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Clofibrate induces expression of hepatic genes encoding fatty acid oxidation and ketogenesis enzymes in pigs during early postnatal development
Author(s) -
Shim Kwanseob,
Xi Lin,
Jacobi Sheila,
Odle Jack
Publication year - 2009
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.23.1_supplement.903.3
Subject(s) - clofibrate , ketogenesis , peroxisome , carnitine , beta oxidation , medicine , endocrinology , carnitine palmitoyltransferase i , chemistry , biology , metabolism , receptor , ketone bodies
The objective of this study was to evaluate the effects of clofibrate on gene expression of hepatic fatty‐acid‐oxidation and ketogenesis enzymes induced in pigs during neonatal development. Evaluations were conducted in 0, 1, 4 and 7 d‐old pigs fed milk replacer and orally gavaged with either vehicle (2 % Tween 80) or clofibrate (75 mg /kg body weight) +/‐ etomoxir (5 mg/ kg body weight). Transcript abundances were measured using qRT‐PCR and were greater for carnitine palmitoyltransfersae I (CPT I; 2.8 fold), carnitine palmitoyltransfersae II (CPT II; 3.1 fold), and mitochondrial 3‐methly‐3‐hydroxyglutaryl‐CoA synthase (mHMG‐CoA‐S; 3.9 fold) in pigs fed clofibrate verses vehicle. Addition of etomoxir had no effects on the transcript abundances induced by clofibrate. Transcript abundance of targeted genes also increased as piglets aged, but the mRNA levels remained relatively constant for CPT I and mHMG‐CoA‐S in pigs after 4 d and for CPT II after 1 d. There was no interaction between clofibrate treatment and age. The abundance of acyl‐CoA oxidase and peroxisome proliferator‐activated receptor αtranscripts were not altered by clofibrate, etomoxir or piglet age. In conclusion, clofibrate strongly induces genes of fatty acid oxidation in the young, postnatal pig, but induction is not influenced by developmental age. Supported by CSREES, USDA NRI program award 2007‐35206‐1 7897.