ISSN:0957-9672    

出版商:OVID    

年代:1998

数据来源: OVID

摘要:

The hypothalamus contains a wealth of peptide and non‐peptide neurotransmitters, many of which have been shown experimentally to influence feeding behaviour and energy metabolism. Regulatory activities as complex as these are likely to be controlled by numerous neurotransmitters interacting at a variety of levels. The hierarchy of command of these neuronal circuits is not known, but it is possible that some converge on to a final common pathway, governed by the actions of a single neurotransmitter, through which all other influences ultimately operate. This review will discuss several of the more recently identified neurotransmitters and consider their validity as candidates in the regulation of energy homeostasis. Curr Opin Lipidol 9:295–299. © 1998 Lippincott–Raven Publishers

ISSN:0957-9672    

出版商:OVID    

年代:1998

数据来源: OVID

摘要:

Although it is well established that dietary saturated fatty acid intake is an important risk factor for coronary heart disease, there remains substantial controversy regarding whether these dietary fatty acids should be replaced with either carbohydrates, monounsaturated fatty acids, polyunsaturated fatty acids or a combination of these. This review highlights recent studies evaluating the role of dietary fatty acids in atherosclerosis, with a particular emphasis on their roles in lipoprotein oxidation and other potential proatherogenic processes. Curr Opin Lipidol 9:301–307. © 1998 Lippincott–Raven Publishers

ISSN:0957-9672    

出版商:OVID    

年代:1998

数据来源: OVID

摘要:

The Barker hypothesis proposes a link between low birth weight and adulthood cardiovascular disease. Recent studies have cast doubt on this hypothesis whilst others have proposed an effect of maternal birth weight that may extend to future generations. Thus, the debate on the effect of birth weight in cardiovascular disease continues. Curr Opin Lipidol 9:309–312. © 1998 Lippincott–Raven Publishers

ISSN:0957-9672    

出版商:OVID    

年代:1998

数据来源: OVID

摘要:

It is now possible to identify the specific gene defect in the majority of patients with familial hypercholesterolaemia. A potential benefit of this knowledge, in addition to helping with family screens, is to be able to predict the future clinical course. In order to do this, detailed genotype/phenotype correlation studies are required. Curr Opin Lipidol 9:313–317. © 1998 Lippincott–Raven Publishers

ISSN:0957-9672    

出版商:OVID    

年代:1998

数据来源: OVID

摘要:

Paraoxonase (PON1) hydrolyses organophosphate insecticides and nerve gases and is responsible for determining the selective toxicity of these compounds in mammals. Human PON1 has two genetic polymorphisms giving rise to amino‐acid substitutions at positions 55 and 192. The 192 polymorphism is the major determinant of the PON1 activity polymorphism towards organophosphates. However, the 55 polymorphism also modulates activity.Ex vivo, the PON1 polymorphisms are important in determining the capacity of HDL to protect LDL against oxidative modificationin vitroand this may explain the relationship between the PON1 alleles and coronary heart disease in case‐control studies. In recent case‐control studies serum PON1 concentration and activity were also found to be decreased in coronary heart disease (CHD) independent of the PON1 polymorphism, and in diabetes serum PON1 specific activity decrease is also independent of the PON1 genetic polymorphism. HDL from transgenic mice lacking PON1 fails to protect LDL against oxidative modification. Thus PON1 may be a determinant of resistance to the development of atherosclerosis by protecting lipoproteins against oxidative modification, perhaps by hydrolysing phospholipid and cholesteryl‐ester hydroperoxides. Curr Opin Lipidol 9:319–324. © 1998 Lippincott–Raven Publishers

ISSN:0957-9672    

出版商:OVID    

年代:1998

数据来源: OVID

摘要:

Many risk factors operate in both coronary heart disease and stroke, especially ischaemic stroke–age, sex, social class, blood pressure, pre‐existing vascular disease (angina, myocardial infarction, cardiac failure, diabetes and peripheral vascular disease, transient ischaemic attack and stroke), atrial fibrillation and fibrinogen, smoking, alcohol and height. Total cholesterol has also recently been recruited to this list. The various mechanisms involved in stroke and its subtypes and the epidemiological problems in evaluating aetiological factors in stroke make the comparison with coronary heart disease more difficult. The recent discrepancy between much of the epidemiology and the clinical trials evaluating the role of lipids in stroke has spurred the systematic review (meta‐analysis) of major prospective observational studies. These will provide a clearer assessment about the quantitative comparison of some of the more important risk factors for stroke and coronary heart disease in the near future. Curr Opin Lipidol 9:325–328. 1998 Lippincott–Raven Publishers

ISSN:0957-9672    

出版商:OVID    

年代:1998

数据来源: OVID

摘要:

Lowering LDL cholesterol (LDL‐C) levels to reduce or prevent coronary artery disease (CAD) progression and cardiac events in hypercholesterolemic subjects is now widely accepted. The clinical benefit of lowering LDL‐C has recently been extended to individuals with normal or mildly elevated LDL‐C. Recent analyses of large primary and secondary CAD prevention trials, however, clearly demonstrated that reducing LDL‐C levels does not entirely account for the coronary event reduction associated with lipid‐lowering therapy. Growing and compelling evidence is emerging on the role of triglyceride‐rich lipoproteins (VLDL and IDL), high density lipoproteins (HDL), and small, dense LDL, as well as non lipid risk factors, in the regression or stabilization of atherosclerotic plaques of mild/moderate severity, which are associated with clinical cardiac events. Enzymes involved in the tight metabolic interrelationship between triglyceride‐rich lipoproteins, small, dense LDL and HDL levels may represent potential therapeutic targets for CAD prevention by favourably altering lipoprotein composition and physical properties in addition to the current therapeutic focus on lipoprotein levels. Curr Opin Lipidol 9:329–336. © 1998 Lippincott–Raven Publishers

ISSN:0957-9672    

出版商:OVID    

年代:1998

数据来源: OVID

摘要:

Basic research has provided strong evidence that oxidation of LDL plays an important role in the pathogenesis of atherosclerosis. Several mechanisms have been identified which can lead to LDL oxidationin vivo. Clinical and epidemiological studies have provided circumstantial evidence that oxidized LDL, as measured by serum autoantibody levels, may be associated with the progression of atherosclerotic vascular disease. This review discusses recent findings regarding the presence of oxidized LDL (ox‐LDL)in vivoand the significance of ox‐LDL autoantibody measurements as a tool to predict cardiovascular diseases in various patient populations. Curr Opin Lipidol 9:337–344. © 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