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Microarray analysis indicates an important role for FABP5 and putative novel FABPs on a Western-type diet
Menno Hoekstra1, Miranda Stitzinger, Eva J A van Wanrooij
1Division of Biopharmaceutics, Leiden/Amsterdam Center for Drug Research, Gorlaeus Laboratories, Leiden University, 2300 RA Leiden, The Netherlands. hoekstra@lacdr.leidenuniv.nl
Journal of Lipid Research
|August 4, 2006
Summary
Feeding a Western-type diet rapidly increases fatty acid binding protein 5 (FABP5) expression in mouse liver cells. This response may protect against lipid toxicity and influences cholesterol homeostasis, impacting atherosclerosis development.
Area of Science:
- Metabolic research
- Molecular biology
- Cardiovascular science
Background:
- Liver parenchymal cells are critical for cholesterol homeostasis and metabolism.
- Atherosclerosis is linked to dietary lipid intake and hepatic responses.
- LDL receptor-deficient mice are a model for studying diet-induced atherosclerosis.
Purpose of the Study:
- To investigate gene expression changes in liver parenchymal cells in response to a Western-type diet.
- To identify key genes and pathways involved in hepatic lipid metabolism under atherogenic conditions.
- To understand the role of specific fatty acid-binding proteins in diet-induced cellular responses.
Main Methods:
- Microarray analysis of liver parenchymal cell gene expression.
- Utilized LDL receptor-deficient mice fed a Western-type diet over 6 weeks.
- ABI Mouse Genome Survey Arrays were employed to profile gene expression.
Main Results:
- Over 7,500 genes were expressed in liver parenchymal cells across all time points.
- Fatty acid binding protein 5 (FABP5) and four novel FABP5-like transcripts showed a 16- to 22-fold increase within 2 weeks.
- Secondary responses included stimulated glycolysis and lipogenesis, leading to an atherogenic lipoprotein profile (increased VLDL/LDL).
Conclusions:
- FABP5 and related transcripts are primary responders to Western-type diets, potentially protecting against lipid toxicity.
- Hepatic gene expression changes influence cholesterol homeostasis and contribute to atherogenic lipoprotein profiles.
- These findings provide insight into the molecular mechanisms underlying diet-induced atherosclerosis.
