Adiponectin and β-Cell Adaptation in Pregnancy.

Abstract

Pregnancy poses a unique physiological challenge to the pancreatic β-cells. For normal glucose tolerance to be maintained in the setting of the insulin resistance of late gestation, the β-cells must markedly increase their secretion of insulin. It is believed that this enhanced secretion is achieved through the expansion of β-cell mass in response to circulating factors, including prolactin and placental lactogens (1,2). Conversely, failure of this compensatory response will result in maternal hyperglycemia or gestational diabetes mellitus (GDM) (3). However, our understanding of the mechanisms underlying normal islet adaptation in pregnancy and its failure in GDM remains limited at this time. In this context, the importance of elucidating the biology of this adaptive response is underscored by the novel insight that it could provide into the pathophysiology of β-cell dysfunction, with implications for not only GDM but also subsequent type 2 diabetes (1,2). Adiponectin is an adipocyte-derived hormone with pleiotropic effects on a broad array of physiological processes including energy homeostasis, vascular function, systemic inflammation, and cell growth (4,5). Most notably, it has emerged as an antidiabetic adipokine, with low serum adiponectin shown to predict incident type 2 diabetes in several populations (6). Similarly, hypoadiponectinemia in early pregnancy, or even prior to gestation, can predict the subsequent development of GDM in the second or third trimester (7). These antidiabetic associations have …