Obesity and fat infiltration of a liver

Obesity is a pathologic excess of TAG in the body. It is an increase of body weight on 10% and more from normal weight.

There are 4 extent of obesity. 1-st extent conforms to excess of body weight 10-29% from normal one; 2-nd extent – 30-49%; 3-rd extent – 50-99%; 4-th extent – 100 and more %.

There are primary (constitutional) and secondary (symptomatic) obesity.

The key mechanism of the primary obesity consists in derangement of hormonal connection between adipose tissue and hypothalamus. In 1994 the hormone of adipocytes was opened. It is named leptin and it is secreted in full state (naurishing). Leptin goes in hypothalamus and joins with ventromedialis nucleus. It causes the feeling of full state. In the obesity the formation and secretion of leptin is decreased and this is accompanied by permanent hunger feeling. Thus, the primary obesity is a deficiency of leptin on dietary-hypodynamic phone.

If the content of TAG in the liver is more than 10% and the fatty drops are histologically revealed in more than half of hepatocytes, are said to be about steatosis of a liver (or fat infiltration of a liver).

The reasons are next: diabetes mellitus, obesity, hyperlipoproteinemia, abuse of alcohol, poisonings, starvation, hypovitaminosis, pregnancy, hereditary defects of oxidation of FFA.

The term “fat transformation of a liver) is referred to situation when the adipocytes appear in stroma of a liver.

The pathogenesis of its can be related with increase of entrance of lipids into hepatocytes; decrease of assembling and secretion of LPVLD; inhibition of oxidation of lipids in liver and combination of these factors. In this connection there are 2 main types of fat infiltrationof a liver: 1-st type results in increase of content of FFA on the blood plasma promoted by mobilization of fats from adipose tissue or hydrolysis of TAG of chylomicrons and LP. In this case the absorption and esterification of FFA by the liver are increased. It results in excess of TAG in liver and lack of LP are observed.

The 2-nd type is related with metabolic block of formation of LP. This derangement can be caused by: a) block of synthesis of apoproteins; b) block of formation of LP; c) insufficient formation of phospholipids; d) derangement of own secretory mechanism. The steatosis of a liver can be developed in the lack of proteins, PUFA, vitamins B3 and B6.

All compounds are being donators of CH3-group promote the secretion of LPVLD and oxidation of FFA. Hence, they are lipotropic factors. The main lipotropic factor is a choline. Vitamins B12, Bc, B6, Met, betain, inosit, pangamic acid, carnitine are referred to lipotropic factors too.

Vitamin PP, ethionine, guanidine acetate are antilipotropic factors. The cells of pancreatic ducts are secreted the lipocain which is lipotropic factor.