β‐Cell adaptation in pregnancy

Abstract

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 to 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.

A mouse model of gestational glucose intolerance through exposure to a low protein diet during fetal and neonatal development

“…The compensatory changes in human BCM remain controversial as the dynamics of BCM expansion are hypothesized to be slightly different from those in mouse (Baeyens et al . ). Nonetheless, the only two human studies conducted to date have both reported an increase in β‐cell area in pancreata of pregnant women at postmortem (Van Assche et al .…”

The maternal plasma proteome changes as a function of gestational age in normal pregnancy: a longitudinal study

“…Reproductive success depends on an intensive and rich dialogue among mother, placenta, and fetus. The adaptations required for pregnancy appear to involve virtually all maternal organs/systems, including the metabolic/ endocrine (1)(2)(3)(4)(5)(6), cardiovascular (7)(8)(9)(10)(11)(12), respiratory (13), gastrointestinal (12,(14)(15)(16)(17)(18)(19)(20)(21), hematologic (22,23), and central nervous systems (24)(25)(26).…”

“…The study of the physiology of pregnancy has spanned decades, and has largely depended upon available technological capabilities to study parameters that change with gestational age. Such parameters have been studied with relatively simple methods, such as hormonal determinations (20,21,27), concentrations of nutrients/fuels (glucose (17)(18)(19), lipids(28-33), proteins(34-40), amino acids(41-43)), blood pressure (8,44), cardiovascular function (9,11), spirometry (13,16), immunological assays (14,24,45), and different tests of central nervous system function (25,26). These studies have been essential to understand changes in body composition (4,18), physiologic adaptation (10,13), pathophysiology of selected pregnancy complications (17,(46)(47)(48).…”

Adiponectin and β-Cell Adaptation in Pregnancy

“…For normal glucose tolerance to be maintained in the setting of the insulin resistance of late gestation, the b-cells must markedly increase their secretion of insulin. It is believed that this enhanced secretion is achieved through the expansion of b-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).…”