Piecing together the puzzle of pancreatic islet adaptation in pregnancy

Ann N Y Acad Sci. 2018 Jan;1411(1):120-139. doi: 10.1111/nyas.13552.


Pregnancy places acute demands on maternal physiology, including profound changes in glucose homeostasis. Gestation is characterized by an increase in insulin resistance, counterbalanced by an adaptive increase in pancreatic β cell production of insulin. Failure of normal adaptive responses of the islet to increased maternal and fetal demands manifests as gestational diabetes mellitus (GDM). The gestational changes and rapid reversal of islet adaptations following parturition are at least partly driven by an anticipatory program rather than post-factum compensatory adaptations. Here, I provide a comprehensive review of the cellular and molecular mechanisms underlying normal islet adaptation during pregnancy and how dysregulation may lead to GDM. Emerging areas of interest and understudied areas worthy of closer examination in the future are highlighted.

Keywords: gestational diabetes; insulin secretion; pregnancy; β cell biology; β cell proliferation.

Publication types

  • Review

MeSH terms

  • Adaptation, Physiological
  • Animals
  • Cell Division
  • Cytokines / physiology
  • Diabetes, Gestational / epidemiology
  • Diabetes, Gestational / physiopathology
  • Energy Metabolism
  • Female
  • Fetus / metabolism
  • Gene Expression Regulation
  • Hormones / physiology
  • Humans
  • Insulin / metabolism
  • Insulin Resistance
  • Intercellular Signaling Peptides and Proteins / physiology
  • Islets of Langerhans / physiology*
  • Neurotransmitter Agents / physiology
  • Pregnancy / physiology*
  • RNA, Untranslated / physiology
  • Transcription Factors / physiology


  • Cytokines
  • Hormones
  • Insulin
  • Intercellular Signaling Peptides and Proteins
  • Neurotransmitter Agents
  • RNA, Untranslated
  • Transcription Factors