Niacin and Cholesterol
|Niacin and Cholesterol -- abstracts states blocks cholesterol absorption ...||Darrell Miller||05/21/05|
May 21, 2005 11:20 AM
Author: Darrell Miller (email@example.com)
Subject: Niacin and Cholesterol -- abstracts states blocks cholesterol absorption ...
The Era of Statins - Is There Still a Place for Other Classes of Lipid-Lowering Drugs? Wascher, Thomas C. Department of Internal Medicine, Diabetes and Metabolism Unit, and Diabetic Angiopathy Research Group, Medical University of Graz, Graz, Austria. HeartDrug (2005), 5(1), 34-38. CODEN: HEARCO ISSN: 1422-9528. Journal; General Review written in English. CAN 142:384798 AN 2005:64730 CAPLUS
A review. Plenty of evidence suggests statins as the first-line therapy for the treatment of lipid disorders. However, further therapeutic options available in the treatment of lipid disorders are fibrates, niacin and cholesterol absorption inhibitors. In the present study, current treatment modalities of lipid disorders are reviewed, and their use was scrutinized based on the available evidence.
Niacin and cholesterol: role in cardiovascular disease (review). Ganji, Shobha H.; Kamanna, Vaijinath S.; Kashyap, Moti L. Atherosclerosis Research Center, Department of Veterans Affairs Healthcare System, Long Beach, CA, USA. Journal of Nutritional Biochemistry (2003), 14(6), 298-305. CODEN: JNBIEL ISSN: 0955-2863. Journal; General Review written in English. CAN 139:291534 AN 2003:542279 CAPLUS
A review. Niacin has been widely used as a pharmacol. agent to regulate abnormalities in blood plasma lipid and lipoprotein metab. and in the treatment of atherosclerotic cardiovascular disease. Although the use of niacin in the treatment of dyslipidemia has been reported as early as 1955, only recent studies have examd. the cellular and mol. mechanism of action of niacin on lipid and lipoprotein metab. The beneficial effects of niacin in decreasing triglyceride and apolipoprotein-B contg. lipoprotein (VLDL and LDL) levels are mainly due to decreased fatty acid mobilization from adipose tissue triglyceride stores and inhibition of hepatocyte diacylglycerol acyltransferase and triglyceride synthesis, leading to increased intracellular apolipoprotein-B degrdn. and subsequent decreased secretion of VLDL and LDL particles. The mechanism of action of niacin to raise HDL levels involves decreasing the fractional catabolic rate of HDL-apolipoprotein A-I without affecting its biosynthetic rates. Niacin selectively increases blood plasma levels of Lp-AI (HDL subfraction without apolipoprotein A-II), a cardioprotective subfraction of HDL in patients with low HDL levels. Using human hepatocytes (Hep G2 cells) as an in vitro model, recent studies indicate that niacin selectively inhibits the uptake/removal of HDL-apolipoprotein A-I (but not HDL-cholesterol ester) by hepatocytes, thereby increasing the capacity of retained HDL-apolipoprotein A-I to augment cholesterol efflux through reverse cholesterol transport pathway. The data provide evidence extending the role of niacin as a lipid-lowering drug beyond its dietary role as a vitamin.
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