Levels of the proinflammatory adipokine leptin are increased in obesity, and this hormone has been called “an active player in the development of NAFLD”.1
The potential for hepatic leptin resistance in NAFLD & NASH, along with leptin’s complex role in energy balance, insulin resistance, hepatic steatosis and fibrosis, has resultin in leptin being considered ”a convincing target for development of novel therapies in liver diseases”.2
High consumption of fructose has been implicated in the development of NAFLD and NASH, and particularly the increased risk of CVD in patients with fatty liver.
Fructose is thought to play a direct role because it is “both a substrate and an inducer of hepatic de novo lipogenesis”3. In addition, fructose may play an indirect role through its link to weight gain, changes in gut permeability & function, insulin resistance, hepatic inflammation, hyperleptinemia and hepatic leptin resistance.