The Impact of Niacin Administration on Plasma Lipids and Gene Expression in the Vervet Monkey Model (Chlorocebus aethiops)

Abstract

Investigations conducted in mice and humans have reported that the nature and the amount of lipids in plasma can predict the likelihood of cardiovascular disease (CVD) development. Although niacin has a history as treatment for dyslipidemia, only a handful of clinical trials have investigated its efficiency in the prevention of the morbidity and mortality associated with CVDs. Therefore, the purpose of this study was to assess the impact of a niacin formulation on gene expression and plasma lipids using 16 vervet monkeys (8 controls and 8 experimental). The control group was given a maintenance diet only, while the experimental group’s diet was supplemented with niacin (100 mg/kg) for a period of 3 months, followed by 4-week washout. The investigated plasma lipids were total cholesterol, low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), and triglycerides. Gene expression of proprotein convertase subtilisin/kexin type 9 (PCSK9), cholesterol ester transfer protein (CETP), low-density lipoprotein receptor (LDLR), apolipoprotein B-100 (APOB-100) and sterol regulatory element–binding protein-2 (SREBP-2), which are involved in the reverse cholesterol transport (RCT) pathway, was also determined. Niacin administration resulted in statistically significant changes for total cholesterol and HDL-C, with the changes also significantly higher in females compared to males in the niacin-treated group. Furthermore, gene expression analysis revealed significant decrease in CETP during niacin treatment. The downregulation suggested that the vervet monkey model supports the HDL-C hypothesis. Future studies aimed at supporting these findings are directed towards exploring the epigenetic biomarkers influencing the RCT pathway to combat CVDs.