist GW501516 reverses multiple abnormalities associated with the metabolic syndrome without increasing oxidative stress. The effect is probably caused by increased fat oxidation in skeletal muscle. OBJECTIEVE-Pharmacological use of peroxisome proliferator-activated receptor (PPAR)delta agonists and transgenic overexpression of PPAR delta in mice suggest amelioration of features of the metabolic syndrome through enhanced fat oxidation in skeletal muscle. We hypothesize a similar mechanism operates in humans. RESEARCH DESIGN AND METHODS-The PPAR delta agonist (10 mg o.d. GW501516), a comparator PPAR alpha agonist (20 mu g o.d. GW590735)), and placebo were given in a double-blind, randomized, three-parallel group, 2-week study to six healthy moderately overweight subjects in each group. Metabolic evaluation was made before and after treatment including liver fat quantification, fasting blood samples, a 6-h meal tolerance test with stable isotope fatty acids, skeletal muscle biopsy for gene expression, and urinary isoprostanes for global oxidative stress. RESULTS-Treatment with GW501516 showed statistically significant reductions in fasting plasma triglycerides (-30%), apolipoprotein B (-26%), LDL cholesterol (-23%), and insulin (-11%), whereas HDL cholesterol was unchanged. A 20% reduction in liver fat content (P < 0.05) and 30% reduction in urinary isoprostanes (P = 0.01) were also observed. Except for a lowering of triglycerides (-30%, P < 0.05), none of these changes were observed in response to GW590735. The relative proportion of exhaled CO, directly originating from the fat content of the meal was increased (P < 0.05) in response to GW501516, and skeletal muscle expression of carnitine palmitoyl-transferase 1b (CPT1b) was also significantly increased. CONCLUSIONS-The PPAR delta agonist GW501516 reverses multiple abnormalities associated with the metabolic syndrome without increasing oxidative stress. The effect is probably caused by increased fat oxidation in skeletal muscle. OBJECTIVE--Pharmacological use of peroxisome proliferator-activated receptor (PPAR)δ agonists and transgenic overexpression of PPARδ in mice suggest amelioration of features of the metabolic syndrome through enhanced fat oxidation in skeletal muscle. We hypothesize a similar mechanism operates in humans. RESEARCH DESIGN AND METHODS--The PPARδ agonist (10 mg o.d. GW501516), a comparator PPARα agonist (20 µg o.d. GW590735), and placebo were given in a double-blind, randomized, three-parallel group, 2-week study to six healthy moderately overweight subjects in each group. Metabolic evaluation was made before and after treatment including liver fat quantification, fasting blood samples, a 6-h meal tolerance test with stable isotope fatty acids, skeletal muscle biopsy for gene expression, and urinary isoprostanes for global oxidative stress. RESULTS--Treatment with GW501516 showed statistically significant reductions in fasting plasma triglycerides (-30%), apolipoprotein B (-26%), LDL cholesterol (-23%), and insulin (-11%), whereas HDL cholesterol was unchanged. A 20% reduction in liver fat content (P < 0.05) and 30% reduction in urinary isoprostanes (P = 0.01) were also observed. Except for a lowering of triglycerides (-30%, P < 0.05), none of these changes were observed in response to GW590735. The relative proportion of exhaled C[O.sub.2] directly originating from the fat content of the meal was increased (P < 0.05) in response to GW501516, and skeletal muscle expression of carnitine palmitoyl-transferase 1b (CPT1b) was also significantly increased. CONCLUSIONS--The PPARδ agonist GWb01516 reverses multiple abnormalities associated with the metabolic syndrome without increasing oxidative stress. The effect is probably caused by increased fat oxidation in skeletal muscle. |
| Audience | Professional |
| Author | Peter Murgatroyd Barbara A. Fielding Leli Sarov-Blat Jay C. Strum Jane Cheeseman Sandy M. Humphreys David Hassall Duncan Richards Pauline Sutton Niall R. Moore Sandra Hirschberg Theodore Danoff Tony Johnson Fredrik Karpe Eric Olson Zeke Fang Ulf Risérus Dennis Sprecher Priti Hegde Stephen O'Rahilly Samar Basu Aixue Liu Keith N. Frayn Tim Willson |
| Author_xml | – sequence: 1 givenname: Ulf surname: Risérus fullname: Risérus, Ulf organization: Oxford Centre for Diabetes, Endocrinology and Metabolism, University of Oxford, Oxford, U.K – sequence: 2 givenname: Dennis surname: Sprecher fullname: Sprecher, Dennis organization: Cardiovascular and Urogenital Center for Excellence in Drug Discovery, GlaxoSmithKline, King of Prussia, Pennsylvania – sequence: 3 givenname: Tony surname: Johnson fullname: Johnson, Tony organization: Cardiovascular and Urogenital Center for Excellence in Drug Discovery, GlaxoSmithKline, King of Prussia, Pennsylvania – sequence: 4 givenname: Eric surname: Olson fullname: Olson, Eric organization: Cardiovascular and Urogenital Center for Excellence in Drug Discovery, GlaxoSmithKline, King of Prussia, Pennsylvania – sequence: 5 givenname: Sandra surname: Hirschberg fullname: Hirschberg, Sandra organization: Cardiovascular and Urogenital Center for Excellence in Drug Discovery, GlaxoSmithKline, King of Prussia, Pennsylvania – sequence: 6 givenname: Aixue surname: Liu fullname: Liu, Aixue organization: Human Target Validation, Cardiovascular and Urogenital Center for Excellence in Drug Discovery, GlaxoSmithKline, King of Prussia, Pennsylvania – sequence: 7 givenname: Zeke surname: Fang fullname: Fang, Zeke organization: Statistics, GlaxoSmithKline, King of Prussia, Pennsylvania – sequence: 8 givenname: Priti surname: Hegde fullname: Hegde, Priti organization: Clinical Pharmacology and Discovery Medicine/Cardiovascular and Urogenital (CPDM CVU) Unit, GlaxoSmithKline, King of Prussia, Pennsylvania – sequence: 9 givenname: Duncan surname: Richards fullname: Richards, Duncan organization: Addenbrooke's Centre for Clinical Investigation (ACCI) Unit, GlaxoSmithKline, Cambridge, U.K – sequence: 10 givenname: Leli surname: Sarov-Blat fullname: Sarov-Blat, Leli organization: Clinical Pharmacology and Discovery Medicine/Cardiovascular and Urogenital (CPDM CVU) Unit, GlaxoSmithKline, King of Prussia, Pennsylvania – sequence: 11 givenname: Jay C. surname: Strum fullname: Strum, Jay C. organization: Clinical Pharmacology and Discovery Medicine/Cardiovascular and Urogenital (CPDM CVU) Unit, GlaxoSmithKline, King of Prussia, Pennsylvania – sequence: 12 givenname: Samar surname: Basu fullname: Basu, Samar organization: Department of Public Health, University of Uppsala, Uppsala, Sweden – sequence: 13 givenname: Jane surname: Cheeseman fullname: Cheeseman, Jane organization: Oxford Centre for Diabetes, Endocrinology and Metabolism, University of Oxford, Oxford, U.K – sequence: 14 givenname: Barbara A. surname: Fielding fullname: Fielding, Barbara A. organization: Oxford Centre for Diabetes, Endocrinology and Metabolism, University of Oxford, Oxford, U.K – sequence: 15 givenname: Sandy M. surname: Humphreys fullname: Humphreys, Sandy M. organization: Oxford Centre for Diabetes, Endocrinology and Metabolism, University of Oxford, Oxford, U.K – sequence: 16 givenname: Theodore surname: Danoff fullname: Danoff, Theodore organization: Human Target Validation, Cardiovascular and Urogenital Center for Excellence in Drug Discovery, GlaxoSmithKline, King of Prussia, Pennsylvania – sequence: 17 givenname: Niall R. surname: Moore fullname: Moore, Niall R. organization: Department of Radiology, Churchill Hospital, University of Oxford, Oxford, U.K – sequence: 18 givenname: Peter surname: Murgatroyd fullname: Murgatroyd, Peter organization: Wellcome Trust Clinical Research Facility, Addenbrooke's Hospital, Cambridge, U.K – sequence: 19 givenname: Stephen surname: O'Rahilly fullname: O'Rahilly, Stephen organization: Department of Clinical Biochemistry and Medicine, University of Cambridge, Cambridge, U.K – sequence: 20 givenname: Pauline surname: Sutton fullname: Sutton, Pauline organization: Oxford Centre for Diabetes, Endocrinology and Metabolism, University of Oxford, Oxford, U.K – sequence: 21 givenname: Tim surname: Willson fullname: Willson, Tim organization: GlaxoSmithKline, Research Triangle Park, North Carolina – sequence: 22 givenname: David surname: Hassall fullname: Hassall, David organization: GlaxoSmithKline, Stevenage, U.K – sequence: 23 givenname: Keith N. surname: Frayn fullname: Frayn, Keith N. organization: Oxford Centre for Diabetes, Endocrinology and Metabolism, University of Oxford, Oxford, U.K – sequence: 24 givenname: Fredrik surname: Karpe fullname: Karpe, Fredrik organization: Oxford Centre for Diabetes, Endocrinology and Metabolism, University of Oxford, Oxford, U.K |
| BackLink | http://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=20181212$$DView record in Pascal Francis https://www.ncbi.nlm.nih.gov/pubmed/18024853$$D View this record in MEDLINE/PubMed https://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-15746$$DView record from Swedish Publication Index |
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| CODEN | DIAEAZ |
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| Snippet | Activation of Peroxisome Proliferator–Activated Receptor (PPAR)δ Promotes Reversal of Multiple Metabolic Abnormalities, Reduces
Oxidative Stress, and Increases... OBJECTIVE— Pharmacological use of peroxisome proliferator–activated receptor (PPAR)δ agonists and transgenic overexpression of PPARδ in mice suggest... Pharmacological use of peroxisome proliferator-activated receptor (PPAR)delta agonists and transgenic overexpression of PPARdelta in mice suggest amelioration... OBJECTIVE--Pharmacological use of peroxisome proliferator-activated receptor (PPAR)δ agonists and transgenic overexpression of PPARδ in mice suggest... OBJECTIEVE-Pharmacological use of peroxisome proliferator-activated receptor (PPAR)delta agonists and transgenic overexpression of PPAR delta in mice suggest... |
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| SubjectTerms | Adolescent Adult Apolipoproteins B - blood Apolipoproteins B - drug effects Biological and medical sciences Care and treatment Cholesterol, HDL - blood Cholesterol, HDL - drug effects Diabetes. Impaired glucose tolerance Double-Blind Method Endocrine pancreas. Apud cells (diseases) Endocrinopathies Etiopathogenesis. Screening. Investigations. Target tissue resistance Fat metabolism Fatty Acids - metabolism Fibric acids Genetic aspects Humans Magnetic Resonance Imaging Male Medical sciences MEDICIN MEDICINE Metabolic diseases Metabolic syndrome X Middle Aged Obesity Obesity - physiopathology Oxidation-Reduction Oxidative stress Oxidative Stress - physiology Peroxisomes Physiological aspects Placebos PPAR delta - agonists PPAR delta - physiology Thiazoles - pharmacology Triglycerides - blood |
| Title | Activation of Peroxisome Proliferator–Activated Receptor (PPAR)δ Promotes Reversal of Multiple Metabolic Abnormalities, Reduces Oxidative Stress, and Increases Fatty Acid Oxidation in Moderately Obese Men |
| URI | http://diabetes.diabetesjournals.org/content/57/2/332.abstract https://www.ncbi.nlm.nih.gov/pubmed/18024853 https://www.proquest.com/docview/70240596 https://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-15746 |
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