The postprandial state and the risk of atherosclerosis

被引:0
|
作者
Hanefeld, M
TemelkovaKurktschiev, T
机构
关键词
postprandial; risk factors; atherosclerosis; acarbose;
D O I
10.1002/(SICI)1096-9136(199708)14:3+<S6::AID-DIA438>3.3.CO;2-8
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
The results of the Diabetes Intervention Study indicate that postprandial hyperglycaemia, but not fasting hyperglycaemia, is an independent risk factor for myocardial infarction and total mortality in newly detected non-insulin-dependent diabetes mellitus (NIDDM). Blood pressure and triglyceride levels were also found to be risk factors. Data from patients in the Study to Prevent NIDDM show that patients with impaired glucose tolerance (IGT) have higher fasting levels of triglycerides, and higher fasting and postprandial levels of pro-insulin, insulin, and C-peptide levels, compared with those who have normal glucose tolerance (NGT). Postprandial data at 2 h showed that hyperinsulinaemia was prolonged in subjects with IGT compared with their NGT counterparts. Postprandial pro-insulin levels at 2 h were also increased in subjects with IGT, and were found to have the best discriminating power between subjects with IGT and NGT. Those with IGT also secreted markedly higher levels of insulin, indicated by C-peptide levels, than those with NGT. These data support the possibility that subjects with IGT are at an increased risk of conditions such as atherosclerotic disease, even though they have not developed manifest NIDDM. Intervention with agents that can affect risk factors, such as triglyceride levels and postprandial hyperglycaemia, are expected to reduce the risk of atherosclerosis. One promising agent is acarbose, an antihyperglycaemic drug that significantly reduces postprandial insulin and triglyceride levels and has no effect on leptin levels. The ability of acarbose to improve glycaemic control without the potential for inducing hyperinsulinaemia and weight gain appears to give it an advantage over oral antidiabetic agents such as the sulphonylureas. (C) 1997 by John Wiley & Sons, Ltd.
引用
收藏
页码:S6 / S11
页数:6
相关论文
共 50 条
  • [1] POSTPRANDIAL STATE AND ATHEROSCLEROSIS
    EBENBICHLER, CF
    KIRCHMAIR, R
    EGGER, C
    PATSCH, JR
    CURRENT OPINION IN LIPIDOLOGY, 1995, 6 (05) : 286 - 290
  • [2] Postprandial hyperglycemia and risk of atherosclerosis - Reply
    Beckman, JA
    Creager, MA
    Libby, P
    JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION, 2002, 288 (08): : 955 - 955
  • [3] Postprandial hypertriglyceridemia as a risk factor of atherosclerosis
    Fujioka, Yoshio
    ANNALS OF NUTRITION AND METABOLISM, 2023, 79 : 221 - 221
  • [4] The postprandial state and risk of cardiovascular disease
    Lefèbvre, P
    Scheen, AJ
    DIABETIC MEDICINE, 1998, 15 (12) : S63 - S68
  • [5] Postprandial lipoproteins and atherosclerosis
    Yu, KCW
    Cooper, AD
    FRONTIERS IN BIOSCIENCE-LANDMARK, 2001, 6 : D332 - D354
  • [6] Postprandial hyperlipidemia and atherosclerosis
    Tamio Teramoto
    Current Atherosclerosis Reports, 2007, 9 (3)
  • [7] Elevated levels of platelet microparticles in carotid atherosclerosis and during the postprandial state
    Michelsen, Annika E.
    Noto, Ann-Trude
    Brodin, Ellen
    Mathiesen, Ellisiv B.
    Brosstad, Frank
    Hansen, John-Bjarne
    THROMBOSIS RESEARCH, 2009, 123 (06) : 881 - 886
  • [8] Effect of the postprandial state on nontraditional risk factors
    Lebovitz, HE
    AMERICAN JOURNAL OF CARDIOLOGY, 2001, 88 (6A): : 20H - 25H
  • [9] GENETIC-CONTROL OF POSTPRANDIAL LIPEMIA - THE ATHEROSCLEROSIS RISK IN COMMUNITIES STUDY
    BOERWINKLE, E
    BROWN, SA
    SHARRETT, AR
    HEISS, G
    PATSCH, W
    CIRCULATION, 1992, 86 (04) : 809 - 809
  • [10] POSTPRANDIAL CHOLESTEROL-METABOLISM IN MICE WITH DIFFERENTIAL GENETIC RISK FOR ATHEROSCLEROSIS
    VAITHILINGAM, D
    ANTAO, V
    KAKIS, G
    CLINICAL RESEARCH, 1988, 36 (03): : A773 - A773