High-density lipoprotein subspecies between patients with type 1 diabetes and type 2 diabetes without/with intensive insulin therapy

被引:22
作者
Fukui, Tomoyasu [1 ]
Hirano, Tsutomu [1 ]
机构
[1] Showa Univ, Sch Med, Div Diabet Metab & Endocrinol,Dept Med, Shinagawa Ku, Tokyo 1428666, Japan
关键词
High-density lipoprotein subspecies; Type; 1; diabetes; 2; Intensive insulin therapy; CORONARY-ARTERY-DISEASE; APOLIPOPROTEIN-A-I; CHOLESTEROL SUBFRACTIONS; HDL3; SUBFRACTIONS; GLUCOSE CONTROL; HEART-DISEASE; PLASMA; SUBCLASSES; MELLITUS; ATHEROSCLEROSIS;
D O I
10.1507/endocrj.EJ11-0329
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
The reduced levels of high-density lipoprotein (HDL) 2-cholesterol (C) in diabetes and other metabolic disorders associated with a high risk of cardiovascular disease are well established. Few studies, however, have compared the HDL subspecies in type I diabetes (T1D) with those in type 2 diabetes (T2D) with or without insulin. We examined HDL subspecies in 27 T1D with insulin, 33 T2D with insulin or insulin plus oral-anti-diabetic drugs (OADs), 36 T2D with OADs or diet/exercise, and 25 non-diabetic controls. Insulin was injected four times daily in a basal-bolus manner for both T1D and T2D. Plasma levels of C, apolipoprotcin (apo) AI, and AII were determined in HDL2 and HDL3 by the single precipitation method. HDL-C levels were significantly higher in T1D and lower in T2D, compared with the controls. Insulin-treated T2D had higher HDL-C than non-insulin-treated T2D. T1D had higher HDL2-C and HDL2-apo AI levels than T2D. Insulin-treated T2D had higher HDL2-C and HDL2-apo AI levels than non-insulin-treated T2D. All of these differences were more pronounced for men than for women. HDL3 levels were comparable among controls,T1D and T2D. HDL2-C levels were inversely associated with BMI, HbA1c, triglyceride, small dense LDL-C, and LDL-C. Multiple regression analysis revealed that HDL2-C was independently associated with triglyceride, LDL-C, and intensive insulin therapy but not with HbA1c. In conclusion, these results suggest that intensive insulin therapy is associated with alterations of HDL subspecies, irrespective of the type of diabetes.
引用
收藏
页码:561 / 569
页数:9
相关论文
共 32 条
[1]   Suppression of plasma cholesteryl ester transfer protein activity in acute hyperinsulinemia and effect of plasma nonesterified fatty acid [J].
Arii, K ;
Suehiro, T ;
Yamamoto, M ;
Ito, H ;
Hashimoto, K .
METABOLISM-CLINICAL AND EXPERIMENTAL, 1997, 46 (10) :1166-1170
[2]   Clinical evaluation of plasma high-density lipoprotein subfractions (HDL2, HDL3) in non-insulin-dependent diabetics with coronary artery disease [J].
Bakogianni, MC ;
Kalofoutis, CA ;
Skenderi, KI ;
Kalofoutis, AT .
JOURNAL OF DIABETES AND ITS COMPLICATIONS, 2001, 15 (05) :265-269
[3]   High density lipoproteins (HDLs) and atherosclerosis; the unanswered questions [J].
Barter, P ;
Kastelein, J ;
Nunn, A ;
Hobbs, R .
ATHEROSCLEROSIS, 2003, 168 (02) :195-211
[4]  
CALVERT GD, 1978, LANCET, V2, P66
[5]  
CHAPMAN MJ, 1981, J LIPID RES, V22, P339
[6]   Lipoprotein subclasses and particle sizes and their relationship with coronary artery calcification in men and women with and without type 1 diabetes [J].
Colhoun, HM ;
Otvos, JD ;
Rubens, MB ;
Taskinen, MR ;
Underwood, SR ;
Fuller, JH .
DIABETES, 2002, 51 (06) :1949-1956
[7]   Association of cholesterol subfractions and carotid lipid core measured by MRI [J].
Desai, MY ;
Rodriguez, A ;
Wasserman, BA ;
Gerstenblith, G ;
Agarwal, S ;
Kennedy, M ;
Bluemke, DA ;
Lima, JAC .
ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY, 2005, 25 (06) :E110-E111
[8]   RELATION OF THE LEVEL OF HIGH-DENSITY-LIPOPROTEIN SUBFRACTIONS TO THE PRESENCE AND EXTENT OF CORONARY-ARTERY DISEASE [J].
DREXEL, H ;
AMANN, FW ;
RENTSCH, K ;
NEUENSCHWANDER, C ;
LUETHY, A ;
KHAN, SI ;
FOLLATH, F .
AMERICAN JOURNAL OF CARDIOLOGY, 1992, 70 (04) :436-440
[9]   PLASMA-LIPOPROTEIN ABNORMALITIES IN TYPE-1 (INSULIN-DEPENDENT) DIABETES-MELLITUS [J].
DULLAART, RPF .
NETHERLANDS JOURNAL OF MEDICINE, 1995, 46 (01) :44-54
[10]   High-density lipoprotein subclasses and apolipoprotein A-I [J].
Duriez, P ;
Fruchart, JC .
CLINICA CHIMICA ACTA, 1999, 286 (1-2) :97-114