Hemorheological abnormalities in lipoprotein lipase deficient mice with severe hypertriglyceridemia
- Institute of Cardiovascular Sciences, Health Science Center, Peking University, Beijing 100083 (China) and Key Laboratory of Molecular Cardiovascular Sciences, Ministry of Education (China)
- Hemorheology Center, Department of Biophysics, Health Science Center, Peking University, Beijing 100083 (China)
- Department of Medical Genetics, University of British Columbia, Centre for Molecular Medicine and Therapeutics, Vancouver (Canada)
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.
- OSTI ID:
- 20798853
- Journal Information:
- Biochemical and Biophysical Research Communications, Vol. 341, Issue 4; Other Information: DOI: 10.1016/j.bbrc.2006.01.067; PII: S0006-291X(06)00155-0; Copyright (c) 2006 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved; Country of input: International Atomic Energy Agency (IAEA); ISSN 0006-291X
- Country of Publication:
- United States
- Language:
- English
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