Many people, doctors and researcher alike, believe that fatty liver diseas develops as a result of abnormal retention of lipid within the body cells. Its occurrence is reversible and develops as a result of large vacuoles fat deposits on the cells of the liver. Morphologically, it is extremely impractical to distinguish alcoholic from the non-alcoholic disease.
Accumulation of fat in the liver cells can always be caused by persistent inflammation of the cells. Usually, the disease is often categorized according to the alcohol intake of the patient because it is mainly due to alcoholism. Thus, it is grouped into either an alcoholic and non-alcoholic disease. Similarly, its severe stages are known as alcoholic and non-alcoholic steatohepatitis conditions.
A part from alcohol, there are also other causal factors, including dislipidemia, obesity, diabetes, and hypertension. The disease attacks the cells of the organ in several stages that follows specific steps. The initial stages involve intracytoplasmatic accumulation of triglycerides, increasing the deposition of fat in the organ. In addition, the hepatocytes deposit small fat vacuoles around the nucleus of the cell.
Similarly, the early stages of attack are also characterized by filling of the organ cells by many fat droplets that do not displace the cell nucleus. However, the vacuoles expand to displace the nucleus to the periphery of the cell wall and form signet rings, in the later phases. The formation of rings dissolves tissue processing and makes the vesicles appear delineated and empty. Thereafter, the large vacuoles coalesce and form irreversible lesions of fatty cysts.
Usually, macro vesicular steatosis is believed to be caused by excessive alcohol consumption, corticosteroids, diabetes, and obesity. Moreover, it can give rise to severe conditions that affect the cells and may even lead to severe conditions such as Reyes syndrome and acute fatty liver of pregnancy. Generally, it is still a daunting task to know the severity of cell damage at the early stages of the organ attack.
This implies that diagnosis can only be conducted when fat accumulation reaches 5-10% in weight. Often, fatty acid metabolism causes pathogenesis of the disease. The metabolism is mainly as a result of two factors, imbalance in consumption and combustion of energy and peripheral insulin resistance, which increases the transport rate of the fat acids to the organ.
Accumulation of fat can also result from inhibition and impairment of the receptor molecules which are responsible for controlling synthesis of enzymes within the fatty acids and also the control of oxidation. Alcohol intake is believed to cause damages to the mitochondria among other cellular components and impairing the energy metabolism process. On the other hand, the non-alcoholic type of disease develops as a result excess metabolic energy in the cells.
Generally, many people believe that fatty liver diseas can be cured through eliminating the causal factors since it develops through a reversible process. Its severe conditions are usually characterized by persistent inflammation of the organ cells. However, the progression to alcoholic steatohepatitis or non-alcoholic steatohepatitis, which are advanced stages, relies on the persistence of the causal factors or failure to fight them at the early stages of attack.