Gestational diabetes pathophysiology
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
Pathophysiology
Pregnancy is a state of relative insulin insensitivity. During the early part of pregnancy there is increase in insulin secretion and beta cell hyperplasia. This leads to an increase in insulin sensitivity with low fasting blood sugar levels, increased glucose uptake by peripheral tissue and glycogen storage as well as decreased hepatic gluconeogenesis. This process is crucial for the build-up of maternal adipose tissue, to be used in the later part of pregnancy. During the late phase, there is an increase in hormones such as cortisol, prolactin, progesterone and human placental lactogen which leads to a state of relative insulin resistance, possibly via a post receptor defect in the cells. This is a critical step which ensures adequate delivery of nutrients to the fetus. The pancreas respond to this increased resistance by doubling the release of insulin.
It has been found that women diagnosed with gestational diabetes already have insulin resistance at baseline with a higher level of plasma insulin levels. This state gets further aggravated by the metabolic changes associated with pregnancy. The pancreas however, is unable to cope with this additional stress of elevated level of insulin resistance. This results in an inadequate release of insulin and elevated blood sugar levels.