Peroxisome Proliferator-Activated Receptors Alpha, Beta, and Gamma mRNA and Protein Expression in Human Fetal Tissues | Zendy

Barbara D. Abbott | Zendy; Carmen R. Wood | Zendy; Andrew M. Watkins | Zendy; Kaberi Das | Zendy; Christopher Lau | Zendy

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Peroxisome Proliferator-Activated Receptors Alpha, Beta, and Gamma mRNA and Protein Expression in Human Fetal Tissues

Author(s) -

Barbara D. Abbott,

Carmen R. Wood,

Andrew M. Watkins,

Kaberi Das,

Christopher Lau

Publication year - 2010

Publication title -

ppar research

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 1.164

H-Index - 49

eISSN - 1687-4765

pISSN - 1687-4757

DOI - 10.1155/2010/690907

Subject(s) - peroxisome proliferator activated receptor , endocrinology , medicine , fetus , kidney , receptor , peroxisome , messenger rna , biology , pregnancy , biochemistry , genetics , gene

Peroxisome proliferator-activated receptors (PPARs) regulate lipid and glucose homeostasis, are targets of pharmaceuticals, and are also activated by environmental contaminants. Almost nothing is known about expression of PPARs during human fetal development. This study examines expression of PPARalpha, beta, and gamma mRNA and protein in human fetal tissues. With increasing fetal age, mRNA expression of PPARalpha and beta increased in liver, but PPARbeta decreased in heart and intestine, and PPARgamma decreased in adrenal. Adult and fetal mean expression of PPARalpha, beta, and gamma mRNA did not differ in intestine, but expression was lower in fetal stomach and heart. PPARalpha and beta mRNA in kidney and spleen, and PPARgamma mRNA in lung and adrenal were lower in fetal versus adult. PPARgamma in liver and PPARbeta mRNA in thymus were higher in fetal versus adult. PPARalpha protein increased with fetal age in intestine and decreased in lung, kidney, and adrenal. PPARbeta protein in adrenal and PPARgamma in kidney decreased with fetal age. This study provides new information on expression of PPAR subtypes during human development and will be important in evaluating the potential for the developing human to respond to PPAR environmental or pharmaceutical agonists.

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