Niacin's therapeutic effect is thought to be related to inhibition of lipolysis in adipose tissue. This limits free fatty acids available for the liver to produce triglycerides and VLDL, and consequently LDL.
Niacin therapy leads to a reduction in hepatic VLDL secretion via decreased free fatty acid availability for the liver to produce TG and VLDL. Decrease in free fatty acids also suppresses hepatic expression of apolipoprotein C3 and leads to reduced VLDL production.
Triglycerides are esters derived from glycerol and three fatty acids. High levels of triglycerides in the bloodstream have been linked to atherosclerosis, and niacin therapy can decrease triglyceride levels in the body.
Low-density lipoprotein (LDL) is associated with health problems, including heart disease, which is why it is commonly called the "bad" cholesterol. Niacin decreases blood LDL levels.
High density lipoprotein particles remove fats like cholesterol from cells and transport it back to the liver for excretion or re-utilization. Therefore, HDL is often referred to as "good" cholesterol. Niacin is associated with increased HDL levels in users.
Flushing is a well known side effect of niacin use. Flushing usually lasts for about 15-30 minutes and is mediated by prostaglandin activation.
Because the flushing related with niacin use is mediated by prostaglandin activation, aspirin can reduce flushing by altering or blocking the prostaglandin mediated pathway.
High doses of niacin have been associated with elevations in blood sugar, thereby worsening diabetes mellitus.
Hyperuricemia is another side effect of taking high doses of niacin and may exacerbate gout in certain patients.
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