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| Content Provider | MDPI |
|---|---|
| Author | He, Yonghui Khan, Imad Bai, Xiumei Odle, Jack Xi, Lin |
| Abstract | The objective of this study was to evaluate the effects of peroxisome proliferator-activated receptor α (PPARα) activation by clofibrate on both mitochondrial and peroxisomal fatty acid oxidation in the developing kidney. Ten newborn pigs from 5 litters were randomly assigned to two groups and fed either 5 mL of a control vehicle (2% Tween 80) or a vehicle containing clofibrate (75 mg/kg body weight, treatment). The pigs received oral gavage daily for three days. In vitro fatty acid oxidation was then measured in kidneys with and without mitochondria inhibitors (antimycin A and rotenone) using [1-14C]-labeled oleic acid (C18:1) and erucic acid (C22:1) as substrates. Clofibrate significantly stimulated C18:1 and C22:1 oxidation in mitochondria (p < 0.001) but not in peroxisomes. In addition, the oxidation rate of C18:1 was greater in mitochondria than peroxisomes, while the oxidation of C22:1 was higher in peroxisomes than mitochondria (p < 0.001). Consistent with the increase in fatty acid oxidation, the mRNA abundance and enzyme activity of carnitine palmitoyltransferase I (CPT I) in mitochondria were increased. Although mRNA of mitochondrial 3-hydroxy-3-methylglutaryl-coenzyme A synthase (mHMGCS) was increased, the β-hydroxybutyrate concentration measured in kidneys did not increase in pigs treated with clofibrate. These findings indicate that PPARα activation stimulates renal fatty acid oxidation but not ketogenesis. |
| File Size | 1171456 |
| File Format | |
| e-ISSN | 14220067 |
| DOI | 10.3390/ijms18122663 |
| Journal | International Journal of Molecular Sciences |
| Issue Number | 12 |
| Volume Number | 18 |
| Language | English |
| Publisher Date | 2017-12-08 |
| Access Restriction | Open |
| Subject Keyword | peroxisome proliferator-activated receptor α (PPARα) clofibrate fatty acid β-oxidation pigs |
| Content Type | Text |
| Resource Type | Article |
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