[The content of individual fatty acids and numbers of double bonds, insulin, C-peptide and unesterified fatty acids in blood plasma in testing tolerance to glucose].

The glucose tolerance test demonstrates that content of unesterified fatty acids in blood plasma decreases up to three times and the content of oleic and linoleic acids is more decreased in the pool of fatty acids lipids. Out of resistance to insulin, hormone secretion increases up to three times. The decreasing of level of individual fatty acids occurs in a larger extent.

[The fatty acids in blood plasma and erythrocytes in test of glucose tolerance].

The sample of 26 patients with ischemic heart disease and syndrome of insulin resistance was subjected to standard test of glucose tolerance. The content of individual fatty acids was detected using technique of gas chromatography and mass spectrometry. In blood plasma, after 2 hours of post-prandial hyperglycemia, reliably decreased content of C 16:1 of palmitoleic mono fatty acid, C 18:1 oleic mono fatty acid and in a lesser degree C 18:2 linoleic unsaturated fatty acid (p < 0.

[The different notions about beta-oxidation of fatty acids in peroxisomes, peroxisomes and ketonic bodies. The diabetic, acidotic coma as an acute deficiency of acetyl-CoA and ATP].

The mechanisms of beta-oxidation of fatty acids developed more than a century before have no compliance with actual physical chemical data. The oxidation of long-chain C 16:0 palmitic saturated fatty acid occurs not by sequential formation of eight molecules of acetyl-KoA but by force of formation of double bond and its hydrolysis on two short-chain C 8:0 fatty acids. Only short-chain fatty acids can become shorter under "chipping" of C 2-acetate with formation of C 4-butyric acid (butyrate) and its metabolites (beta-hidroxibutirate, acetoacetate, acetone).

[Alloxan cytotoxicity: a new aspect of the problem].

The effect of alloxan on human intact erythrocytes (in the suspension and whole blood) was studied using an original potentiometric apparatus permitting continuous registration of the flow rate of reducing equivalents ('RE) through a plasmatic membrane. Acceleration of RE flow from erythrocytes due to the activation of hexosomonophosphate shunt (HMPS) was established. This effect was inhibited by P-chlormercury benzoate proving the involvement of the SH-groups of erythrocyte membrane proteins in the interaction of alloxan with erythrocytes.