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Postprandial lipid metabolism in relation to coronary heart disease.
| Content Provider | Semantic Scholar |
|---|---|
| Author | Karpe, Fredrik |
| Copyright Year | 1997 |
| Abstract | The issue of whether chylomicron remnants are atherogenic has been much debated. A number of reports, which will be discussed later, point to a relationship between impaired metabolism of postprandial triacylglycerol-rich lipoproteins and the presence of coronary artery disease (CAD). For the purpose of standardization, the levels of plasma lipids and lipoproteins are generally measured in the fasting state, despite the fact that most of our lives are spent between regular meals. For obvious reasons, no consensus has been reached on how postprandial lipoproteins should be quantified in the clinical setting. A large body of studies from the 1950s and 1960s focused on plasma levels of triacylglycerols after a fatty meal in case-control studies. Unfortunately, the interest declined when it was found that the postprandial triacylglycerol level was closely reflected by fasting plasma concentrations (Nestel, 1964). A few fairly recent studies have used vitamin A supplementation of the test meal leading to retinyl ester (mainly retinyl palmitate; RP) incorporation into chylomicrons and their remnants as a means of tracing intestinal lipoproteins in plasma. It was shown that postprandial plasma concentrations of RP were higher in CAD patients than in healthy subjects (Simpson et al. 1990; Groot ef al. 1991). With the discovery of the normal truncated variant of apolipoprotein (apo) B, the apo B-48 which in human subjects is the structural protein of intestinally-derived triacylglycerol-rich lipoproteins, a specific marker for chylomicrons and their remnants was found (Kane et al. 1980). The simultaneous quantification of apo B-48 and apo B-100 in subfractions of triacylglycerol-rich lipoproteins after fat intake has led to a better understanding of the metabolism of postprandial triacylglycerol-rich lipoproteins and of their relationship with CAD. However, there is a complete lack of prospective studies in which postprandial lipid metabolism has been related to future events of CAD or progression of atherosclerosis. |
| Starting Page | 10 |
| Ending Page | 10 |
| Page Count | 1 |
| File Format | PDF HTM / HTML |
| Alternate Webpage(s) | https://www.cambridge.org/core/services/aop-cambridge-core/content/view/S0029665197000207 |
| PubMed reference number | 9264117v1 |
| Volume Number | 56 |
| Issue Number | 2 |
| Journal | The Proceedings of the Nutrition Society |
| Language | English |
| Access Restriction | Open |
| Subject Keyword | Apolipoprotein B-100 Apolipoprotein B-48 Apolipoprotein E4 Apolipoproteins Arteriopathic disease Atherosclerosis BLOC1S3 gene Chylomicrons Coronary Artery Disease Coronary heart disease Fatty acid glycerol esters Heart Diseases Lipase Lipid Metabolism Disorders Lipoproteins NG-Nitroarginine Methyl Ester Patients Reactive hypoglycemia Retinitis Pigmentosa Triglycerides Vitamin A retinyl palmitate |
| Content Type | Text |
| Resource Type | Article |
