IMPROVED BLOOD-GLUCOSE CONTROL BY INSULIN THERAPY IN TYPE-2 DIABETIC-PATIENTS HAS NO EFFECT ON LIPOPROTEIN(A) LEVELS

被引:26
作者
WOLFFENBUTTEL, BHR
LEURS, PB
SELS, JPJE
RONDASCOLBERS, GJWM
MENHEERE, PPCA
KRUSEMAN, ACN
机构
[1] Department of Internal Medicine, Division of Endocrinology, University Hospital Maastricht
[2] Department of Clinical Chemistry, University Hospital Maastricht
关键词
TYPE-2; DIABETES-MELLITUS; INSULIN THERAPY; BLOOD GLUCOSE CONTROL; LIPOPROTEINS LIPOPROTEIN(A);
D O I
10.1111/j.1464-5491.1993.tb00093.x
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
The effects of improved blood glucose control by insulin therapy on lipoprotein(a) and other lipoproteins were studied in 54 patients with Type 2 diabetes (mean +/- SD: age 67 +/- 9 years, body mass index 26.1 +/- 4.4 kg m-2, Median duration of diabetes 10 (range 1-37) years, 23 males, 31 females), who were poorly controlled despite diet and maximal doses of oral hypoglycaemic agents. After 6 months of insulin treatment, mean fasting blood glucose concentrations had decreased from 14.1 +/- 2.2 mmol l-1 to 8.4 +/- 1.8 mmol l-1 (p < 0.001), and HbA1c had fallen from 11.1 +/- 1.4 % to 8.2 +/- 1.1 % (p < 0.001). Significant decreases of total and LDL cholesterol, triglycerides, apolipoprotein B, and free fatty acids were observed, while HDL-cholesterol and apoA1 increased by 10 %. Baseline serum Lp(a) levels were elevated compared to non-diabetic subjects of similar age (median 283, range 8-3050 mg l-1, vs 101, range 8-1747 mg l-1, p < 0.05), but did not change with insulin, and there was no correlation with the degree of metabolic improvement and changes in Lp(a) levels. It is concluded that improved blood glucose control by insulin therapy does not alter elevated Lp(a) levels in Type 2 diabetic patients, but has favourable effects on the other lipoproteins.
引用
收藏
页码:427 / 430
页数:4
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共 38 条
  • [1] Kostner GM, Avogaro P., Cazzolato G., Marth E., Bittolo-Bon G., Qunici GB., Lipoprotein Lp(a) and the risk for myocardial infarction, Atherosclerosis, 38, pp. 51-61, (1981)
  • [2] Mbewu AD, Durrington PN., Lipoprotein(a): structure, properties and possible involvement in thrombogenesis and atherogenesis, Atherosclerosis, 85, pp. 1-14, (1990)
  • [3] Rosengren A., Wilhelmsen L., Eriksson E., Risberg B., Wedel H., Lipoprotein(a) and coronary heart disease: a prospective case‐control study in a general population sample of middle aged men, Br Med J, 301, pp. 1248-1251, (1990)
  • [4] Berg K., A new serum type system in man: the Lp system, Acta Pathol Microbiol Scand, 59, pp. 369-382, (1963)
  • [5] Scanu AM., Lipoprotein(a)—a potential bridge between the fields of atherosclerosis and thrombosis, Arch Pathol Lab Med, 112, pp. 1045-1047, (1988)
  • [6] Utermann G., The mysteries of lipoprotein(a), Science, 246, pp. 904-910, (1989)
  • [7] Cushing GL, Gaubatz JW, Nava ML, Burdick BJ, Bocan TMA, Guyton JR, Et al., Quantitation and localization of apolipoprotein(a) and B in coronary artery bypass vein grafts resected at re‐operation, Arteriosclerosis, 9, pp. 593-603, (1989)
  • [8] Rath M., Niendorf A., Reblin T., Dietel M., Krebber HJ, Beisiegel U., Detection and quantification of lipoprotein(a) in the arterial wall of 107 coronary bypass patients, Arteriosclerosis, 9, pp. 579-592, (1989)
  • [9] Thiery J., Armstrong VW, Schleef J., Creutzfeldt C., Creutz-feldt W., Seidel D., Serum lipoprotein Lp(a) concentrations are not influenced by an HMG CoA reductase inhibitor, Klin Wochenschr, 66, pp. 462-463, (1988)
  • [10] Kostner GM, Gavish D., Leopold B., Bolzano K., Weintraub MS, Breslow JL., HMG CoA reductase inhibitors lower LDL cholesterol without reducing Lp(a) levels, Circulation, 80, pp. 1313-1319, (1989)