This lecture discussed recent works pertaining to diet-induced weight loss in patients with NAFLD, which is already the number one chronic liver disease in the US. By imaging, 11-30% of the population has it; by liver enzymes this figure is only 2-9%. Progression to NASH occurs more frequently in the morbidly obese.
Many treatment options have been studied, including: weight loss, exercise, insulin sensitizers, fibrates, statins, urso, and antioxidants like vitamin E. Very few studies include solely a dietary intervention (most have pharmacologic, some have exercise). Therefore, the impact of diet alone is not fully understood.
In studies that look at exercise, or exercise + drug, decreased steatosis has been observed, ranging from 28 to 46% (Chan et al. 2010) and 40-60% (Samson et al. 2011). Of course, degrees of steatosis may be helpful as a biomarker for severity of disease, since steatosis is part of the NAS scoring system for NASH.
Fibroblast growth factor 21 (FGF21) is a key mediator of lipid metabolism and fatty acid oxidation in white adipose tissue and the liver in mice. Levels of this protein correlate with BMI in humans (Zhang et al. 2008). Research is ongoing to determine whether dieting may decrease levels of FGF21 and can be used as a marker of hepatic steatosis. Early results are promising.