Low Cholesterol Provision from HDL<sub>2b</sub> to Lymphocytes in FH Heterozygotes

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  • IWATA Seiji
    The Third Department of Internal Medicine, Nagoya City University Medical School
  • SAKUMA Nagahiko
    The Third Department of Internal Medicine, Nagoya City University Medical School
  • ICHIKAWA Takayoshi
    The Third Department of Internal Medicine, Nagoya City University Medical School
  • IKEUCHI Reiko
    The Third Department of Internal Medicine, Nagoya City University Medical School
  • HIBINO Takeshi
    The Third Department of Internal Medicine, Nagoya City University Medical School
  • KAMIYA Yoshinobu
    The Third Department of Internal Medicine, Nagoya City University Medical School
  • KAWAGUCHI Masanobu
    The Third Department of Internal Medicine, Nagoya City University Medical School
  • FUJINAMI Takao
    The Third Department of Internal Medicine, Nagoya City University Medical School
  • KUNIMATSU Mitoshi
    The Second Department of Biochemistry, Nagoya City University Medical School

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Other Title
  • リンパ球に対するHDL<sub>2b</sub>のコレステロール供給能について
  • ―家族性高コレステロール血症ヘテロ患者における検討―

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When endogenous synthesis of cholesterol is blocked by an HMG-CoA reductase inhibitor (pravastatin), proliferation of phytohemagglutinin (PHA)-stimulated human lymphocytes is markedly inhibited unless an exogenous source ofcholesterol is supplied. Based on this principle, we simplified and modified the method of Lipsky et al. to assay functional LDL receptors. Using our method, we examined the capacity of HDL2b and LDL to supply cholesterol to lymphocytes from FH heterozygotes or normal subjects. Peripheral blood lymphocytes were isolated from the venous blood of 5 patients with heterozygous FH and 10 healthy adults. LDL and HDL2b were isolated by ultracentrifugation from the serum of normal fasting adults, and the HDL2b fraction that contained Apo E but not Apo B was prepared by a heparin-Sepharose column. The ability of HDL2b cholesterol to reverse pravastatinmediated inhibition of lymphocyte proliferation in FH heterozygotes was concentration-dependent. However, the effect of HDL2b was weaker than that of LDL. In addition, HDL2b provided less cholesterol to lymphocytes in FH heterozygotes than in normal subjects. These findings suggested that provision of cholesterol from not only LDL but also HDL2b was depressed by dysfunction of LDL receptor in FH heterozygotes.

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