Role of Ceramide in Apoptosis and Development of Insulin Resistance.

This review presents data on the functional biochemistry of ceramide, one of the key sphingolipids with properties of a secondary messenger. Molecular mechanisms of the involvement of ceramide in apoptosis in pancreatic ß-cells and its role in the formation of insulin resistance in pathogenesis of type 2 diabetes are reviewed. One of the main predispositions for the development of insulin resistance and diabetes is obesity, which is associated with ectopic fat deposition and significant increase in intracellular concentrations of cytotoxic ceramides. A possible approach to the restoration of tissue sensitivity to insulin in type 2 diabetes based on selective reduction of the content of cytotoxic ceramides is discussed.

Functional activity of sphingomyelin cycle in rat liver in chronic toxic hepatitis.

Activities of sphingomyelinase and ceramidase decreased in the liver in chronic toxic hepatitis and the balance between the levels of proapoptotic ceramide and antiapoptotic sphyngosine-1-phosphate shifts towards the latter substance. Pronounced changes in the qualitative and quantitative composition of fatty acids in the sphingomyelin cycle effector molecules were revealed.

[Oxidative stress in adipose tissue as a primary link in pathogenesis of insulin resistance].

Obesity is a leading risk factor of diabetes mellitus type 2, impairments of lipid metabolism and cardiovascular diseases. Dysfunctions of the accumulating weight of the visceral fat are primarily linked to pathogenesis of systemic insulin resistance. The review considers modern views about biochemical mechanisms underlying formation of oxidative stress in adipocytes at obesity, as one of key elements of impairments of their metabolism triggering formation of systemic insulin resistance.

Morphological changes of the red blood cells treated with metal oxide nanoparticles.

The toxic effect of Al2O3, SiО2 and ZrО2 nanoparticles on red blood cells of Wistar rats was studied in vitro using the atomic force microscopy and the fluorescence analysis. Transformation of discocytes into echinocytes and spherocytes caused by the metal oxide nanoparticles was revealed. It was shown that only extremely high concentration of the nanoparticles (2mg/ml) allows correct estimating of their effect on the cell morphology. Besides, it was found out that the microviscosity changes of red blood cell membranes treated with nanoparticles began long before morphological modifications of the cells. On the contrary, the negatively charged ZrO2 and SiO2 nanoparticles did not affect ghost microviscosity up to concentrations of 1µg/ml and 0.1mg/ml, correspondingly. In its turn, the positively charged Al2O3 nanoparticles induced structural changes in the lipid bilayer of the red blood cells already at a concentration of 0.05µg/ml. A decrease in microviscosity of the erythrocyte ghosts treated with Al2O3 and SiO2 nanoparticles was shown. It was detected that the interaction of ZrO2 nanoparticles with the cells led to an increase in the membrane microviscosity and cracking of swollen erythrocytes.

Activity of sphingomyelinase in rat liver in acute and chronic toxic hepatitis: proportion between peroxidative and phospholipase pathways of lipid bilayer modification.

We showed that sphingomyelinase activity in the liver increased only during the acute phase of toxic hepatitis. Peroxidative modification of hepatocyte membrane bilayer prevailed during the acute phase, while after transformation of the process to the chronic phase phospholipase pathway predominated.