Obesity is conducive to liver diseases since it results in disturbances of liver activity that are manifested in increase of liver sizes, amplification of biochemical hepatic indices and changes at the cellular level such as large-cellular steatosis, fatty hepatosis, fibrosis and cirrhosis. Though this pathology is submitted in reviews as a series of particular cases, most likely such disturbances can be attributed to the signs and symptoms of the disease known as non-alcoholic fatty liver degeneration. As the volume of the data is rather small, the incidence of liver diseases in obesity is unknown.
The most characteristic feature of the condition is the increase in hepatic enzymes such as alanine aminotransferase  (ALAT) and aspartate aminotransferase (ASAT). But usually the indices of these enzymes do not exceed the doubled value of the top norm border. Besides, the level of increase in hepatic enzymes does not correspond to the severity of histologic changes. The diet itself can cause a temporary increase in concentration of hepatic enzymes within the first 6 weeks of weight reduction. The retrospective analysis of the samples of the hepatic tissue taken for research from the patients with excessive weight or suffering from obesity showed that 30 % of patients had hepatic fibrosis, and in one third of them (10 % of all group) the latent liver cirrhosis was found.
Besides this, many patients with the symptoms of fatty liver degeneration of non-alcoholic origin suffer from obesity. According to the cumulative data of several researches from 40 % to 100 % of patients with non-alcoholic steatohepatitis (NASH) suffer from obesity. According to the data of autopsy (postmortem examination) of the patients who suffered from obesity doctors find:
•    steatosis in 75 % of cases
•    steatohepatitis in 20 % of cases
•    liver cirrhosis in 2 % of cases
The liver enlargement is detected in 75 % of the patients. The relation of ASAT/ ALAT  is usually less than 1, in contrast to value of this parameter in the patients with alcoholic steatohepatitis. The observation over the patients within 1 to 7 years revealed the progression of the liver disease in 40 % of the patients, and 10 % of the patients developed cirrhosis.
Besides this, in the majority of patients with simple steatosis the disease took a benign course, while steatohepatitis, fibrosis, and cirrhosis frequently resulted in the development of complications and more serious course of the malady. Though, ultima analysi, cirrhosis develops only in a small number of patients with non-alcoholic fatty liver affection, in the countries with a wide incidence of obesity this pathology becomes one of principal causes of liver cirrhosis.
Moreover, obesity increases the risk of fibrosis and cirrhosis development in patients with alcoholic liver affection and hepatitis C. At present, it is not completely clear why people suffering from obesity develop the non-alcoholic fatty liver degeneration. There are grounds to believe that the development of this pathology is frequently associated with the intra-abdominal obesity (determined by the measurements around the waist), insulin resistance (the increase in the levels of glucose on an empty stomach and insulin in blood), diabetes, raised triglyceride levels in blood, low concentration of serum high-density lipoproteins (HDL) and arterial hypertension.
Doctors presuppose that the development of this disease is associated with two or more damaging influences on the liver. First of all, it is steatosis, which most often results from the lipid metabolism alteration due to obesity and namely the increase of triglyceride decomposition in the fatty tissue that in turn increases the accumulation of free fatty acids in the liver. Secondly, it is lipid peroxidation in the liver and liberation of cytokines that can have direct damaging effect upon the cells of the liver and promote the development of inflammation and fibrosis.
Though weight reduction is the typical recommendation for patients with obesity and non-alcoholic fatty affection of the liver, it is not yet known whether such therapy influences upon the nature of the disease. Gradual weight reduction by 10 % and more may correct the level of hepatic enzymes and favor the reduction of the liver sizes, the fat amount in a hepatic tissue and ease the manifestations of steatohepatitis. However, fast weight reduction during the therapy with the help of a very low-calorie diet or starvation may provoke the inflammation.