@techreport{oai:kanazawa-u.repo.nii.ac.jp:00044611,
 month = {May},
 note = {常染色体劣性高コレステロール血症のLDL異化率は正常者に比し75%低下し、VLDLの直接異化率は著明に亢進していた。スタチンによりLDL異化率は正常化し、VLDL直接異化率は上昇した。PCSK9遺伝子異常ホモ接合体のLDL異化率は正常者に比し52%低下し、VLDL合成率、VLDL直接異化率はいずれも亢進していた。スタチンによりLDL異化率は正常化したが、VLDL合成率、直接異化率は不変であった。, The fractional catabolic rate(FCR) of low-density lipoprotein(LDL) apolipoprotein B(apoB) in a patient with autosomal recessive hypercholesterolemia(ARH) was 75% smaller, whereas direct removal of very-LDL apoB was dramatically greater compared with those of normal control subjects. Statin therapy normalized FCR of LDL apoB and increased direct removal of very-LDL in ARH patient. On the other hand, the FCR of patients with homozygous proprotein convertase subtilisin/kexin 9(PCSK9) gene mutation was 52% smaller than that of normal control subjects and normalized by statin therapy. Whereas, both production rate and direct removal of very-LDL was increased compared with those of normal control subjects, which were not changed by statin therapy., 研究課題/領域番号:21591160, 研究期間(年度):2009-2011, 出典：研究課題「家族性高コレステロール血症の原因遺伝子別系統的病態解析」課題番号21591160
（KAKEN：科学研究費助成事業データベース（国立情報学研究所）） 
（https://kaken.nii.ac.jp/report/KAKENHI-PROJECT-21591160/21591160seika/）を加工して作成},
 title = {家族性高コレステロール血症の原因遺伝子別系統的病態解析},
 year = {2012}
}