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Related Experiment Video

Updated: Feb 15, 2026

Measurement of Fatty Acid &#946;-Oxidation in a Suspension of Freshly Isolated Mouse Hepatocytes
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PIK3R3 regulates PPARα expression to stimulate fatty acid β-oxidation and decrease hepatosteatosis.

Xi Yang1, Yinjia Fu1, Fuqing Hu1

  • 1Department of Gastrointestinal Surgery Center, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.

Experimental & Molecular Medicine
|January 20, 2018
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Summary
This summary is machine-generated.

The regulatory subunit PIK3R3 enhances hepatic lipid metabolism by boosting fatty acid oxidation through the HNF4α-PPARα axis. This finding suggests PIK3R3 as a potential therapeutic target for non-alcoholic fatty liver disease (NAFLD).

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Area of Science:

  • Biochemistry
  • Molecular Biology
  • Metabolic Diseases

Background:

  • Phosphatidylinositol 3-kinase (PI3K) signaling is crucial for cellular lipid metabolism and non-alcoholic fatty liver disease (NAFLD).
  • The specific roles of PI3K regulatory subunits in lipid metabolism and NAFLD remain largely unexplored.

Purpose of the Study:

  • To investigate the functional role of PIK3R3, a PI3K regulatory subunit, in regulating hepatic lipid metabolism, particularly during fasting.
  • To elucidate the molecular mechanisms by which PIK3R3 influences hepatic lipid homeostasis and its potential as a therapeutic target for NAFLD.

Main Methods:

  • Characterization of PIK3R3 function in hepatic lipid metabolism using overexpression and knockout mouse models.
  • Analysis of gene expression related to lipid metabolism, including PPARα and HNF4α.
  • Assessment of hepatic lipid levels and fatty liver phenotypes in response to high-fat diet (HFD) and PIK3R3 manipulation.

Main Results:

  • Overexpression of PIK3R3 promoted hepatic fatty acid oxidation by inducing PPARα expression, thereby ameliorating fatty liver in HFD-induced mice.
  • Hepatic PIK3R3 knockout in normal mice resulted in elevated hepatic triglyceride (TG) levels.
  • PIK3R3-mediated PPARα expression was found to be dependent on HNF4α, establishing a PIK3R3-HNF4α-PPARα signaling axis.

Conclusions:

  • The PIK3R3-HNF4α-PPARα signaling pathway is a significant regulator of hepatic lipid metabolism.
  • Activation of PIK3R3 demonstrates a therapeutic potential by reducing hepatosteatosis.
  • PIK3R3 represents a promising novel therapeutic target for the treatment of NAFLD and metabolic syndrome.