title: The role of non-placental signals in the adaptation of islets to pregnancy.
abstract: 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.
authors.affiliation: Diabetes Research Group, Division of Diabetes and Nutritional Sciences, King's College, London, UK.
authors.forename: R
authors.initials: R
authors.lastname: Drynda
authors.affiliation: Department of Endocrinology, Great Ormond Street Hospital, London, UK.
authors.forename: C J
authors.initials: CJ
authors.lastname: Peters
authors.affiliation: Diabetes Research Group, Division of Diabetes and Nutritional Sciences, King's College, London, UK.
authors.forename: P M
authors.initials: PM
authors.lastname: Jones
authors.affiliation: Diabetes Research Group, Division of Diabetes and Nutritional Sciences, King's College, London, UK.
authors.forename: J E
authors.initials: JE
authors.lastname: Bowe
mesh_terms: D000222:Adaptation, Physiological; D000818:Animals; D049109:Cell Proliferation; D005260:Female; D005951:Glucose Tolerance Test; D006984:Hypertrophy; D050417:Insulin-Secreting Cells / Q000378:metabolism* / Q000473:pathology; D008813:Mice, Inbred ICR; D010920:Placenta / Q000378:metabolism*; D011247:Pregnancy; D015398:Signal Transduction