High density lipoprotein and coronary heart disease.

Betteridge, D. J.

doi:10.1136/bmj.298.6679.974

Cited by 23 publications

(6 citation statements)

References 21 publications

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“…It is the number one cause of death of women. Part of the body's cholesterol is derived from dietary intake, but majority is synthesized by the liver and other tissues [2]. Lipids have important roles in virtually all aspects of biological life -serving as hormone precursors, aiding digestion, providing energy storage and metabolic fuels, acting as functional and structural components in bio-membranes and forming insulation to allow nerve conduction or to prevent heat loss [3].…”

Section: Introductionmentioning

confidence: 99%

Menopausal syndrome: Effect on serum lipid and lipoprotein profiles

Ikekpeazu¹,

Neboh²,

Maduka³

et al. 2009

Biomed Res

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Plasma lipids have been known to be altered by the within-month variations in the female hormonal system. The female hormonal system also controls the menstrual cycle in the pre-menopausal women. This study is, therefore, aimed at finding the possible effects of menopause on plasma lipids and lipoprote ins, as shown by the lipid profile. The lipid profiles of 200 post-menopausal women and 100 pre-meno pausal control women were estimated. The results obtained show a statistically significant increase (P less than 0.05) in the total cholesterol level of early menopausal subjects (6.05 plus/minus 1.03mmol/L) and slightly higher values in late menopausal subjects (6.80 plus/minus 0.81mmol/L), when compared with the control subjects (4.6 plus/minus 0.62mmol/L). Triglycerides (TG) showed slight but significant increase (P less than 0.05) in the early menopausal subjects (1.40 plus/minus 0.80 mmol/L) and higher levels in late menopausal subjects(1.96 plus/minus 0.45 mmol/L) in comparison with the control subjects (1.02 plus/minus 0.44 mmol/L). High density lipoprotein (HDL) levels were however reduced significantly (P less than 0.05) in early menopausal subjects (1.20 plus/minus 0.27 mmol/L) and even lower in late menopausal subjects (1.17 plus/minus 0.28 mmol/L) when compared to the controls; while Low density lipoprotein (LDL) and very low density lipoprotein (VLDL) levels were significantly increased (P less than 0.05) in early menopausal subjects (4.21 plus/minus 0.81 and 0.63 plus/minus 0.37 mmol/L), and higher in late menopausal subjects (4.70 plus/minus 0.55 and 0.81 plus/minus 0.41 mmol/L) when compared with the control subjects. The findings suggest the probability that menopausal syndrome can lead to hyperlipidaemia, dyslipidaemia and possibly predispose women to coronary artery disease.

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Section: Introductionmentioning

confidence: 99%

Menopausal syndrome: Effect on serum lipid and lipoprotein profiles

Ikekpeazu¹,

Neboh²,

Maduka³

et al. 2009

Biomed Res

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“…Intoxication with alcohol, chloroform, ether causes the increase in lipoids in the blood (cholesterol and phosphatides). At the base of the lipemia pathogenesis, there is often a disorder of the transport of fat from the fat deposits in the organs and vice versa (transport lipemia), as well as the delayed passage of blood lipids into the organs or the retention of lipids in the blood (retentive lipemia) (in anemia) [1][2][3][4].…”

Section: Resorption and Fat Depositing Disordersmentioning

confidence: 99%

Biological Chemistry in Intermediate Lipid Metabolism Disorder

Condratovici¹,

Elisei²,

Vasincu³

et al. 2019

Rev. Chim.

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Any pathological process is accompanied by quantitative and qualitative changes in metabolism, which is the main form of life manifestation. Metabolism disorders (it is the permanent exchange of substances between the body and the environment) arise if the activity of the central nervous system is affected; the trophic function of the nervous system directs nutrition and metabolism. In this function, the coordinating role belongs to the central nervous system and is made by means of the endocrine glands. Lipids introduced into the body are digested mainly with the help of the pancreatic and intestinal juice and are resorbed through the walls of the small intestine. Even in the intestinal wall, the re-synthesis of fatty acids and glycerine fat occurs. A certain amount of neutral fat is probably resorbed without being split into fatty acids and glycerine. Fats are mainly resorbed through the lymphatic system, in part (about 30%) by means of the portal vein system; the entire fat emulsion penetrates into the blood and its main mass is deposited in certain fat deposits: the adipose subcutaneous cell tissue, the epiploon and the mesenterium of the abdominal cavity, as well as in the fatty layers of the various organs. In fat deposits, processes of lipid formation from carbohydrates and of transformation of higher fatty acids can occur. Lipids from fat deposits are subject to oxidation, especially at the liver level.

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“…These lipoproteins exert their protective role through several mechanisms, including the facilitation of reverse cholesterol transport (Pieters et al 1994), the stimulation of prostacyclin production and stability (Betteridge 1989, Yoi etal. 1988, the prevention of LDL aggregation (Khoo et al 1990), the inhibition of platelet activation (Knorr et al 1988), and the reducion of oxidized-LDLinduced cellular toxicity (Hessler et al 1979).…”

Section: Introductionmentioning

confidence: 99%

High-density lipoproteins protect endothelial cells from apoptosis induced by oxidized low-density lipoproteins

et al. 2000

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Summary. Endotheliai lesion by oxidized low-density liproproteins(LDL) is one of the first stages in the development of atherosclerosis. The effect of these lipoproteins can range from a functional lesion of the endothelium to death of the endothelial cells by apoptosis. High-density lipoproteins (HDL) are one of the factors which can have a protective effect against the development of atheromatous plaques. The aim of this study is to establish whether the death of endothelial cells by apoptosis induced by oxidized LDLs is prevented by HDLs. ECV304 endothelial cells and bovine aorta endothelial cells were incubated with native LDLs, oxidized LDLs, and a combination of both oxidized LDLs and HDLs. Oxidized LDLs caused a significant increase of mortality mainly by apoptosis. However, when HDLs were added together with oxidized LDLs the percentage of total mortality, the degree of lipoprotein oxidation in the medium, and the percentage of cells in apoptosis were all significantly decreased. HDLs protect against the cytotoxicity of oxidized LDLs possibly by preventing the propagation of the oxidative chain in these lipoproteins.

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High density lipoprotein and coronary heart disease.

Abstract: of rear seat occupants in frontal impacts than prevent whiplash in front seat occupants struck from behind.'2 The compulsory wearing of rear seat belts with rear seat head restraints would lessen the incidence of this and other injuries.

Cited by 23 publications

References 21 publications

Menopausal syndrome: Effect on serum lipid and lipoprotein profiles

Menopausal syndrome: Effect on serum lipid and lipoprotein profiles

Biological Chemistry in Intermediate Lipid Metabolism Disorder

High-density lipoproteins protect endothelial cells from apoptosis induced by oxidized low-density lipoproteins

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