New Perspectives on the Management of Low Levels of High-Density Lipoprotein Cholesterol

Harper, Charles R.; Jacobson, Terry A.

doi:10.1001/archinte.159.10.1049

Cited by 64 publications

(32 citation statements)

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“…Both ApoA-and HDL promote cellular cholesterol efflux via ATP-binding cassette transporters (ABCA1 and ABCG1); this is the early stage of RCT, when cholesterol is removed from extrahepatic tissues and transferred to the liver [8][9][10][11] . Scavenger receptor class B type 1 may also be involved in the cellular efflux of cholesterol and play a key role in RCT 12) .…”

Section: Discussionmentioning

confidence: 99%

HMG-CoA Reductase Inhibitor, Simvastatin Improves Reverse Cholesterol Transport in Type 2 Diabetic Patients with Hyperlipidemia

Guan

Tamasawa

Murakami

et al. 2008

JAT

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Aim: ApoA-and HDL promote cellular cholesterol efflux in the early stages of the reverse cholesterol transport (RCT) pathway. A low plasma HDL-C level is characteristic of atherogenic dyslipidemia in patients with type 2 diabetes. We evaluated plasma lipid levels and the expression of factors related to RCT in type 2 diabetic patients, and the effects of an HMG-CoA reductase inhibitor, simvastatin, were studied. Methods: Messenger RNA (mRNA) expression in circulating mononuclear cells was analyzed by reverse transcription-polymerase chain reaction (RT-PCR), focusing on the following factors: liver X receptor (LXR ), ATP-binding cassette A1 (ABCA1), scavenger receptor class B type 1 (SR-B1), apolipoprotein E (ApoE), apolipoprotein A-1 (ApoA-1), caveolin, and cholesterol ester transfer protein (CETP). Type 2 diabetic subjects (n 29) were divided into three subgroups: patients with normolipidemia (DM group, n 11), patients with untreated hyperlipidemia (DMHL group, n 10), and those with hyperlipidemia treated with simvastatin 5-10 mg/day (DMST group, n 8). The control group (CNT group) included seven healthy volunteers. Results: Simvastatin treatment significantly increased plasma levels of ApoA-compared to the other three groups. Simvastatin treatment improved the expression of mRNA for LXR , ABCA1, and ApoA-compared with DMHL or control groups. Conclusion: Our data suggest that RCT may be reduced in type 2 diabetic patients with hyperlipidemia, and simvastatin may be able to improve reverse cholesterol transport for this population of diabetic patients. J Atheroscler

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Section: Discussionmentioning

confidence: 99%

HMG-CoA Reductase Inhibitor, Simvastatin Improves Reverse Cholesterol Transport in Type 2 Diabetic Patients with Hyperlipidemia

Guan

Tamasawa

Murakami

et al. 2008

JAT

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“…This is in contrast to individuals who have low HDL-C as an isolated risk factor. 4,11 Fourth, as a negative acute-phase reactant, low HDL-C can serve as a surrogate marker for a systemic inflammation, which causes or aggravates atherosclerosis (eg, smoking or chronic infections), or as a disease marker for local inflammation, especially in unstable plaques. 19 In support of the importance of this association, low HDL-C is a more powerful risk factor in short-term follow-ups than in long-term follow-ups of prospective epidemiological studies.…”

Section: Epidemiological Backgroundmentioning

confidence: 99%

High Density Lipoproteins and Arteriosclerosis

Eckardstein

Nofer

Assmann

2001

ATVB

604

128

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Abstract-High density lipoprotein (HDL) cholesterol is an important risk factor for coronary heart disease, and HDL exerts various potentially antiatherogenic properties, including the mediation of reverse transport of cholesterol from cells of the arterial wall to the liver and steroidogenic organs. Enhancement of cholesterol efflux and of reverse cholesterol transport (RCT) is considered an important target for antiatherosclerotic drug therapy. Levels and composition of HDL subclasses in plasma are regulated by many factors, including apolipoproteins, lipolytic enzymes, lipid transfer proteins, receptors, and cellular transporters. In vitro experiments as well as genetic family and population studies and investigation of transgenic animal models have revealed that HDL cholesterol plasma levels do not necessarily reflect the efficacy and antiatherogenicity of RCT. Instead, the concentration of HDL subclasses, the mobilization of cellular lipids for efflux, and the kinetics of HDL metabolism are important determinants of RCT and the risk of atherosclerosis. (Arterioscler Thromb Vasc Biol. 2001;21:13-27.)

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“…The negative relationship between low HDL cholesterol and the risk of heart disease is well stablished in the general population (Abbott et al, 1988;Abbott et al, 1998;Castelli, 1983;Gordon et al, 1989;Harper & Jacobson, 1999;Rosenson, 2005) (figure-2). In the Framingham Heart study, the protective role of HDL has been well described (Kannel et al, 1971).…”

Section: Hdl Cholesterolmentioning

confidence: 99%