Nicotinamide Riboside Ameliorates Fructose-Induced Lipid Metabolism Disorders in Mice by Activating Browning of WAT, and May Be Also Related to the Regulation of Gut Microbiota

• Published in: Nutrients 2024-11, Vol.16 (22), p.3920
• Main Authors: Zhang, Huaqi, Zhao, Xuenuo, Zhang, Li, Sun, Dan, Ma, Yanzhen, Bai, Yixian, Bai, Xue, Liang, Xi, Liang, Hui
• Format: Article
• Language: English
• Subjects: Adipocytes; Adipose Tissue, Brown - drug effects; Adipose Tissue, Brown - metabolism; Adipose Tissue, White - drug effects; Adipose Tissue, White - metabolism; Adipose tissues; Analysis; Animals; Body fat; Body weight; Cholesterol; Fructose; Fructose - adverse effects; Gastrointestinal Microbiome - drug effects; Genes; Genetic transcription; High density lipoprotein; Kinases; Lipid Metabolism - drug effects; Lipid Metabolism Disorders - chemically induced; Lipid Metabolism Disorders - drug therapy; Lipid Metabolism Disorders - metabolism; Lipids; Liver; Liver - drug effects; Liver - metabolism; Male; Metabolic disorders; Mice; Mice, Inbred C57BL; Microbiota; Microbiota (Symbiotic organisms); Microscopy; Niacinamide; Niacinamide - analogs & derivatives; Niacinamide - pharmacology; Protein kinases; Proteins; Pyridinium Compounds - pharmacology; Variance analysis
• ISSN: 2072-6643; 2072-6643
• DOI: 10.3390/nu16223920

This study aims to observe the preventive effect of nicotinamide riboside (NR) on fructose-induced lipid metabolism disorders and explore its mechanism. Male C57BL/6J mice were fed a 20% fructose solution and given 400 mg/kg NR daily by gavage for 10 weeks. The results indicated that NR supplementation significantly reduced the body weight, liver weight, white adipose tissue (WAT) weight, serum, and hepatic lipid levels. NR upregulated the protein expression levels of sirtuin-1 (SIRT1), AMP-activated protein kinase (AMPK), PR domain containing 16 (PRDM16), uncoupling protein 1 (UCP1), peroxisome proliferator-activated receptor-gamma coactiva-tor-1-alpha (PGC-1α), nuclear respiratory factor 1-encoding gene (NRF1), mitochondrial transcription factor A (TFAM), cluster of differentiation 137 (CD137), transmembrane protein 26 (TMEM26), and T-box 1 (TBX1). Moreover, NR enhanced the and abundance. Spearman's correlation analysis revealed that significant correlations exist between and with browning-related indicators. In conclusion, NR could alleviate lipid metabolic abnormalities induced by fructose through activating SIRT1/AMPK-mediated browning of WAT. The mechanism by which NR improves fructose-induced lipid metabolism disorders may also be associated with the modulation of intestinal flora.