, Volume 53, Issue 10, pp 2089-2092
Date: 10 Jul 2010

Beta cell adaptation in pregnancy: a major difference between humans and rodents?

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Increasing evidence demonstrates that the insulin-producing beta cells can dynamically adapt their size, number and function in response to a variety of experimental and pathological conditions. Whether this dynamic adaptation also takes place under physiological conditions is less clear, with the notable exception of pregnancy [1, 2]. Under this condition, it has long been known that rodents undergo a rapid and substantial expansion of beta cell mass [35] due to increased beta cell size (hypertrophy) and replication (hyperplasia) [4], without detectable evidence of islet neogenesis [5]. These changes are induced by prolactin, placental lactogen and growth hormone, whose receptors are upregulated in beta cells after two-thirds of the gestational duration [1, 6]. They are also rapidly reversed at about the time of delivery, due to progesterone-controlled activation of beta cell apoptosis [7]. Recent studies have implicated selected genes controlling beta cell replication, survival and ...