Document Detail


Maternal diabetes impairs gastrulation and insulin and IGF-I receptor expression in rabbit blastocysts.
MedLine Citation:
PMID:  20631000     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Women with type 1 diabetes are subfertile. Diabetes negatively affects pregnancy by causing early miscarriage and poor prenatal outcomes. In this study we examine consequences of maternal type 1 diabetes on early embryo development, metabolic gene expression, and the pattern of insulin receptor (IR) and IGF-I receptor (IGF-IR) distribution in rabbit blastocysts. In female rabbits, type 1 diabetes was induced by alloxan treatment. Six-day-old blastocysts were recovered and assessed for receptor distribution and metabolic gene expression. In vitro culture of blastocysts was performed in medium containing 1 mm, 10 mm, or 25 mm glucose, simulating normo- and hyperglycemic developmental condition in vitro. The fertility rate of the diabetic rabbits clearly mirrored subfertility with a drop in blastocyst numbers by 40% (13.3 blastocysts in diabetic vs. 21.9 in control females). In blastocysts onset and progression of gastrulation was delayed and expression of IR and IGF-IR and their metabolic target genes (hexokinase, phosphoenolpyruvate carboxykinase), both in vivo and in vitro, was down-regulated. The amount of apoptotic cells in the embryonic disc was increased, correlating closely with the reduced transcription of the bcl-x(L) gene. Blastocyst development is clearly impaired by type 1 diabetes during early pregnancy. Insulin-stimulated metabolic genes and IR and IGF-IR are down-regulated, resulting in reduced insulin and IGF sensitivity and a delay in development. Dysregulation of the IGF system and embryonic glucose metabolism are potential reasons for diabetogenous subfertility and embryopathies and start as soon as during the first days of life.
Authors:
Nicole Ramin; René Thieme; Sünje Fischer; Maria Schindler; Thomas Schmidt; Bernd Fischer; Anne Navarrete Santos
Publication Detail:
Type:  Journal Article     Date:  2010-07-14
Journal Detail:
Title:  Endocrinology     Volume:  151     ISSN:  1945-7170     ISO Abbreviation:  Endocrinology     Publication Date:  2010 Sep 
Date Detail:
Created Date:  2010-08-25     Completed Date:  2010-10-04     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  0375040     Medline TA:  Endocrinology     Country:  United States    
Other Details:
Languages:  eng     Pagination:  4158-67     Citation Subset:  AIM; IM    
Affiliation:
Department of Anatomy and Cell Biology, Martin Luther University Faculty of Medicine, Grosse Steinstrasse 52, D-06097 Halle (Saale), Germany.
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MeSH Terms
Descriptor/Qualifier:
Alloxan
Animals
Apoptosis / physiology
Blastocyst / cytology,  metabolism*
Blood Glucose / metabolism
Diabetes Mellitus, Experimental / blood,  chemically induced,  physiopathology
Diabetes Mellitus, Type 1 / blood,  chemically induced,  physiopathology*
Embryo Culture Techniques
Embryo, Mammalian / cytology,  embryology,  metabolism
Enzyme-Linked Immunosorbent Assay
Female
Gastrulation / genetics,  physiology
Gene Expression Regulation, Developmental
Immunoblotting
In Situ Nick-End Labeling
Insulin / blood,  genetics*,  metabolism
Phosphoenolpyruvate Carboxykinase (ATP) / genetics,  metabolism
Pregnancy
Pregnancy in Diabetics / blood,  physiopathology
Rabbits
Receptor, IGF Type 1 / genetics*,  metabolism
Receptor, Insulin / genetics,  metabolism
Reverse Transcriptase Polymerase Chain Reaction
Chemical
Reg. No./Substance:
0/Blood Glucose; 11061-68-0/Insulin; 50-71-5/Alloxan; EC 2.7.10.1/Receptor, IGF Type 1; EC 2.7.10.1/Receptor, Insulin; EC 4.1.1.49/Phosphoenolpyruvate Carboxykinase (ATP)

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