Gestational diabetes

Diabetes mellitus is an endocrine disorder in which insulin production or action is insufficient, resulting in hyperglycaemia. Insulin is produced in pancreatic beta (b) cells and is required for the uptake of glucose into cells, as well as the storage of glycogen, protein and fats. Thus, insufficient insulin action results in hyperglycaemia, and the breakdown of storage forms of fuel (glycogen, fats, and proteins) for use by the body's cells, due to lack of availability of glucose. There are three main types of diabetes (Table 1): type 1 diabetes is characterised by early age of onset, destruction of pancreatic b cells, and the need for therapeutic insulin. Type 2 is characterised by older age of onset, insulin resistance and insufficient insulin production to variable degrees, and is associated with obesity and a sedentary lifestyle. Gestational diabetes mellitus is seen only in pregnancy, typically in the third trimester, and it is thought to result from the metabolic changes brought on by pregnancy, along with an underlying predisposition to developing this condition (Crandall and Shamoon, 2015; American Diabetes Association (ADA), 2017; Rankin, 2017). This article will discuss the aetiology of gestational diabetes, how it is identified in pregnancy and controversies around this, adverse effects associated with it for the mother, fetus and child, and interventions aimed at preventing its development as well the associated adverse outcomes.