17beta-estradiol upregulates the expression of peroxisome proliferator-activated receptor alpha and lipid oxidative genes in skeletal muscle

Campbell, S, Mehan, K, Tunstall, R, Febbraio, M and Cameron-Smith, David 2003, 17beta-estradiol upregulates the expression of peroxisome proliferator-activated receptor alpha and lipid oxidative genes in skeletal muscle, Journal of molecular endocrinology, vol. 31, no. 1, pp. 37-45.

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Title 17beta-estradiol upregulates the expression of peroxisome proliferator-activated receptor alpha and lipid oxidative genes in skeletal muscle
Author(s) Campbell, S
Mehan, K
Tunstall, R
Febbraio, M
Cameron-Smith, David
Journal name Journal of molecular endocrinology
Volume number 31
Issue number 1
Start page 37
End page 45
Publisher Society for Endocrinology
Place of publication Bristol, England
Publication date 2003
ISSN 0952-5041
1479-6813
Summary This study examined the actions of 17β-estradiol (E2) and progesterone on the regulation of the peroxisome proliferator-activated receptors (PPARα and PPARγ) family of nuclear transcription factors and the mRNA abundance of key enzymes involved in fat oxidation, in skeletal muscle. Specifically,
carnitine palmitoyltransferase I (CPT I), β-3-hydroxyacyl CoA dehydrogenase (β-HAD), and pyruvate dehydrogenase kinase 4 (PDK4) were examined. Sprague–Dawley rats were ovariectomized and treated with placebo (Ovx), E2, progesterone, or both hormones in combination (E+P). Additionally,
sham-operated rats were treated with placebo (Sham) to serve as controls. Hormone (or vehicle only) delivery was via time release pellets inserted at the time of surgery, 15 days prior to analysis. E2 treatment increased PPARα mRNA expression and protein content (P<0·05), compared with Ovx treatment. E2 also resulted in upregulated mRNA of CPT I and PDK4 (P<0·05). PPARγ mRNA expression was also increased (P<0·05) by E2 treatment, although protein content remained unaltered. These data
demonstrate the novel regulation of E2 on PPARα and genes encoding key proteins that are pivotal in regulating skeletal muscle lipid oxidative flux.
Language eng
Field of Research 111601 Cell Physiology
HERDC Research category C1 Refereed article in a scholarly journal
Copyright notice ©2003, Society for Endocrinology
Persistent URL http://hdl.handle.net/10536/DRO/DU:30008592

Document type: Journal Article
Collection: School of Exercise and Nutrition Sciences
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