These authors contributed equally to this work.
Long-term adaptation of global transcription and metabolism in the liver of high-fat diet-fed C57BL/6J mice
Article first published online: 25 MAY 2011
Copyright © 2011 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim
Molecular Nutrition & Food Research
Special Issue: Lipids as Effectors
Supplement: Lipids as Effectors
Volume 55, Issue Supplement 2, pages S173–S185, September 2011
How to Cite
Do, G.-M., Oh, H. Y., Kwon, E.-Y., Cho, Y.-y., Shin, S.-k., Park, H.-J., Jeon, S.-M., Kim, E., Hur, C.-G., Park, T.-S., Sung, M.-K., McGregor, R. A. and Choi, M.-S. (2011), Long-term adaptation of global transcription and metabolism in the liver of high-fat diet-fed C57BL/6J mice. Mol. Nutr. Food Res., 55: S173–S185. doi: 10.1002/mnfr.201100064
- Issue published online: 26 SEP 2011
- Article first published online: 25 MAY 2011
- Manuscript Accepted: 8 MAR 2011
- Manuscript Revised: 24 FEB 2011
- Manuscript Received: 28 JAN 2011
- SRC program (Center for Food & Nutritional Genomics) of the National Research Foundation (NRF) of Korea funded by the Ministry of Education, Science and Technology. Grant Number: 2010-0001886
- Diet-induced obesity;
- Insulin resistance;
- Metabolic profile;
- Transcriptional response
Scope: This study investigated the global transcriptional and metabolic changes occurring at multiple time points over 24 wk in response to a high-fat diet (HFD).
Methods and results: C57BL/6J mice were fed a HFD or normal diet (ND) over 24 wk. HFD-fed mice developed early clinical indicators of obesity-related co-morbidities including fatty liver, insulin resistance, hyperglycemia and hypercholesterolemia. Time-course microarray analysis at eight time points over 24 wk identified 332 HFD responsive genes as potential targets to counteract diet-induced obesity (DIO) and related co-morbidities. Glucose regulating enzyme activity and gene expression were altered early in the HFD-fed mice. Fatty acid (FA) and triglyceride (TG) accumulation in combination with inflammatory changes appear to be likely candidates contributing to hepatic insulin resistance. Cidea seemed to be one of representative genes related to these changes.
Conclusion: Global transcriptional and metabolic profiling across multiple time points in liver revealed potential targets for nutritional interventions to reverse DIO. In future, new approaches targeting HFD responsive genes and hepatic metabolism could help ameliorate the deleterious effects of an HFD and DIO-related complication.