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Cdc2-Like Kinase 2 Suppresses Hepatic Fatty Acid Oxidation and Ketogenesis Through Disruption of the PGC-1α and MED1 Complex
Cdc2-like kinase 2 reduces liver fat breakdown and ketone production by interfering with the PGC-1α and MED1 protein complex
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Abstract
Liver-specific knockout of in mice fed a high-fat diet leads to increased fasting levels of blood ketone bodies.
- Clk2 suppresses fatty acid oxidation and ketone body production during diet-induced obesity.
- In lean mice, Clk2 protein levels are low during fasting but increase during feeding, while they remain elevated in obese mice.
- Knockout of Clk2 in the liver results in a reduced respiratory exchange ratio and increased expression of genes involved in fatty acid oxidation and ketogenesis.
- Clk2 acts in a cell-specific manner, influencing fatty acid utilization through its effects in hepatocytes.
- Clk2 phosphorylates a protein that disrupts its interaction with another protein, leading to decreased activation of genes associated with fatty acid metabolism.
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Key numbers
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Increase in Serum β-Hydroxybutyrate Levels
Observed in liver-specific knockout mice fed a high-fat diet.
N/A
Decrease in Liver Triglyceride Concentration
Noted in liver-specific knockout mice compared to controls.
N/A
Respiratory Exchange Ratio Decrease
Measured during fasting in knockout mice.