engleski

Changes in the fatty acid profile of the rat liver and brain induced by high streptozotocin dosage or low dosage and fructose supplementation

We have investigated the effects of severe and mild hyperglycemia with insulin resistance on the fatty acid profile of the liver and brain tissue. For this purpose, a single, intraperitoneal dosage of streptozotocin (STZ, 55mg/kg) was used to induce severe hyperglycemia, characteristic for type 1 diabetes mellitus (T1DM) (H-STZ group), while a low dosage of STZ (35mg/kg) and fructose in drinking water was used to mimic mild hyperglycemia and insulin resistance characteristic for the type 2 diabetes mellitus (T2DM) prediabetic state and metabolic syndrome (L-STZ-FRU group). The content of fatty acids varied significantly depending on the treatment, as well on the lipid class and origin (whole cell or microsomes). The variations in the brain fatty acids were much less pronounced and they depended on the brain region. The most significant changes, in the liver tissue of the H-STZ rats were a decrease in monounsaturated fatty acids (MUFA), particularly palmitoleic and cis-vaccenic, while these fatty acids increased in the L-STZ- FRU rats. In the brain tissue of the H-STZ rats the most significant changes included an increase in linoleic acid, while in the L-STZ- FRU rats the changes were minimal. Arachidonic acid decreased in the liver phospholipids of the H-STZ group due to the partitioning into neutral lipids, and in the L-STZ- FRU rats it decreased in liver phospholipids, brain cortex and medulla. The content of docosahexaenoic acid increased in the cerebellum and medulla of the H-STZ rats and decreased in the liver phospholipids of the L-STZ-FRU rats. The influence of hyperglycemia on the fatty acid profile of the liver and brain tissue demands additional investigation, especially in T2DM and metabolic syndrome. However, the presented data could improve knowledge on supplementation of patients with adequate dietary fatty acids.

hyperglycemia; fatty acids; rodent model; diabetes; metabolic syndrome

nije evidentirano