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<p>Elevation of interstitial fluid hydrostatic pressure is observed in the early stages of fatty liver disease. We herein examined the hypothesis that elevated hydrostatic pressure dysregulates lipid metabolism in hepatocytes and thereby contributes to the progression of fatty liver disease. Human hepatocytes were exposed to 20 and 50 mmHg hydrostatic pressure for 1 and 24&#xa0;h. RT-qPCR data on the expression of fatty acid metabolism-associated genes suggested the alteration of lipid metabolism. Although we did not observe an obvious change of cell growth, the accumulation of lipid droplets increased in hepatocytes at 1 and 24&#xa0;h after the exposure to 20 and 50 mmHg hydrostatic pressure. Hydrostatic pressure exposure also enhanced the expression of p-ACC1, FASN, CPT1, and induced the translocation of CD36 to cell membrane. However, all changes under hydrostatic pressure exposure were effectively attenuated by the F-actin polymerization inhibitor latrunculin B. Our in vitro experimental data suggests that elevated interstitial fluid hydrostatic pressure under pathological conditions may dysregulate lipid metabolism to promote the development of liver fatty diseases through regulating the F-actin polymerization.</p>

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Elevated hydrostatic pressure dysregulates lipid metabolism of hepatocytes

  • 期刊论文

  • 发表日期：

    2025年8月11日

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  • Zisheng Huang,
  • Weili Gu,
  • Tao-Sheng Li

摘要

Elevation of interstitial fluid hydrostatic pressure is observed in the early stages of fatty liver disease. We herein examined the hypothesis that elevated hydrostatic pressure dysregulates lipid metabolism in hepatocytes and thereby contributes to the progression of fatty liver disease. Human hepatocytes were exposed to 20 and 50 mmHg hydrostatic pressure for 1 and 24 h. RT-qPCR data on the expression of fatty acid metabolism-associated genes suggested the alteration of lipid metabolism. Although we did not observe an obvious change of cell growth, the accumulation of lipid droplets increased in hepatocytes at 1 and 24 h after the exposure to 20 and 50 mmHg hydrostatic pressure. Hydrostatic pressure exposure also enhanced the expression of p-ACC1, FASN, CPT1, and induced the translocation of CD36 to cell membrane. However, all changes under hydrostatic pressure exposure were effectively attenuated by the F-actin polymerization inhibitor latrunculin B. Our in vitro experimental data suggests that elevated interstitial fluid hydrostatic pressure under pathological conditions may dysregulate lipid metabolism to promote the development of liver fatty diseases through regulating the F-actin polymerization.