Nonalcoholic fatty liver disease (NAFLD) is a recently identified phenomenon, whereby the liver becomes diseased through a mechanisms that is independent of alcohol consumption. Nonalcoholic fatty liver disease is almost identical pathologically to alcoholic fatty liver disease, but while the latter is associated with excess alcohol ingestion, the former is associated with obesity, the metabolic syndrome and insulin resistance. Pathologically, both forms of liver disease involve the accumulation of fatty acids in the liver, and this causes a raft of metabolic dysfunctions and aberrations that impairs liver function. Certain liver enzymes become elevated and nonalcoholic fatty liver is now through to account for around 80 % of cases of such elevated liver enzymes. Clinical tests for these enzymes can be used as a diagnostic tool for the presence of nonalcoholic fatty liver disease. As the liver damage progresses, fibrosis and inflammation occur which can lead to nonalcoholic steatohepatitis (NASH) and cirrhosis of the liver.
It is estimated that 25 % of adults in the United States population now has nonalcoholic fatty liver disease, but in most cases the disease does not progress to severe liver disease. Nonalcoholic fatty liver disease is associated with obesity and shares many of the clinical changes with the metabolic syndrome, because they likely both originate from the same insulin resistant state. The similarity between the conditions also extends to the prevalence in the general adult population which is also around 25 % for the metabolic syndrome. Metabolic syndrome increases in prevalence with body weight such that at normal weight only 18 % have the condition, but this rises to 67 % in the obese. Analysis has shown that obese individuals with nonalcoholic fatty liver disease have shown that the risk of developing nonalcoholic steatohepatitis increases if metabolic syndrome is also present1. Severe liver disease therefore seems to develop from disorders that centre on the development of insulin resistance.
The cause of nonalcoholic fatty liver disease is an insulin resistant state that includes elevated production of fatty acids and triglycerides. This implicates fructose as a causative agent in the development of nonalcoholic fatty liver disease. Evidence from studies involving feeding fructose to animals suggests that nonalcoholic fatty liver disease may be caused by fructose overconsumption, in the same way that alcohol overconsumption leads to alcoholic fatty liver disease. The similarity in the metabolic fate of both fructose and alcohol (ethanol) suggests that this theory has some merit. Both alcohol and fructose are metabolised largely in the liver, both increase the production of fatty acids and both cause accumulation of fatty acids in liver tissue. The main difference between fructose overconsumption and alcohol overconsumption is that the former is associated with obesity and the latter is associated with leanness. However, nonalcoholic fatty liver disease can develop in normal weight individuals.
RdB
