β‐Cell adaptation in pregnancy

Pregnancy in placental mammals places unique demands on the insulin‐producing β‐cells in the pancreatic islets of Langerhans. The pancreas anticipates the increase in insulin resistance that occurs late in pregnancy by increasing β‐cell numbers and function earlier in pregnancy. In rodents, this β‐cell expansion depends on secreted placental lactogens that signal through the prolactin receptor. Then at the end of pregnancy, the β‐cell population contracts back to its pre‐pregnancy size. In the current review, we focus on how glucose metabolism changes during pregnancy, how β‐cells anticipate these changes through their response to lactogens and what molecular mechanisms guide the adaptive compensation. In addition, we summarize current knowledge of β‐cell adaptation during human pregnancy and what happens when adaptation fails and gestational diabetes ensues. A better understanding of human β‐cell adaptation to pregnancy would benefit efforts to predict, prevent and treat gestational diabetes.