Hemorheological abnormalities in lipoprotein lipase deficient mice with severe hypertriglyceridemia

Tieqiang Zhao, Jun Guo, Hui Li, Wei Huang, Xunde Xian, Colin J D Ross, Michael R. Hayden, Zongyao Wen, George Liu

Research output: Contribution to journalArticlepeer-review

24 Scopus citations


Severe hypertriglyceridemia (HTG) is a metabolic disturbance often seen in clinical practice. It is known to induce life-threatening acute pancreatitis, but its role in atherogenesis remains elusive. Hemorheological abnormality was thought to play an important role in pathogenesis of both pancreatitis and atherosclerosis. However, hemorheology in severe HTG was not well investigated. Recently, we established a severe HTG mouse model deficient in lipoprotein lipase (LPL) in which severe HTG was observed to cause a significant increase in plasma viscosity. Disturbances of erythrocytes were also documented, including decreased deformability, electrophoresis rate, and membrane fluidity, and increased osmotic fragility. Scanning electron microscopy demonstrated that most erythrocytes of LPL deficient mice deformed with protrusions, irregular appearances or indistinct concaves. Analysis of erythrocyte membrane lipids showed decreased cholesterol (Ch) and phospholipid (PL) contents but unaltered Ch/PL ratio. The changes of membrane lipids may be partially responsible for the hemorheological and morphologic abnormalities of erythrocytes. This study indicated that severe HTG could lead to significant impairment of hemorheology and this model may be useful in delineating the role of severe HTG in the pathogenesis of hyperlipidemic pancreatitis and atherosclerosis.

Original languageEnglish (US)
Pages (from-to)1066-1071
Number of pages6
JournalBiochemical and Biophysical Research Communications
Issue number4
StatePublished - Mar 24 2006


  • Hemorheology
  • Hypertriglyceridemia
  • Lipoprotein lipase

ASJC Scopus subject areas

  • Biophysics
  • Biochemistry
  • Molecular Biology
  • Cell Biology


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