ISSN:0957-9672    

出版商:OVID    

年代:1998

数据来源: OVID

摘要:

Familial combined hyperlipidaemia is the most common inherited hyperlipidaemia and is found in up to 10% of patients with premature myocardial infarction. The genetic and metabolic bases of the disorder have not yet been defined. This review discusses the important advances in the past year in our understanding of the different metabolic pathways contributing to the pathogenesis of familial combined hyperlipidaemia. Curr Opin Lipidol 9:189–196. © 1998 Lippincott–Raven Publishers

ISSN:0957-9672    

出版商:OVID    

年代:1998

数据来源: OVID

摘要:

Apolipoprotein B‐100‐containing lipoprotein assembly is dependent on the successive addition of triglyceride by microsomal transfer protein. Assembly may end at this point and the lipoprotein secreted or it may continue with the bulk addition of triglyceride by an unknown transfer process. These steps are independently regulated and result in the secretion of a spectrum of apolipoprotein B‐100‐containing particles. The production of small, dense LDL is determined by the type of VLDL secreted by the liver. Large, triglyceride‐rich VLDL1 results in the formation of small, dense LDL through triglyceride exchange and subsequent hydrolysis. Small, dense LDL are cleared from plasma relatively slowly and tend to accumulate in the circulation where they exert their atherogenic effects. Curr Opin Lipidol 9:197–202. © 1998 Lippincott–Raven Publishers

ISSN:0957-9672    

出版商:OVID    

年代:1998

数据来源: OVID

摘要:

Recent cloning and sequencing of plasma phospholipid transfer protein complementary DNA revealed that phospholipid transfer protein belongs to the lipid transfer/lipopolysaccharide binding protein family that includes the cholesteryl ester transfer protein, the bactericidal permeability increasing protein and the lipopolysaccharide‐binding protein. In addition to structural similarities, members of the lipid transfer/lipopolysaccharide‐binding protein family might share some common functional properties, and recent studies demonstrated that phospholipid transfer protein can act in several distinct metabolic processes. In particular, the molecular transfer of phospholipids, unesterified cholesterol, α‐tocopherol and lipopolysaccharides by phospholipid transfer protein suggests that it might be involved both in lipoprotein metabolism and in antimicrobial defence, resulting in a growing interest in this protein. Curr Opin Lipidol 9:203–209. © 1998 Lippincott–Raven Publishers

ISSN:0957-9672    

出版商:OVID    

年代:1998

数据来源: OVID

摘要:

In addition to its traditional role in the hydrolysis of lipoprotein triglycerides and phospholipids, recent studies have implicated hepatic lipase in other aspects of cellular lipid and/or lipoprotein metabolism and atherosclerosis. Hepatic lipase may serve as a ligand that mediates the interaction of lipoproteins to cell surface receptors and/or proteoglycans as well as modulating aortic lesion development in different animal models. Over the past several years significant advances have been made in our understanding of new, alternative mechanisms by which hepatic lipase may modulate lipoprotein metabolism and the development of atherosclerosisin vivo. Curr Opin Lipidol 9:211–219. © 1998 Lippincott–Raven Publishers

ISSN:0957-9672    

出版商:OVID    

年代:1998

数据来源: OVID

摘要:

The lipolysis stimulated receptor is a lipoprotein receptor that was initially described in 1992. In the presence of free fatty acids, the lipolysis stimulated receptor recognizes either apolipoprotein B or apolipoprotein E, and as a consequence, leads to the internalization and degradation of the lipoprotein particles. Its affinity is highest for those lipoproteins most susceptible to lipolysis, triglyceride‐rich lipoproteins. Since the initial biochemical identification and description of the lipolysis stimulated receptor, several reports have been published by our group that provide circumstantial evidence for its rolein vivofor the clearance of triglyceride‐rich lipid particles. In this review, we bring the readers up‐to‐date on the evidence for the role of the lipolysis stimulated receptor in lipoprotein metabolism, as well as the recent developments in its molecular characterization. Curr Opin Lipidol 9:221–224. © 1998 Lippincott–Raven Publishers

ISSN:0957-9672    

出版商:OVID    

年代:1998

数据来源: OVID

摘要:

The enterohepatic circulation of bile acids is maintained by a series of membrane transport proteins. Recent studies of the cloned sodium bile acid cotransporters have provided new insights into their tissue expression, regulation, and their relationship to cholesterol homeostasis and human diseases such as primary bile acid malabsorption. Curr Opin Lipidol 9:225–229. © 1998 Lippincott–Raven Publishers

ISSN:0957-9672    

出版商:OVID    

年代:1998

数据来源: OVID

摘要:

It has long been recognized that skeletal muscle can contain modest stores of triglyceride and that this depot of fuel can make a major contribution to energy production during exercise. More recently, an adverse effect of muscle triglyceride has begun to be defined within the context of insulin resistance. Animal and clinical investigations have revealed a significant relation between increased muscle triglyceride and insulin resistance, at least among mostly sedentary individuals. These observations have stimulated the development, or at least the refinement, of new methodologies to assess this aspect of ‘regional’ fat deposition. In parallel, there has also been important new work designed to enable better understanding of the factors that regulate muscle triglyceride and to determine whether fatty acids taken up by skeletal muscle are oxidized or stored, and how these pathways might be either altered by the presence of insulin resistance or, in turn, contribute to the pathogenesis of insulin resistance. Curr Opin Lipidol 9:231–236. © 1998 Lippincott–Raven Publishers

ISSN:0957-9672    

出版商:OVID    

年代:1998

数据来源: OVID

摘要:

Hypercholesterolaemia is associated with endothelial dysfunction and increased risk of atheromatous disease. Although endothelial dysfunction has been demonstrated early in the course of the disease process, it remains difficult to establish a causal relationship. Despite this, endothelial function has been used as a surrogate marker in small trials to identify and assess the effectiveness of therapeutic interventions to reduce cardiovascular mortality, before large scale clinical trials are undertaken. Recently, arterial stiffness has emerged as an independent risk factor for cardiovascular disease and may provide a link between hypercholesterolaemia, endothelial dysfunction, hypertension and stroke. Curr Opin Lipidol 9:237–242. © 1998 Lippincott–Raven Publishers

ISSN:0957-9672    

出版商:OVID    

年代:1998

数据来源: OVID

ISSN:0957-9672    

出版商:OVID    

年代:1998

数据来源: OVID