**5. Conclusion**

Another factor that significantly affects this process is HL activation. As we have already mentioned, HL is associated with proteoglycans of liver blood vessels endothelial cells and hydrolyzes TAGs and phospholipids (PL) in the composition of the various lipoprotein

It is known that activation of increased HL activity under CE transfer and growth of blood TAG content determined in our experiments is one of the main reasons of HDL-cholesterol content decrease. This is linked with the fact that TAG hydrolysis in the HDL3 composition leads to their transformation to HDL2, which are rapidly removed from the blood stream by

According to our data, the HL activity increase is accompanied by LAL activity increase in the liver (compared with Figures 2 and 10), which shows the intense lipoprotein uptake (probably

Hence, our results suggest that changes in VLDL secretion are associated with the MS development FFA accumulation in the blood and elevated hepatic FFA uptake then followed changes in the CE transfer activity and after all was HL activation. This leads to the LDL*B*

At the same time, it is apparent that changes in lipoprotein enzymatic transformations are led to their abnormal composition. This fact is confirmed by earlier enzymatic changes compared with changes in the blood lipid fractions content. Furthermore, the lipoprotein content changes earlier than their composition, which should reflect the balance disorder of their secretion and absorption. Probably, the latter is related with HDL metabolism in the blood and liver uptake

Thus, the TAG-enriched apoB-LP accumulation, which was accompanied by an increased CE transfer rate and increased HL activity, was found out in blood serum of male Syrian hamsters fed high-calorie die. It is known that such changes have a pronounced proatherogenic character, because they lead to the formation of atherogenic LDL fractions – LDL*B* and lower

The reason for hypertriacylglycerolemia development in the experimental animals in our investigation, probably, is the lipolysis activation in adipose tissue due to cortisol secretion elevation and decreased adiponectin secretion, which was observed under body weight gain. The absence of a positive correlation between the serum TAG content and apoB-LP, as well as the serum and liver TAG content in experimental animals, suggests that the serum TAG content increase in females fed high calorie diet is not associated with increased hepatic VLDL

Based on these statements we can suggest that the cause of hypertriacylglycerolemia in females in our experiments, probably, is the predominant only liver VLDL1 fraction secretion by liver

As is mentioned above, the intensive formation of TAG-enriched VLDL1 in liver and their secretion to the blood may occur due to the growth of the intracellular TAG content, including the intensive FFA inflow from the blood, and reducing of the hepatocytes sensitivity to insulin.

and/or diminished VLDL utilization because of the LDL activity decrease.

fractions and plays a leading role in their metabolism.

accumulation and cholesterol reverse transport disorder.

the liver.

HDL) from the blood stream.

48 Lipoproteins - From Bench to Bedside

under the condition of EC enrichment.

of HDL cholesterol.

secretion.

The obtained results suggest that the MS begins to develop differently in individuals of different sex. In males, the starting point for MS development is the increase in adipose tissue mass, changes of its endocrine activity, and as a result the hypercortisolemia development, decreased adiponectin secretion, which is caused by the lipolysis activation in adipose tissue and with time, provokes metabolic and hormonal shifts and the IR development. In females, the MS development begins with the IR appearance, which activates the other pathogenetic factors, although they are delayed by estrogens in the first stages.

Our data are consistent with literature data and demonstrate that feeding high-calorie diet causes the atherogenic dyslipidemia development in experimental animals, which is the consequence of metabolic disorders in adipose tissue and liver as well as lipid and lipoprotein metabolic disorders in the bloodstream.

Our current studies revealed some age and gender features of lipid metabolism disorders mediated by body weight gain. In particular, it was demonstrated that the tendency to atherogenic dyslipidemia in males does not significantly depend on age, but it increases with age in females.

The hormonal disturbances that cause lipolysis activation in adipose tissue in males are the bases of hypertriacylglycerolemia development, which in turn provokes the further blood lipid profile deterioration. The hypertriacylglycerolemia in females is associated with lipid metab‐ olism disorders in the liver due to hepatic IR. The body weight gain of the experimental animals is of great importance as to the formation of these disorders.
