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‐c...
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Published in | Diabetes, obesity & metabolism Vol. 18; no. S1; pp. 63 - 70 |
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Main Authors | , , , |
Format | Journal Article |
Language | English |
Published |
Oxford, UK
Blackwell Publishing Ltd
01.09.2016
Wiley Subscription Services, Inc |
Subjects | |
Online Access | Get full text |
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Summary: | 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. |
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Bibliography: | Larry L. Hillblom Foundation - No. 2014-D-004_NET NIH - No. P30 DK063720 ark:/67375/WNG-KWP19Z7T-0 UCSF Diabetes Research Center istex:85891B84506EBBA4F0C6F3625E62F42ED6D26BF7 ArticleID:DOM12716 ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-3 content type line 23 ObjectType-Review-1 |
ISSN: | 1462-8902 1463-1326 |
DOI: | 10.1111/dom.12716 |