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KLF15 Enables Rapid Switching between Lipogenesis and Gluconeogenesis during Fasting
Yoshinori Takeuchi1, Naoya Yahagi1, Yuichi Aita1
1Nutrigenomics Research Group, Faculty of Medicine, University of Tsukuba, Ibaraki 305-8575, Japan.
Cell Reports
|August 23, 2016
Summary
Fasting-induced KLF15 protein complexes with LXR/RXR to reduce SREBP-1c expression, thereby decreasing hepatic lipogenesis. This mechanism ameliorates hypertriglyceridemia, offering therapeutic potential for hyperlipidemia.
Area of Science:
- Molecular biology
- Metabolic regulation
- Nutritional adaptation
Background:
- Hepatic lipogenesis is tightly regulated by nutritional status.
- Transcription factor SREBP-1c is crucial for lipogenesis, but upstream regulators are unclear.
Purpose of the Study:
- To elucidate the upstream mechanisms controlling Srebf1 expression during fasting.
- To investigate the role of KLF15 in regulating hepatic lipogenesis.
Main Methods:
- Chromatin immunoprecipitation assays to detect KLF15 binding to the Srebf1 promoter.
- Analysis of gene expression in response to KLF15 overexpression.
- Biochemical assays to assess triglyceride and cholesterol levels.
Main Results:
- KLF15 forms a complex with LXR/RXR on the Srebf1 promoter during fasting.
- This complex recruits the corepressor RIP140, reducing Srebf1 expression and downstream lipogenic enzymes.
- KLF15 overexpression ameliorates hypertriglyceridemia without impacting cholesterol metabolism.
Conclusions:
- KLF15 acts as a key regulator linking glucose and lipid metabolism.
- KLF15-mediated repression of hepatic lipogenesis offers a therapeutic strategy for hypertriglyceridemia.
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