Postprandial dysmetabolism and cardiovascular disease in type 2 diabetes

被引：67

作者：

Tushuizen, ME ^{[1
]}

Diamant, M ^{[1
]}

Heine, RJ ^{[1
]}

机构：

[1] Vrije Univ Amsterdam Med Ctr, Dept Endocrinol, Ctr Diabet, NL-1007 MB Amsterdam, Netherlands

来源：

POSTGRADUATE MEDICAL JOURNAL | 2005年 / 81卷 / 951期

关键词：

D O I：

10.1136/pgmj.2004.020511

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

The worldwide prevalence of type 2 diabetes mellitus has reached epidemic proportions. The so-called traditional risk factors cannot fully explain the excessive cardiovascular disease risk of type 2 diabetic patients. Numerous studies indicate that postprandial metabolic derangements, most notably hyperglycaemia and hypertriglyceridaemia, which are exaggerated and prolonged in type 2 diabetes, are important cardiovascular disease risk factors since they induce oxidative stress and endothelial dysfunctions. This review discusses the current evidence showing that postprandial dysmetabolism may indeed constitute an important cardiovascular disease risk factor as well as the mechanisms underlying this association. Finally, some possible therapeutic options and recommendations for future research are discussed.

引用

页码：1 / 6

页数：6

共 65 条

[1] SERUM TRIGLYCERIDES IN CORONARY ARTERY DISEASE [J].

ALBRINK, MJ ;

MAN, EB .

ARCHIVES OF INTERNAL MEDICINE, 1959, 103 (01) :4-8

[2] The relationships between post-prandial lipaemia, endothelial function and oxidative stress in healthy individuals and patients with type 2 diabetes [J].

Anderson, RA ;

Evans, ML ;

Ellis, GR ;

Graham, J ;

Morris, K ;

Jackson, SK ;

Lewis, MJ ;

Rees, A ;

Frenneaux, MP .

ATHEROSCLEROSIS, 2001, 154 (02) :475-483

[3] Impact of postprandial hypertriglyceridemia on vascular responses in patients with coronary artery disease: effects of ACE inhibitors and fibrates [J].

Bae, JH ;

Bassenge, E ;

Lee, HJ ;

Park, KR ;

Park, CG ;

Park, KY ;

Lee, MS ;

Schwemmer, M .

ATHEROSCLEROSIS, 2001, 158 (01) :165-171

[4] THE EFFECT OF SHORT-TERM ALPHA-GLUCOSIDASE INHIBITION ON CARBOHYDRATE AND LIPID-METABOLISM IN TYPE-II (NONINSULIN-DEPENDENT) DIABETES [J].

BARON, AD ;

ECKEL, RH ;

SCHMEISER, L ;

KOLTERMAN, OG .

METABOLISM-CLINICAL AND EXPERIMENTAL, 1987, 36 (05) :409-415

[5]

Borch-Johnsen K, 1999, LANCET, V354, P617

[6] A combination of high concentrations of serum triglyceride and non-high-density-lipoprotein-cholesterol is a risk factor for cardiovascular disease in subjects with abnormal glucose metabolism - The Hoorn Study [J].

Bos, G ;

Dekker, JM ;

Nijpels, G ;

de Vegt, F ;

Diamant, M ;

Stehouwer, CDA ;

Bouter, LM ;

Heine, RJ .

DIABETOLOGIA, 2003, 46 (07) :910-916

[7] Alimentary lipemia enhances the membrane expression of platelet P-selectin without affecting other markers of platelet activation [J].

Bröijersén, A ;

Karpe, F ;

Hamsten, A ;

Goodall, AH ;

Hjemdahl, P .

ATHEROSCLEROSIS, 1998, 137 (01) :107-113

[8] Biochemistry and molecular cell biology of diabetic complications [J].

Brownlee, M .

NATURE, 2001, 414 (6865) :813-820

[9] Increased PAI activity and PAI-1 antigen occurring with an oral fat load:: associations with PAI-1 genotype and plasma active TGF-β levels [J].

Byrne, CD ;

Wareham, NJ ;

Martensz, ND ;

Humphries, SE ;

Metcalfe, JC ;

Grainger, DJ .

ATHEROSCLEROSIS, 1998, 140 (01) :45-53

[10] Hyperglycemia-induced circulating ICAM-1 increase in diabetes mellitus:: The possible role of oxidative stress [J].

Ceriello, A ;

Falleti, E ;

Motz, E ;

Taboga, C ;

Tonutti, L ;

Ézsol, Z ;

Gonano, F ;

Bartoli, E .

HORMONE AND METABOLIC RESEARCH, 1998, 30 (03) :146-149

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