Piecing together the puzzle of pancreatic islet adaptation in pregnancy

被引：30
作者：
Banerjee, Ronadip R. [1 ,2 ]
机构：
[1] Univ Alabama Birmingham, Dept Med, Div Endocrinol Diabet & Metab, Sch Med, 1808 7th Ave South,Boshell Diabet Bldg B730, Birmingham, AL 35294 USA
[2] Univ Alabama Birmingham, Comprehens Diabet Ctr, Sch Med, Birmingham, AL 35294 USA
来源：
ANNALS OF THE NEW YORK ACADEMY OF SCIENCES | 2018年 / 1411卷 / 01期
关键词：
beta cell biology; pregnancy; gestational diabetes; insulin secretion; beta cell proliferation; BETA-CELL PROLIFERATION; STIMULATED INSULIN-SECRETION; GESTATIONAL DIABETES-MELLITUS; HEPATOCYTE GROWTH-FACTOR; PROLACTIN RECEPTOR; GENE-EXPRESSION; PLACENTAL-LACTOGEN; GLUCOSE-HOMEOSTASIS; MATERNAL METABOLISM; RESEARCH RESOURCE;
D O I：
10.1111/nyas.13552
中图分类号：
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号：
07 ; 0710 ; 09 ;
摘要：
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 beta 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.
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收藏
页码：120 / 139
页数：20
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