Emerging Concepts on the Pathogenesis of Non‐Alcoholic Steatohepatitis (NASH)

Yin Yang 1 and farnesoid X receptor: a balancing act in non-alcoholic fatty liver disease?

“…This preliminary evidence, added to other emerging data,3 supports the possibility that the first cause of NAFLD, and possibly other consequences of obesity, might be the triggering of innate/inflammatory effectors, secondarily affecting lipid and glucose homeostasis. Indeed the route to NAFLD/NASH might not be the highroad of liver fat accumulation increasing the susceptibility to a second injurious hit as first proposed, but rather a labyrinth of diverse reciprocally amplifying signals (inflammatory, metabolic, oxidative, etc) and tissue origin (liver, adipose tissue, gut, brain, etc) 9 19. Up to now, efforts to improve treatment of NASH have focused on improving insulin sensitivity (metformin, PPARγ agonists, etc), on interfering with lipid metabolism to decrease lipid storage (PPARα agonist, olistat, etc) or on protecting against lipotoxicity and oxidative stress (vitamin E, ursodeoxycholic acid, etc) 20.…”

Exploiting the biological effect exerted by lipid nanocapsules in non-alcoholic fatty liver disease

“…In this model, there were no significant improvements in the liver when compared to the untreated mice fed a WDF, which could be due in part to the presence of fructose in the drinking water. Fructose can lead to an increase in fat storage in the liver via the stimulation of the de novo lipogenesis pathway [ 21 , 22 ]. It has been shown that the use of fructose in combination with a western diet leads to increased lipid deposition in the liver and to loss of insulin sensitivity while maintaining caloric intake [ 23 ].…”