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.
Keywords: Htr1d; Htr2b; Htr3a; gestational diabetes; insulin; placenta; placental lactogen; pregnancy; serotonin; β-cell.
© 2016 John Wiley & Sons Ltd.