J Vet Sci.
2003 Dec;4(3):239-244.
Phenotype of peroxisome proliferator-activated receptor-alpha(PPARalpha)deficient mice on mixed background fed high fat diet
- Affiliations
-
- 1Department of Toxicology, National Institute of Toxicological Research, Korea Food and Drug Administration, Seoul 122-704, Korea.
- 2Genetic Resources Center, Korea Research Institute of Bioscience and Biotechnology, Daejeon 305-600, Korea.
- 3Department of Life Science, Mokwon University, Daejeon 302-729, Korea.
- 4Department of Pathology, College of Veterinary Medicine and School of Agricultural Biotechnology, Seoul National University, Seoul 151-742, Korea. daeyong@snu.ac.kr
Abstract
- Considerable controversy exists in determining the role of peroxisome proliferator-activated receptor-alpha(PPARalpha) on obesity. Previous reports demonstrated that PPARalpha is a critical modulator of lipid homeostasis, but the overt, obese phenotypic characterization in the strain of PPAR deficient (PPARalpha-/-) mice is influenced by other factors, including diet and genetics. Therefore, it is necessary to establish the phenotypic characterization of PPARalpha-/- mice prior to the obesity-related study. In this study, we observed phenotype of PPARalpha-/- mice on mixed genetic background (C57BL/6Nx129/Sv) fed a high fat diet for 16 weeks. PPARalpha-/- mice, regardless of sex, raised body growth rate significantly comparing with wild type and showed male-specific fatty change in the liver. They were shown to lack hepatic induction of PPARalpha target genes encoding enzymes for fatty acid beta-oxidation.
Keyword
MeSH Terms
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Adipose Tissue/metabolism
Animals
Body Weight
Cholesterol/blood
Crosses, Genetic
Dietary Fats/*administration & dosage
Female
Histocytochemistry
Liver/enzymology/metabolism
Male
Mice
Mice, Inbred C57BL
Mice, Knockout
Obesity/genetics/*metabolism
Phenotype
RNA/chemistry/genetics
Receptors, Cytoplasmic and Nuclear/*deficiency/genetics/metabolism
Reverse Transcriptase Polymerase Chain Reaction
Specific Pathogen-Free Organisms
Transcription Factors/*deficiency/genetics/metabolism
Triglycerides/blood
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