Pharmaco-epi-genetic and patho-physiology of gestational diabetes mellitus (GDM): An overview

Gestational diabetes mellitus (GDM) is a medical complication of glycaemic intolerance that develops in 2^nd or 3^rd trimester of pregnancy. The speculative cause behind insulin resistance or chronic glycemic intolerance occurs due to pancreatic β-cell alterations during gestation. Women who have GDM are more likely to acquire type 2 diabetes mellitus (T2DM) and other metabolic problems later in life. GDM is linked to several risk factors including gestational age, diabetic family history, polycystic ovary syndrome, obesity, ethnicity, hypertension during pregnancy, and spontaneous pregnancy loss. GDM causes several adverse effects in the mother and fetus like pre-eclampsia, neonatal hypoglycemia, macrosomia, hypocalcemia, and congenital malformations. T2DM and GDM share similar pathophysiology and a common genetic background. Previous studies suggested that alterations in insulin homeostatic genes associated with T2DM could also be responsible for the development of GDM. GDM development is influenced by several placental hormones like progesterone, estrogen, and insulin insensitivity. In the past few years, there has been a significant focus on molecular biomarkers in the field of GDM prognosis/diagnosis and use for screening. The present review suggests the role of genetic and epigenetic alterations in the pathophysiology of GDM.