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Co-option of PPARα ...
Co-option of PPARα in the regulation of lipogenesis and fatty acid oxidation in CLA-induced hepatic steatosis
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- Cai, Demin (författare)
- College of Animal Science and Technology, Yangzhou University, Yangzhou, Jiangsu, China.
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- Li, Yanwei (författare)
- College of Animal Science and Technology, Yangzhou University, Yangzhou, Jiangsu, China.
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- Zhang, Kexin (författare)
- College of Animal Science and Technology, Yangzhou University, Yangzhou, Jiangsu, China.
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- Zhou, Bo (författare)
- Institute of Digestive Disease, Zhengzhou University, Zhengzhou, China.
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- Guo, Feilong (författare)
- Department of General Surgery, Jinling Hospital, School of Medicine, Nanjing University, Nanjing, China.
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- Holm, Lena (författare)
- Uppsala universitet,Integrativ Fysiologi
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- Liu, Haoyu (författare)
- Uppsala universitet,Institutionen för medicinsk cellbiologi,College of Animal Science and Technology, Yangzhou University, Yangzhou, Jiangsu, China
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College of Animal Science and Technology, Yangzhou University, Yangzhou, Jiangsu, China Institute of Digestive Disease, Zhengzhou University, Zhengzhou, China. (creator_code:org_t)
- 2020-11-13
- 2021
- Engelska.
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Ingår i: Journal of Cellular Physiology. - : Wiley. - 0021-9541 .- 1097-4652. ; 236:6, s. 4387-4402
- Relaterad länk:
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https://urn.kb.se/re...
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https://doi.org/10.1...
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Abstract
Ämnesord
Stäng
- Nonalcoholic-fatty-liver-disease (NAFLD) is the result of imbalances in hepatic lipid partitioning and is linked to dietary factors. We demonstrate that conjugated linoleic acid (CLA) when given to mice as a dietary supplement, induced an enlarged liver, hepatic steatosis, and increased plasma levels of fatty acid (FA), alanine transaminase, and triglycerides. The progression of NAFLD and insulin resistance was reversed by GW6471 a small-molecule antagonist of peroxisome proliferator-activated receptor α (PPARα). Transcriptional profiling of livers revealed that the genes involved in FA oxidation and lipogenesis as two core gene programs controlled by PPARα in response to CLA and GW6471 including Acaca and Acads. Bioinformatic analysis of PPARα ChIP-seq data set and ChIP-qPCR showed that GW6471 blocks PPARα binding to Acaca and Acads and abolishes the PPARα-mediated local histone modifications of H3K27ac and H3K4me1 in CLA-treated hepatocytes. Thus, our findings reveal a dual role of PPARα in the regulation of lipid homeostasis and highlight its druggable nature in NAFLD.
Ämnesord
- MEDICIN OCH HÄLSOVETENSKAP -- Klinisk medicin -- Gastroenterologi (hsv//swe)
- MEDICAL AND HEALTH SCIENCES -- Clinical Medicine -- Gastroenterology and Hepatology (hsv//eng)
Nyckelord
- GW6471
- PPARα
- conjugated linoleic acid
- fatty acid oxidation
- hepatic steatosis
- lipogenesis
Publikations- och innehållstyp
- ref (ämneskategori)
- art (ämneskategori)
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