Long-term adaptation of global transcription and metabolism in the liver of high-fat diet-fed C57BL/6J mice

Gyeong Min Do, Hea Young Oh, Eun Young Kwon, Yun Young Cho, Su Kyung Shin, Hae Jin Park, Seon Min Jeon, Eunjung Kim, Cheol Goo Hur, Taesun Park, Mi Kyung Sung, Robin A. Mcgregor, Myung Sook Choi

Research output: Contribution to journalArticle

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Abstract

Scope: This study investigated the global transcriptional and metabolic changes occurring at multiple time points over 24wk 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.

Original languageEnglish
JournalMolecular Nutrition and Food Research
Volume55
Issue numberSUPPL. 2
DOIs
Publication statusPublished - 2011 Sep 1

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High Fat Diet
high fat diet
Inbred C57BL Mouse
transcription (genetics)
liver
metabolism
Liver
mice
obesity
Obesity
Diet
insulin resistance
diet
Insulin Resistance
Genes
Morbidity
nutritional intervention
genes
hypercholesterolemia
fatty liver

All Science Journal Classification (ASJC) codes

  • Biotechnology
  • Food Science

Cite this

Do, Gyeong Min ; Oh, Hea Young ; Kwon, Eun Young ; Cho, Yun Young ; Shin, Su Kyung ; Park, Hae Jin ; Jeon, Seon Min ; Kim, Eunjung ; Hur, Cheol Goo ; Park, Taesun ; Sung, Mi Kyung ; Mcgregor, Robin A. ; Choi, Myung Sook. / Long-term adaptation of global transcription and metabolism in the liver of high-fat diet-fed C57BL/6J mice. In: Molecular Nutrition and Food Research. 2011 ; Vol. 55, No. SUPPL. 2.
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Do, GM, Oh, HY, Kwon, EY, Cho, YY, Shin, SK, Park, HJ, Jeon, SM, Kim, E, Hur, CG, Park, T, Sung, MK, Mcgregor, RA & Choi, MS 2011, 'Long-term adaptation of global transcription and metabolism in the liver of high-fat diet-fed C57BL/6J mice', Molecular Nutrition and Food Research, vol. 55, no. SUPPL. 2. https://doi.org/10.1002/mnfr.201100064

Long-term adaptation of global transcription and metabolism in the liver of high-fat diet-fed C57BL/6J mice. / Do, Gyeong Min; Oh, Hea Young; Kwon, Eun Young; Cho, Yun Young; Shin, Su Kyung; Park, Hae Jin; Jeon, Seon Min; Kim, Eunjung; Hur, Cheol Goo; Park, Taesun; Sung, Mi Kyung; Mcgregor, Robin A.; Choi, Myung Sook.

In: Molecular Nutrition and Food Research, Vol. 55, No. SUPPL. 2, 01.09.2011.

Research output: Contribution to journalArticle

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T1 - Long-term adaptation of global transcription and metabolism in the liver of high-fat diet-fed C57BL/6J mice

AU - Do, Gyeong Min

AU - Oh, Hea Young

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AU - Cho, Yun Young

AU - Shin, Su Kyung

AU - Park, Hae Jin

AU - Jeon, Seon Min

AU - Kim, Eunjung

AU - Hur, Cheol Goo

AU - Park, Taesun

AU - Sung, Mi Kyung

AU - Mcgregor, Robin A.

AU - Choi, Myung Sook

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N2 - Scope: This study investigated the global transcriptional and metabolic changes occurring at multiple time points over 24wk 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.

AB - Scope: This study investigated the global transcriptional and metabolic changes occurring at multiple time points over 24wk 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.

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