Niacin reduced

In general, niacin reduces LDL cholesterol from 5% to 25%, reduces triglycerides by 20% to 50%, and increases HDL cholesterol by 15% to 35% (Table 9-8). Niacin has been shown to reduce CHD events and total mortality31 as well as the progression of atherosclerosis when combined with a statin.31... 

Niacin reduces plasma LDL cholesterol, lipoprotein (a), triglycerides and raises HDL cholesterol in all types of hyperlipoproteinemia [26]. Although available on the market for more than 40 years, the mechanisms of action of niacin are poorly understood. Putative mechanisms are the activation of adipose tissue LPL, diminished HTGL activity, a reduced hepatic production and release of VLDL, and composi-... 

This familial disorder, which is associated with increased atherogenesis, is determined chiefly by alleles that dictate increased production of the (a) protein moiety. Niacin reduces levels of Lp(a) in many patients. 

Neomycin is indicated for the suppression of intestinal bacteria of the bowel as a preoperative prophylaxis for elective colorectal surgery. The treatment begins 3 days prior to surgery with liquid diets with minimum residue, oral capsule of bisacodyl, magnesium sulfate, enema, and repeated oral administration of neomycin and erythromycin (1 gram of each). Neomycin has been used as an adjunctive therapy in hepatic coma by reduction in the ammonia-forming bacteria in the intestinal tract. The subsequent reduction in blood ammonia has resulted in neurologic improvement. Neomycin combined with niacin reduces the cholesterol level. 

The cholesterol reducing effect of megadoses of niacin has been known for more than 50 years (Altschul et al. 1955). While the daily allowance for niacin is in the order of 15 mg per day, the cholesterol reducing effect requires doses of about 1.5-3 g of nicotinic acid per day (Knopp 1999). In these doses, niacin reduces the atherogenic very low-density lipoprotein (VLDL) and low-density lipoprotein (LDL) cholesterol, but raises the level of high-density lipoprotein... 

These dehydrogenases use nicotinamide adenine dinucleotide (NAD ) or nicotinamide adenine dinucleotide phosphate (NADP )—or both—and are formed in the body from the vitamin niacin (Chapter 45). The coenzymes are reduced by the specific substrate of the dehydrogenase and reoxidized by a suitable electron acceptor (Figure 11-4). They may freely and reversibly dissociate from their respective apoenzymes. 

Reducing LDL cholesterol while substantially raising HDL cholesterol (statin + niacin) appears to reduce the risk of atherosclerotic disease progression to a greater degree than statin monotherapy. 

Niacin (vitamin B3) has broad applications in the treatment of lipid disorders when used at higher doses than those used as a nutritional supplement. Niacin inhibits fatty acid release from adipose tissue and inhibits fatty acid and triglyceride production in liver cells. This results in an increased intracellular degradation of apolipoprotein B, and in turn, a reduction in the number of VLDL particles secreted (Fig. 9-4). The lower VLDL levels and the lower triglyceride content in these particles leads to an overall reduction in LDL cholesterol as well as a decrease in the number of small, dense LDL particles. Niacin also reduces the uptake of HDL-apolipoprotein A1 particles and increases uptake of cholesterol esters by the liver, thus improving the efficiency of reverse cholesterol transport between HDL particles and vascular tissue (Fig. 9-4). Niacin is indicated for patients with elevated triglycerides, low HDL cholesterol, and elevated LDL cholesterol.3... 

The predominant effects of fibrates are a decrease in triglyceride levels by 20% to 50% and an increase in HDL cholesterol levels by 9% to 30% (Table 9-8). The effect on LDL cholesterol is less predictable. In patients with high triglycerides, however, LDL cholesterol may increase. Fibrates increase the size and reduce the density of LDL particles much like niacin. 

Some patients, in particular those with genetic forms of hypercholesterolemia (Table 9-2), will require three or more drugs to manage their disorder. Regimens using a statin, resin, and niacin were found to reduce LDL cholesterol up to 75%.42 These early studies were conducted with lovastatin, so larger reductions would be expected with the more potent statins available today. 

Prior to the discovery of niacin receptors, medicinal chemistry efforts were mainly directed toward small heterocyclic carboxylic acids that are structurally similar to niacin. Systematic study of nitrogen-containing five- and six-membered heterocyclic carboxylic acids revealed that activity at GPR109A was significantly reduced for any of the variants of niacin shown in general structures (A and B) [45,46]. These heterocycles include pyrazole, isoxazole, thiazole, pyrazine, and pyrimidine. 

Niacin (nicotinic acid) reduces the hepatic synthesis of VLDL, which in turn leads to a reduction in the synthesis of LDL. Niacin also increases HDL by reducing its catabolism. 

Gemfibrozil reduces the synthesis of VLDL and, to a lesser extent, apolipoprotein B with a concurrent increase in the rate of removal of triglyceride-rich lipoproteins from plasma. Clofibrate is less effective than gemfibrozil or niacin in reducing VLDL production. 

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