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Folly Beach Library
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Wando Mount Pleasant Library
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Village Library
9 a.m. - 1 p.m.
Phone: (843) 884-9741
St. Paul's/Hollywood Library
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McClellanville Library
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Hurd/St. Andrews Library
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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.
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- Author(s): Risérus, Ulf; Sprecher, Dennis; Johnson, Tony; Olson, Eric; Hirschberg, Sandra; Liu, Aixue; Fang, Zeke; Hegde, Priti; Richards, Duncan; Sarov-Blat, Leli; Strum, Jay C.; Basu, Samar; Cheeseman, Jane; Fielding, Barbara A.; Humphreys, Sandy M.; Danoff, Theodore; Moore, Niall R.; Murgatroyd, Peter; O'Rahilly, Stephen; Sutton, Pauline
- Source:
Diabetes. Feb2008, Vol. 57 Issue 2, p332-339. 8p. 3 Charts, 4 Graphs. - Source:
- Additional Information
- Subject Terms:
- 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[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 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. Diabetes 57: 332-339, 2008 [ABSTRACT FROM AUTHOR]
- Abstract: Copyright of Diabetes is the property of American Diabetes Association and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
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