Role of insulin, adenosine, and adipokine receptors in the foetoplacental vascular dysfunction in gestational diabetes mellitus

摘要: Gestational diabetes mellitus (GDM) is a disease of pregnancy associated with maternal and foetal hyperglycaemia altered foetoplacental vascular function. Human microvascular macrovascular endothelium from GDM show increased maximal l-arginine transport capacity via the human cationic amino acid transporter 1 (hCAT-1) isoform nitric oxide (NO) synthesis by endothelial NO synthase (eNOS). These alterations are paralleled lower activity endogenous nucleoside adenosine equilibrative (hENT1) activation receptors. A causal relationship has been described for adenosine-activation A2A receptors, hCAT-1, eNOS (i.e. Adenosine/l-Arginine/Nitric Oxide, ALANO, signalling pathway). Insulin restores these in insulin receptor (IR-A) form but IR-A IR-B forms microcirculation placenta. Adipokines secreted adipocytes influencing metabolic Various adipokines dysregulated GDM, adiponectin leptin playing major roles. Abnormal plasma concentration or their receptors involved pathophysiology GDM. However, involvement adipokines, adenosine, membrane transporters aetiology this unknown. This review focuses on membranes giving an overview key vasculature article part Special Issue entitled: Membrane Transporters Receptors Pregnancy Metabolic Complications edited Luis Sobrevia.