ИСТИНА

Insulin resistance is the earliest event in pathogenesis of type 2 diabetes mellitus. It is defined as inability of insulin to decrease postprandial glucose levels in blood. At the cellular level, it is due to inability of insulin to stimulate glucose uptake by insulin-sensitive skeletal muscle, liver and fat cells. At the molecular level, this is caused by disruption of intracellular cascade initiated by insulin receptor in these cells. Physiological conditions that promote IR include obesity, inflammation, chronic hypoxia, oxidative and cellular stresses. However, the intimate mechanisms linking to dysregulated insulin signaling remain largely unclear. Furthermore, it is unknown whether these mechanisms are typical only for differentiated muscle, liver and fat cells, whereas their precursor cells are less affected and have a potential against IR. We explore this possibility using mouse preadipocytes 3T3L1 that can be maintained in culture or fully differentiated into adult adipocytes.