Guarding Your Liver Against Nicotine and Coca-Cola™-Induced Steatosis with NR
Introduction
Cigarettes containing nicotine (Nic) and sugar-sweetened beverages (SSBs) with high fructose corn syrup (HFCS) have been uncovered to induce hepatic steatosis, which are the risk factors for the development of metabolic diseases including non-alcoholic fatty liver disease (NAFLD). Noteworthily, nicotinamide riboside (NR) can elevate mitochondrial nicotinamide adenine dinucleotide (NAD+) to exert a protect role against hepatic steatosis in NAFLD.About NAFLD
NAFLD, which is marked by excessive neutral fat accumulation in the liver, is a frequent chronic liver disease unrelated to alcohol and other well-defined liver-damaging factors, with a global prevalence of 25%. With the epidemic trend of obesity and metabolism-associated syndromes worldwide, NAFLD has been regarded as a type of metabolic stress liver injury with tight association with insulin resistance and genetic predisposition.The association between Nic/Coke and hepatic steatosis in NAFLD
Nic plus Coke administration causes hepatic steatosis. In addition, Nic plus Coke also leads to a striking increase in lipid accumulation and mitochondrial swelling as well as loss of the mitochondrial cristae (arrowhead), with a decrease in the amount of endoplasmic reticulum (arrow) and glycogen deposition (asterisk).
The preventive role of NR against hepatic steatosis in NAFLD
NR leads to a decrease in the calorie intake to reduce hepatic steatosis through the increased of the NAD+ concentration, and triggers the downstream signaling of NAD+, with a reduction in oxidative stress markers and mitochondrial damage.
Underpinned mechanism of NR in ameliorating Nic plus Coke-induced hepatic steatosis
Nic plus Coke consumption reduces the protein levels of the NAMPT, diminishing NAD+-dependent enzyme Sirt1 and downstream PGC1α. This combined treatment also enhances SREBP1c and ACC activity, increasing intracellular triglyceride deposits and reducing AMPK phosphorylation. The decline in PGC1α can result in the retention of damaged mitochondria with increased oxidative stress, indicated by higher MDA and HO1 levels as well as lower SOD2 level.
Importantly, the reduced hepatic NAD+ level is a risk factor to develop NAFLD. NR is a precursor of NAD+ that reduces plasma triglycerides and total cholesterol levels, in turn preventing hepatic lipid accumulation in mice and humans. Sirt1, an NAD+-dependent enzyme, has a protective effect in NAFLD. Sirt1 promotes mitochondrial biogenesis through PGC1α. NR supplementation activates Sirt1 signaling to repress the progression of NAFLD.
Conclusion
NR supplement has the potential to mitigate oxidative stress and mitochondrial abnormalities, and prevent hepatic steatosis induced by Nic plus Coke, which may be promissory candidates for the management of NAFLD.Reference
Rivera JC, Espinoza-Derout J, Hasan KM, et al. Hepatic steatosis induced by nicotine plus Coca-Cola™ is prevented by nicotinamide riboside (NR). Front Endocrinol (Lausanne). 2024;15:1282231. Published 2024 May 2. doi:10.3389/fendo.2024.1282231BONTAC NR
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