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The role of non-placental signals in the adaptation of islets to pregnancy

Research output: Contribution to journalArticle

R. Drynda, C. J. Peters, P. M. Jones, J. E. Bowe

Original languageEnglish
Pages (from-to)64-71
Number of pages8
JournalHormone and Metabolic Research
Issue number1
Published1 Jan 2015

King's Authors


It is well established that the maternal β-cell mass increases during pregnancy in both humans and rodents to compensate insulin resistance and increased metabolic demand, and rapidly returns to normal levels post-partum. However, the mechanisms underlying this adaptation are not well understood. It is established that this process is driven partly by placental signals, but the contribution of non-placental signals is still unclear. This study aimed to differentiate between the role of placental and non-placental signals in regulating the β-cell mass and glucose homeostasis during and after pregnancy. Pseudopregnant, pregnant and lactating mice were used to study the effects of maternal hormones on β-cell function during early pregnancy, mid-to-late pregnancy and post-partum, respectively. Pseudopregnant mice, with circulating hormone levels mirroring those during pregnancy but lacking placental signals, had significantly increased β-cell proliferation compared to non-pregnant controls but no change in glucose homeostasis, suggesting a role for non-placental hormones in increasing β-cell mass. The rate of β-cell proliferation rate dropped immediately after parturition, but lactating mice still had a significantly higher rate of β-cell proliferation compared to non-lactating post-partum mice, suggesting that lactation-related hormones play a role in the controlled involution of β-cell mass post-partum. These results implicate a role for both non-placental and placental signals in regulating β-cell mass during and after pregnancy.

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