Gestational diabetes promotes germ cell cCyst breakdown and primordial follicle formation in newborn mice via the AKT signaling pathway

Type 1 diabetes (T1D) is a common disease in which pancreatic β cells are impaired due to auto-immunity, pregnancy in women with it is associated with increased risk of neonatal morbidity, mortality. However, the effects of gestational diabetes on the reproduction of newborn offspring are still poor...

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Bibliographic Details
Published in:PloS one 2019-04, Vol.14 (4), p.e0215007-e0215007
Main Authors: Xu, Junjun, Huang, Jiaojiao, Pan, Qingjie, Du, Miao, Li, Zhen, Dong, Huansheng
Format: Article
Language:English
Subjects:
1-Phosphatidylinositol 3-kinase
AKT protein
Animal sciences
Animals
Animals, Newborn
Biology and Life Sciences
Breakdown
Complications
Cysts
Diabetes
Diabetes mellitus
Diabetes mellitus (insulin dependent)
Diabetes Mellitus, Experimental - drug therapy
Diabetes Mellitus, Experimental - metabolism
Diabetes Mellitus, Experimental - pathology
Diabetes, Gestational - drug therapy
Diabetes, Gestational - metabolism
Diabetes, Gestational - pathology
Diagnosis
Disease susceptibility
DNA methylation
Embryonic development
Endoplasmic reticulum
Female
Folliculogenesis
Genomics
Gestational diabetes
Glucose
House mouse
Immunity
Infertility
Insulin
Insulin - pharmacology
Kinases
Medicine and Health Sciences
Metabolism
Mice
Mice, Inbred ICR
Morbidity
Neonates
Newborn babies
Newborn infants
Offspring
Ovarian Follicle - growth & development
Ovarian Follicle - pathology
Ovaries
Pancreas
Pancreatic beta cells
Phosphatidylinositol 3-Kinases - metabolism
Physical Sciences
Physiological aspects
Pregnancy
Pregnancy complications
Proto-Oncogene Proteins c-akt - metabolism
Research and Analysis Methods
Signal Transduction
Signaling
Stem cells
Streptozocin
Type 1 diabetes
Women
Zoology
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Summary:Type 1 diabetes (T1D) is a common disease in which pancreatic β cells are impaired due to auto-immunity, pregnancy in women with it is associated with increased risk of neonatal morbidity, mortality. However, the effects of gestational diabetes on the reproduction of newborn offspring are still poorly understood. Here, we determined the cyst breakdown and primordial follicle formation in neonatal offspring born by streptozotocin (STZ)-induced diabetic or non-diabetic female mice, and found that the germ cell cyst breakdown was promoted in neonatal offspring of STZ -induced diabetic mice at postnatal Day 1, which sequentially accelerated the primordial follicle formation. Further investigation revealed that, the expression level of PI3K and p-AKT were significantly increased in ovaries of offspring born by T1D mice. These results indicated that STZ -induced gestational diabetes promotes germ cell cyst breakdown and primordial follicle formation by regulating the PI3K/AKT signaling pathway in the newborn offspring. In addition, this effect can be rescued by an insulin supplement. Taken together, our results uncover the intergenerational effects of gestational diabetes on neonatal offspring folliculogenesis, and provide an experimental model for treating gestational diabetes and its complications in neonatal offspring.
ISSN:1932-6203
1932-6203
DOI:10.1371/journal.pone.0215007