Non-Alcoholic Steatohepatitis (NASH) or Fatty Liver

Non-alcoholic steatohepatitis was first reported in 1980 by Ludwig et al. It is the fat deposition in the liver that is unrelated to alcoholic, iatrogenic, and hemochromatosis history. NASH is defined as an excessive accumulation of fat in the liver, usually exceeding 5 per cent of the total liver weight. Since alcohol related liver disease also causes fatty liver, the name NASH is used to distinguish non-alcohol related cases of fatty liver.

The precise cause of this condition have not yet been clearly defined but some factors such obesity, diabetes, and mal-nutrition are possible culprits. More than 50% of the fat is composed of triglyceride (TG), which was has been called fatty liver or diabetic hepatitis. It is often associated with obesity, type II diabetes, and high blood lipids levels. Although it is possible for a person of average weight to develop NASH, in most cases, obesity is often a pre-condition. In the USA, about two-thirds of the population is considered overweight and among these people, about twenty percent could develop fatty liver, or steatosis.  This means that as much as 12% of the US population may be affected by fatty liver (steatosis or NASH).

Approximately twenty percent of individuals that have NASH may progress to cirrhosis. Of the total population, up to 2.4% could develop cirrhosis induced by NASH. This number is greater than the total estimated US Hepatitis C patient population(1.8%), making non-alcoholic steatohepatitis a serious health problem.

The dysfunction of the Golgi apparatus and rough-surfaced reticular membrane of the liver cell causes the retention of TG and blockage of the secretion of very low-density lipid (VLDL) from the liver cells. Diabetes is a common cause of NASH and obesity and for those whose body weight is 40% heavier than normal, the incidence rate of NASH is about 18%. In NASH patients, more than 50% have diabetes and high blood lipids. The deposit of fat in the liver cell causes hyper oxidation of lipids, which promote the secretion of cytokines and inflammatory agents. These cytokines and inflammatory agents in turn cause the liver cells to become inflamed. As the condition persists, liver cell apoptosis, inflammatory cells infiltration, and fibrosis begin to develop. If left untreated, severe cases will progress to cirrhosis and transplantations may become necessary if the condition of the liver continues to deteriorate.