ISSN:0957-9672    

出版商:OVID    

年代:2000

数据来源: OVID

摘要:

Although the biochemistry of triglyceride synthesis has been studied for decades, an understanding of the molecular processes involved has been lacking. The recent cloning of a gene encoding acyl coenzyme A : diacylglycerol acyltransferase, an enzyme that catalyses the final step in triglyceride synthesis, has opened this area to molecular investigation and has begun to provide new insights into triglyceride metabolism.

ISSN:0957-9672    

出版商:OVID    

年代:2000

数据来源: OVID

摘要:

Several lines of clinical and experimental data suggest that postprandial lipemia is an independent risk factor for atherosclerosis. There are a number of reasons why processes that occur in the period immediately after eating could be deleterious to arteries. By understanding the links between postprandial lipemia and the accumulation of lipid within vessels, a more global understanding of how lipoproteins cause disease may be forthcoming. In this article recent information on the control of postprandial lipemia and the biological effects of chylomicron remnants and lipolysis products will be reviewed. Because this topic is broad, we will focus on the roles played by lipoprotein lipase and proteoglycans in this process.

ISSN:0957-9672    

出版商:OVID    

年代:2000

数据来源: OVID

摘要:

Apolipoprotein E plays a key protective role in atherosclerosis. Its capacity to safeguard against this disease can be attributed to at least three distinct functions. First, plasma apolipoprotein E maintains overall plasma cholesterol homeostasis by facilitating efficient hepatic uptake of lipoprotein remnants. Second, lesion apolipoprotein E in concert with apolipoprotein A-I facilitates cellular cholesterol efflux from macrophage foam cells within the intima of the lesion. Third, lesion apolipoprotein E directly modifies both macrophage- and T lymphocyte-mediated immune responses that contribute to this chronic inflammatory disease.

ISSN:0957-9672    

出版商:OVID    

年代:2000

数据来源: OVID

摘要:

Lipid-poor apolipoproteins remove cellular cholesterol and phospholipids by an active transport pathway controlled by an ATP binding cassette transporter called ABCA1 (formerly ABC1). Mutations in ABCA1 cause Tangier disease, a severe HDL deficiency syndrome characterized by a rapid turnover of plasma apolipoprotein A-I, accumulation of sterol in tissue macrophages, and prevalent atherosclerosis. This implies that lipidation of apolipoprotein A-I by the ABCA1 pathway is required for generating HDL particles and clearing sterol from macrophages. Thus, the ABCA1 pathway has become an important therapeutic target for mobilizing excess cholesterol from tissue macrophages and protecting against atherosclerosis.

ISSN:0957-9672    

出版商:OVID    

年代:2000

数据来源: OVID

摘要:

Amino acid precursors labelled with stable isotopes have been successfully used to explore the metabolism of the apolipoproteins of HDL. Some methodological and mathematical modelling problems remain, mainly related to amino acid recycling in a plasma protein such as apolipoprotein A-I with a long residence time (the reciprocal of the fractional catabolic rate) of 4-5 days. Apolipoprotein A-I, apolipoprotein E, and apolipoprotein A-IV in triglyceride-rich lipoproteins (containing chylomicrons, VLDL, and remnants) exhibit more complex kinetics. The small amounts of apolipoprotein A-I and of apolipoprotein A-IV in the triglyceride-rich lipoproteins have a residence time similar to that of the apolipoprotein A-I of HDL. In contrast, the apolipoprotein E in triglyceride-rich lipoproteins has been found to have an average residence time of 0.11 days. Diets low in saturated fat and cholesterol, which lower HDL levels, do so by decreasing the secretion of apolipoprotein A-I, with apolipoprotein A-II kinetics unaffected. Individuals with impaired glucose tolerance have a decreased residence time of apolipoprotein A-I but no change in secretion rate or in apolipoprotein A-II kinetics. This suggests a link between insulin resistance and the risk of atherosclerosis. In heterozygous familial hypercholesterolemia, both the fractional catabolic rate and the secretion rate of apolipoprotein A-I are increased, resulting in no change in the plasma level. Stable isotope studies have strengthened the evidence that triglyceride enrichment of HDL increases its catabolism Laboratory.

ISSN:0957-9672    

出版商:OVID    

年代:2000

数据来源: OVID

摘要:

In the past several years significant advances have been made in our understanding of lecithin-cholesterol acyltransferase (LCAT) function. LCAT beneficially alters the plasma concentrations of apolipoprotein B-containing lipoproteins, as well as HDL. In addition, its proposed role in facilitating reverse cholesterol transport and modulating atherosclerosis has been demonstratedin vivo. Analysis of LCAT transgenic animals has established the importance of evaluating HDL function, as well as HDL plasma levels, to predict atherogenic risk.

ISSN:0957-9672    

出版商:OVID    

年代:2000

数据来源: OVID

摘要:

Hepatic lipase is a lipolytic enzyme that has been suggested to have a role in HDL metabolism. Evidence suggests that HDL-cholesterol level is at least partly regulated by hepatic lipase level. Recent studies have shown that hepatic lipase not only hydrolyzes triglyceride and phospholipid in HDL, but also stimulates HDL cholesterol ester uptake by hepatocytes. Therefore, hepatic lipase, together with lipid transfer proteins, determines both HDL-cholesterol level and its function in reverse cholesterol transport. These conclusions are based on observations from in-vitro model substrate studies, cell culture studies, transgenic animal studies, and clinical studies. At present time, it is not known whether hepatic lipase action increases or decreases risk of developing atherosclerosis.

ISSN:0957-9672    

出版商:OVID    

年代:2000

数据来源: OVID

摘要:

Phospholipid transfer protein (PLTP) is one of the main modulators of plasma HDL size and composition. The publications discussed in the present review have substantially increased our knowledge on the physiological importance of PLTP-mediated phospholipid transfer, especially between triglyceride-rich lipoproteins and HDL. Furthermore, novel data have provided clues about the transfer mechanism, and evidence for the direct involvement of PLTP in atheroprotection has recently been presented. The development of assays for PLTP mass determination has offered new tools for the elucidation of the physiological role of PLTP.

ISSN:0957-9672    

出版商:OVID    

年代:2000

数据来源: OVID

摘要:

The storage and release of energy by adipocytes is of fundamental biologic importance. Not surprisingly, therefore, the rate at which these processes occur can be modulated by a variety of physiologic molecules. A newly recognized participant is produced by adipocytes themselves: acylation-stimulating protein (ASP). This article focuses on the most recent in-vivo evidence regarding how the ASP pathway may influence energy storage and release. In brief, the rate at which triglycerides are cleared from plasma (i.e. the rate at which they are hydrolysed) is determined by lipoprotein lipase and insulin, which is the principal hormone that regulates lipoprotein lipase. By contrast, the ASP pathway modulates the rate at which fatty acids are taken up and converted to triglycerides by adipocytes. Under certain circumstances, however, reduction of activity of the ASP pathway may negatively impact on the first step of the process. ASP also influences the rate at which fatty acids are released by adipocytes, and it is clear that insulin and ASP interact in a variety of ways that involve energy storage and release. Accordingly, to understand the impact of any intervention on energy storage and release by adipocytes, the effects of both insulin and ASP must be taken into account.

ISSN:0957-9672    

出版商:OVID    

年代:2000

数据来源: OVID