The pancreas and the placenta: understanding gestational diabetes and why some islets fail to cope with pregnancy
Author(s) -
Lorna Smith,
James E. Bowe
Publication year - 2021
Publication title -
the biochemist
Language(s) - English
Resource type - Journals
eISSN - 1740-1194
pISSN - 0954-982X
DOI - 10.1042/bio_2021_115
Subject(s) - placental lactogen , gestational diabetes , pregnancy , hormone , human placental lactogen , diabetes mellitus , prolactin , endocrinology , medicine , placenta , insulin , insulin resistance , fetus , pancreas , type 2 diabetes , endocrine system , gestation , biology , genetics
During healthy pregnancy there is a progressive decrease in sensitivity of the mother’s cells to insulin signalling, known as insulin resistance, in order to divert glucose towards the growing fetus. To compensate for this, the pancreatic β-cells must adapt through various mechanisms to increase the amount of insulin produced. A failure of the β-cells to sufficiently adapt can lead to gestational diabetes and clinical consequences for both mother and baby. The necessary β-cell adaptations are coordinated in large part by the placenta, which acts as an endocrine organ producing and releasing hormones into the maternal blood circulation. Hormones such as prolactin, placental lactogen, and kisspeptin have been identified to play important roles in initiating and maintaining the changes in the β-cells necessary for a healthy pregnancy. Further work towards understanding how the β-cells adapt to pregnancy in humans, the signals underlying these changes, and why these adaptations fail in gestational diabetes is essential in allowing us to address this increasingly prevalent form of diabetes.
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