Data from: Hepatic steatosis induced by nicotine plus Coca-Cola™ is prevented by nicotinamide riboside (NR)

Introduction. Cigarettes containing nicotine (Nic) are a risk factor for
the development of cardiovascular and metabolic diseases. We reported that
Nic delivered via injections or e-cigarette vapor led to hepatic steatosis
in mice fed with a high-fat diet. High-fructose corn syrup (HFCS) is the
main sweetener in sugar-sweetened beverages (SSBs) in the US. Increased
consumption of SSBs with HFCS is associated with increased risks of
non-alcoholic fatty liver disease (NAFLD). Nicotinamide riboside (NR)
increases mitochondrial nicotinamide adenine dinucleotide (NAD+) and
protects mice against hepatic steatosis. This study evaluated if Nic plus
Coca-Cola™ (Coke) with HFCS can cause hepatic steatosis and that can be
protected by NR. Methods. C57BL6 mice received twice daily intraperitoneal
(IP) injections of Nic or saline and were given Coke (HFCS), or Coke with
sugar, and NR supplementation for 10 weeks. Results. Our results show that
Nic+Coke caused increased caloric intake and induced hepatic steatosis,
and the addition of NR prevented these changes. Western blot analysis
showed lipogenesis markers were activated (increased cleavage of the
sterol regulatory element-binding protein 1 [SREBP1c] and reduction of
phospho-Acetyl-CoA Carboxylase [p-ACC]) in the Nic+Coke compared to the
Sal+Water group. The hepatic detrimental effects of Nic+Coke were mediated
by decreased NAD+ signaling, increased oxidative stress, and mitochondrial
damage. NR reduced oxidative stress and prevented mitochondrial damage by
restoring protein levels of Sirtuin1 (Sirt1) and peroxisome
proliferator-activated receptor coactivator 1-alpha (PGC1a) signaling.
Discussion. We conclude that Nic+Coke has an additive effect on producing
hepatic steatosis, and NR is protective. This study suggests concern for
the development of NAFLD in subjects who consume nicotine and drink SSBs
with HFCS.