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Department of Advanced Medical Technology and Development, BML, Inc. (T.I., T.K., M.I., M. N., H.H.), Kawagoe 50-1101, Japan; Third Department of Internal Medicine, Faculty of Medical Sciences (S.T., Y.Z., J.Su., I. M.), and Second Department of Pathology (H. N.), University of Fukui, Fukui 910-1193, Japan; Department of Cardiovascular Surgery, Hiratsuka Kyosai Hospital (M.T.), Hiratsuka 254-8502, Japan; Laboratory for Systems Biology and Medicine, Research Center for Advanced Science and Technology, University of Tokyo (J.Sa.), Komaba 153-8904, Japan; Exploratory Research for Advanced Technology of Japan Science and Technology Corp. (J.Sa.), Aomi 135-0064, Japan; Department of Bioscience, Integrated Center for Science, Ehime University (T.F.), Shigenobu 791-0295, Japan; Department of Cardiovascular Biochemistry, St. Barts and the Royal London School of Medicine (N.E.M.), London EC1A 7BE, United Kingdom; and Center for Advanced Genome Research, Institute of Aging, Development, and Cancer, Tohoku University (T.T.Y.), Sendai 981-8555, Japan
Address all correspondence and requests for reprints to: Dr. Sadao Takahashi, Third Department of Internal Medicine, Faculty of Medical Sciences, University of Fukui, Matsuoka-cho, Fukui 910-1193, Japan. E-mail: sadaost{at}fmsrsa.fukui-med.ac.jp.
Hyperlipidemia is a common feature of diabetes and is related to cardiovascular disease. The very low-density lipoprotein receptor (VLDL-R) is a member of the low-density lipoprotein receptor (LDL-R) family. It binds and internalizes triglyceride-rich lipoproteins with high specificity. We examined the etiology of hyperlipidemia in the insulin-deficient state. VLDL-R expression in heart and skeletal muscle were measured in rats with streptozotocin (STZ)-induced diabetes. STZ rats showed severe hyperlipidemia on d 21 and 28, with a dramatic decline in VLDL-R protein in skeletal muscle (>90%), heart (
50%) and a loss of adipose tissues itself on d 28. The reduction of VLDL-R protein in skeletal muscle could not be explained simply by a decrease at the transcriptional level, because a dissociation between VLDL-R protein and mRNA expression was observed. The expression of LDL-R and LDL-R-related protein in liver showed no consistent changes. Furthermore, no effect on VLDL-triglyceride production in liver was observed in STZ rats. A decrease in postheparin plasma lipoprotein lipase activity started on d 7 and continued to d 28 at the 50% level even though severe hyperlipidemia was detected only on d 21 and 28. In rat myoblast cells, serum deprivation for 24 h induced a reduction in VLDL-R proteins. Insulin (10–6 M), but not IGF-I (10 ng/ml), restored the decreased VLDL-R proteins by serum deprivation. These results suggest that the combination of VLDL-R deficiency and reduced plasma lipoprotein lipase activity may be responsible for severe hyperlipidemia in insulin-deficient diabetes.
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