Postprandial lipid metabolism and thrombosis

Miller, George

doi:10.1079/pns19970074

Cited by 5 publications

(4 citation statements)

References 34 publications

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“…This brief review covers the authors work and views in relation to other researchers work on the associations between postprandial triglycerides and hemostatic function underlying CHD. Different aspects of the subject have been published by Miller (1997 and1998) and by Mennen et al (1996).…”

Section: Pai-1 and Postprandial Triglyceridesmentioning

confidence: 99%

Postprandial triglycerides and blood coagulation

Silveira¹

2001

Exp Clin Endocrinol Diabetes

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Most of our lifetime we spend in the postprandial state. Postprandial triglyceridemia may represent a procoagulant state involving disturbances of both blood coagulation and fibrinolysis, in particular due to elevation of the plasma levels of activated factor VII (VIIa) and plasminogen activator inhibitor (PAI-1). Therefore, disturbances of the hemostatic system might, at least partly, account for by the link between hypertriglyceridemia and coronary heart disease (CHD). Factor VIIa is the first enzyme of the blood coagulation system and serves a priming function for triggering of the clotting cascade. The coagulant activity of factor VII (VIIc, total activity of factor VII in plasma) was identified as an independent predictor of myocardial infarction in initially healthy middle-aged men, and particularly of fatal coronary events, and both serum cholesterol and triglyceride concentrations correlated positively with the VIIc level. Addition of fat to diet has been consistently shown to cause a rapid conversion of the factor VII zymogen into its active form (VIIa) whereas the concentration of total protein is unaffected. Postprandial activation of factor VII is dependent on lipolytic activity and it is mainly supported by large triglyceride-rich lipoprotein of the VLDL class. Studies in vivo with specific coagulation factor-deficient patients indicate that factor IX is essential for the postprandial activation of factor VII. The basal generation of thrombin seems to be unaffected by increased plasma levels of VIIa. However, since VIIa-tissue factor complex is responsible for the initiation of the coagulation cascade, increased generation of VIIa in the postprandial state would increase the potential for thrombin production in the event of plaque rupture. Plasminogen activator inhibitor-1 (PAI-1) is the major physiological inhibitor of the plasminogen activators in the circulation and thereby the principal inhibitor of the fibrinolytic system. Postprandial triglyceridemia has been observed in many, not all, studies to increase PAI-1 plasma levels, which would further strengthen the chances of thrombotic occlusion of a vessel after rupture of an atherosclerotic plaque.

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Section: Pai-1 and Postprandial Triglyceridesmentioning

confidence: 99%

Postprandial triglycerides and blood coagulation

Silveira¹

2001

Exp Clin Endocrinol Diabetes

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“…The involvement of postprandial TRL (chylomicrons (CM) and VLDL) in the pathogenesis of atherosclerosis and thrombosis is dealt with by other speakers in the symposium (Karpe, 1997;Miller, 1997;Sniderman et al 1997). A brief outline of the relationships between CM and VLDL, and cholesterol-rich lipoproteins (LDL-cholesterol and HDL-cholesterol), is given here to illustrate how an elevated postprandial lipaemic response may be related to other lipid abnormalities of the 'metabolic syndrome', such as low HDL, raised fasting triacylglycerols and a preponderance of the LDL-3 (small dense) subtype.…”

Section: Postprandial Triacylglycerol-rich Lipoproteins As a Lipid Rimentioning

confidence: 99%

Postprandial lipid metabolism: effects of dietary fatty acids

Williams

1997

Proc. Nutr. Soc.

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“…Since then, numerous studies have linked the postprandial increases in plasma TAG concentrations with CHD via effects on atherosclerosis (Havel 1994; Karpe 1997), either directly through the atherogenic properties of chylomicron remnants, and/or indirectly by influencing compositional changes in other lipoproteins (LDL and HDL) involved in the process of atherosclerosis. Postprandial lipaemia may also increase the risk of thrombosis by increasing the activation of factor VII (FVII), which promotes blood clotting, and by decreasing fibrinolytic activity, which promotes the breakdown of blood clots (Hoak 1994; Miller 1997, 1998). Figure 2 outlines some of the mechanisms by which postprandial lipaemia may increase risk of CHD, discussed in detail below.…”

Section: Mechanisms Whereby Postprandial Lipaemia Increases Risk Of Chdmentioning

confidence: 99%

Postprandial lipaemia – the influence of diet and its link to coronary heart disease

Berry

2005

Nutrition Bulletin

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Coronary heart disease (CHD) is the leading cause of death worldwide, and dietary fat intake is one of the major environmental risk factors implicated in its causation. In the drive to prevent CHD, much attention has focused on reducing the amount of energy derived from fat in the diet. However, little attention has been given to the amount of fat consumed in an individual meal and its postprandial effects. Postprandial lipaemia is the term used to describe the series of metabolic events that occur following the consumption of a fatty meal. The extent of postprandial lipaemia is indicated by the size or duration of the increase in plasma triacylglycerol (TAG) concentrations. There is evidence to indicate that exaggerated postprandial lipaemia is linked to an increased risk of CHD. There are several mechanisms by which it may influence the pathological processes that result in CHD, including effects on lipoproteins involved in atherosclerosis and acute effects on haemostatic function . The postprandial response to dietary fat is influenced by non-dietary factors (such as age, gender and activity level) as well as background diet and the amount and type of fat consumed in a meal. This review focuses on the mechanisms linking postprandial lipaemia and CHD risk and the factors affecting the level of postprandial lipaemia.

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Postprandial lipid metabolism and thrombosis

Cited by 5 publications

References 34 publications

Postprandial triglycerides and blood coagulation

Postprandial triglycerides and blood coagulation

Postprandial lipid metabolism: effects of dietary fatty acids

Postprandial lipaemia – the influence of diet and its link to coronary heart disease

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