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

ABSTRACT

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 161 of palmitoleic mono fatty acid, C 181 oleic mono fatty acid and in a lesser degree C 182 linoleic unsaturated fatty acid (p < 0.05). The level C 140 of myristic unsaturated fatty acid, C 160 of palmitic unsaturated fatty acid and with 180 of stearic unsaturated fatty acid, ratio C 160/C 161 and C 180/C 181 had no changes content of both (omega-6 C 203 digomo-gamma-linoleic unsaturated fatty acid and essential polyenoic fatty acids remained the same. The significant differences between initial content in blood plasma of palmitic saturated fatty acid and oleic monoenic fatty acid was noted. The alteration in content of fatty acids in membranes of erythrocytes is the most expressed. In erythrocytes reliable (p < or = 0.05) decrease of content of C 160 palmitic fatty acid, C 180 stearic fatty acid and C 181 oleic fatty acid is established. The reliable decrease is noted in content of linoleic unsaturated fatty acid. In erythrocytes, moderate decrease is detected in levels of C 204 arachidonic polyenoic fatty acid, C 205 eicosapentaenoic polyenoic fatty acid. It is assumed that under post-prandial hyperglycemia insulin regulates metabolism of fatty acids, blocks lipolysis, decreases in cytosol of cells content of oleic and palmitic fatty acids inform of acetyl-KoA and forces mitochondrions intensively oxidate acetyl-KoA formed from pyruvate, from GLU. On surface of membrane, insulin increases number of glucose carriers GLUT4. Hypoglycemic effect of insulin is mediated by regulation first of all of metabolism of fatty acids. Hyperglycemia and insulin are two phylogenetically different humoral regulators. Insulin initiates blockade of lipolysis in adipocytes and positioning on membrane GLUT4. Hyperglycemia passively (activated) increases absorption by cells GLU on gradient of concentration inter-cellular medium--cytosol and synthesis of glycogen.