Abstract
Introduction
Gestational diabetes mellitus (GDM) is carbohydrate intolerance of varied severity with first onset or first recognition during pregnancy [1]. GDM is one of the most prevalent medical conditions in pregnant population. Global prevalence of GDM is on the rise. A study conducted among pregnant population in south Kerala had shown a prevalence as high as11.2%.[2]
Gestational diabetes seems to stem from the placenta and several placental hormones that help the development of fetus during pregnancy. During the second and third trimesters, these “insulin-antagonist” hormone levels increase and can cause insulin resistance. Insulin resistance makes it difficult for the mother’s body to properly utilize insulin, the hormone that manages glucose or blood sugar levels. This causes a higher-than-normal blood sugar level or hyperglycemia. Hence GDM usually develops between the 24th and 28th week of pregnancy. Normally, after delivery, these hormone levels, as well as glucose levels, return to normal[3]. According to American Diabetes Association (ADA), GDM is pathophysiologically similar to Type 2 diabetes in that the abnormality is in islets cell function or peripheral insulin resistance at receptor level. Studies suggest that the peripheral insulin resistance that characterize GDM likely results from several integrated mechanisms including a decrease in insulin receptor number, a post-receptor defect in insulin action and alterations in glucose transport systems[4,5].
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Corresponding Author
Dr Sreekala K N
Assistant Professor, Department of Physiology, SUT AMS, TVM
DOI: https://dx.doi.org/10.18535/jmscr/v5i10.41
