Niacin (vitamin B3, nicotinic acid) Decreases VLDLA‐polipoprotein B Secretion and Reduces Hepatic and Blood Lipid Concentrations: Roles of Niacin Metabolism and Autophagy Degradation

Niacin therapy, used either alone or in combination with another agent to reduced the risk of coronary heart disease, is effective in raising and lowering, respectively, HDL‐c and apoB/VLDL triglyceride (TG) levels in dyslipidemia. To further understand if part of the mechanism is by reducing the secretion of apoB‐containing lipoproteins through autophagy, we did a series of niacin studies in isolated primary hepatocytes or in intact mice. Metabolic labeling and pulse‐chase results showed niacin increased intracellular apoB degradation by 30%, and decreased apoB/VLDL TG secretions by 40%. These effects were lost in autophagy‐deficient cells. Mice fed with diet containing 3% niacin had 40% increases in plasma HDL‐c. Feeding high fat diet (HFD) with niacin lowered LDL‐c by 50%. Niacin was able to suppress postprandial plasma triglyceride by 30%. Niacin reduced hepatic triglyceride and cholesterol concentrations by 40% and 50%, respectively, in mice fed with HFD. These data suggest niacin decreases hepatic lipid concentrations, apoB/VLDL secretion, and modifies plasma cholesterol levels. Some of the effects required niacin metabolism and autophagy degradation. Supported by grants from the NIH (HL58541) and Merck & Co., Inc. Grant Funding Source : NIH (HL58541) and Merck & Co., Inc.