This highlights a critical gap in clinical practice, emphasizing the need for hepatologists and gastroenterologists to be more proactive in identifying smoking as a risk factor for liver disease progression and in implementing strategies to promote smoking cessation among their patients
Volume 100E: A Review of Human Carcinogens
JNK is activated in various animal models of obesity and also in patients with NASH and its deletion results in attenuation of fatty liver (60) or nicotine plus HFD-induced hepatic steatosis in obese mice (42)
Simultaneously, it may impair the liver's ability to export fat as very-low-density lipoproteins (VLDL), creating a situation where fat accumulates faster than it can be removed
The additive effects of nicotine on the severity of HFD-induced hepatic steatosis was associated with significantly greater oxidative stress, increased hepatic TG levels, higher incidence of hepatocellular apoptosis, inactivation (dephosphorylation) of AMPK, and activation of its downstream target ACC (42)
Research indicates that smokers with NAFLD are more likely to develop advanced fibrosis (scarring) compared to non-smokers
