Potential Effects of Nicotinamide on Serum HDL-Cholesterol Levels and Hepatic Oxidative Stress, ABCA1 Gene and Protein Expression in Rats Fed a High-Fat/Fructose Diet

TL;DR

This study shows that nicotinamide may help improve cholesterol levels and reduce liver stress in rats on a high-fat diet.

Contribution

The study reveals nicotinamide's potential to modulate HDL-cholesterol and ABCA1 expression in hypercaloric diet-induced metabolic stress.

Findings

Nicotinamide improved HDL-cholesterol levels in rats fed a high-fat/fructose diet.

Nicotinamide reduced systemic lipid peroxidation and enhanced hepatic antioxidant response.

Nicotinamide modulated hepatic ABCA1 gene and protein levels affected by the diet.

Abstract

A hypercaloric diet is associated with oxidative stress and the dysfunction of ATP-Binding Cassette transporter A1 (ABCA1), a key element in high-density lipoprotein (HDL) biogenesis and reverse cholesterol transport. Nicotinamide (NAM) presents antioxidant properties, which may contribute to maintaining lipid metabolism. Therefore, we aimed to evaluate the effect of NAM on HDL-cholesterol (HDL-C) level, oxidative stress markers, and the gene expression and protein levels of ABCA1 in Sprague-Dawley rats fed a hypercaloric diet. Forty male rats were divided into five groups: one group received a standard diet, and the remaining groups received a single high-fat, high-fructose diet (HFDF). Three of the HFDF groups received NAM treatment (5, 10, and 15 mM) in drinking water for 16 weeks (5 h/day). While HDL-C and oxidative stress were measured in serum samples, oxidative stress markers, and the gene expression and protein levels of ABCA1 were quantified in liver samples. The HDL-C level altered by the HFDF was improved by treatment with NAM. Furthermore, NAM reduces systemic lipid peroxidation levels and enhances the hepatic antioxidant response affected by the HFDF. In addition, NAM modulates the hepatic ABCA1 gene expression and protein level, altered by the HFDF. Our results suggest that NAM may modify the serum HDL-C level by an improvement of antioxidant response, and a possible modulation of the hepatic ABCA1 gene and protein expression. Further metabolic and molecular studies are needed to support the potential therapeutic role of NAM to prevent or treat lipid alterations promoted by a hypercaloric diet.

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