The purpose of this review article is to analyze current information on the molecular mechanisms of gestational diabetes and the prospects for their use in the further development of new effective treatments for this common pathology. Decreased ability of insulin to bind to its receptor, decreased IRS-1 expression and GLUT-4 translocation, and increased levels of p85α-PI-3 kinase subunits are involved in the development of insulin resistance during pregnancy. In gestational diabetes, there are not only more significant changes of the above mentioned indicators, but also increased levels of pro-inflammatory factors: TNF-α, IL-6, leptin and decreased insulin-sensitizing factors: adiponectin and PPAR-γ. Therapeutic measures aimed at normalizing the secretion of cytokines and adipokines reduce the risk of gestational diabetes mellitus and its complications and require further development