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-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.
Diabetes Center, University of California San Francisco, San Francisco.|Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research, University of California San Francisco, San Francisco.
L
L
Baeyens
Diabetes Center, University of California San Francisco, San Francisco.|Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research, University of California San Francisco, San Francisco.|Department of Medicine, University of California San Francisco, San Francisco.
S
S
Hindi
Department of Genetics, Cell Biology and Development, University of Minnesota Medical School, Minneapolis.
R L
RL
Sorenson
Diabetes Center, University of California San Francisco, San Francisco. michael.german@ucsf.edu.|Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research, University of California San Francisco, San Francisco. michael.german@ucsf.edu.|Department of Medicine, University of California San Francisco, San Francisco. michael.german@ucsf.edu.
M S
MS
German
D000222:Adaptation, Physiological; D000818:Animals; D049109:Cell Proliferation; D016640:Diabetes, Gestational / Q000378:metabolism; D005260:Female; D005947:Glucose / Q000378:metabolism*; D006801:Humans; D007328:Insulin / Q000378:metabolism*; D007333:Insulin Resistance; D000078790:Insulin Secretion; D050417:Insulin-Secreting Cells / Q000166:cytology / Q000378:metabolism*; D051379:Mice; D010928:Placental Lactogen / Q000378:metabolism; D049590:Postpartum Period; D011247:Pregnancy / Q000378:metabolism*; D051381:Rats; D012701:Serotonin / Q000378:metabolism
D007328:Insulin; D012701:Serotonin; D010928:Placental Lactogen; D005947:Glucose
Htr1d; Htr2b; Htr3a; gestational diabetes; insulin; placenta; placental lactogen; pregnancy; serotonin; β-cell