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Gemfibrozil-Induced Intracellular Triglyceride Increase in SH-SY5Y, HEK and Calu-3 Cells
Cornel Manuel Bachmann1, Daniel Janitschke1, Anna Andrea Lauer1,2
1Experimental Neurology, Saarland University, 66421 Homburg, Germany.
International Journal of Molecular Sciences
|February 11, 2023
Summary
Gemfibrozil increases intracellular triglycerides in brain, lung, and kidney cells. This finding is crucial for understanding gemfibrozil
Area of Science:
- Biochemistry
- Cell Biology
- Pharmacology
Background:
- Gemfibrozil is a long-standing medication for lowering blood triglycerides.
- It acts as a ligand for peroxisome proliferative-activated receptor-alpha (PPARα), influencing carbohydrate and lipid metabolism genes.
- The impact of gemfibrozil on intracellular lipid homeostasis, particularly triglycerides, remains largely unknown.
Purpose of the Study:
- To investigate the effects of gemfibrozil on intracellular lipid levels.
- To determine if gemfibrozil influences triglyceride accumulation in metabolically active cells.
Main Methods:
- Incubation of SH-SY5Y (brain), HEK (kidney), and Calu-3 (lung) cells with gemfibrozil.
- Semi-quantitative analysis of intracellular lipid levels using mass spectrometry.
Main Results:
- Significant increases in intracellular triglycerides were observed across all cell lines (SH-SY5Y: 170.3%, HEK: 272.1%, Calu-3: 448.1%).
- Cell-line specific alterations in acylcarnitines were detected.
- Gemfibrozil appears to enhance fatty acid transport to mitochondria, particularly in neuronal cells, boosting energy supply.
Conclusions:
- Gemfibrozil treatment leads to a substantial increase in intracellular triglycerides.
- The drug may enhance cellular uptake of triglycerides.
- Gemfibrozil's effect on fatty acid metabolism, especially in neuronal cells, could have implications for energy supply in diseases like Alzheimer's.
