Abstract：
:Embryo implantation requires a hospitable uterine environment. A key metabolic change that occurs during the peri-implantation period, and throughout early pregnancy, is the rise in endometrial glycogen content. Glycogen accumulation requires prior cellular uptake of glucose. Here we show that both human and murine endometrial epithelial cells express the high affinity Na+-coupled glucose carrier SGLT1. Ussing chamber experiments revealed electrogenic glucose transport across the endometrium in wild type (Slc5a1 +/+) but not in SGLT1 deficient (Slc5a1 -/-) mice. Endometrial glycogen content, litter size and weight of offspring at birth were significantly lower in Slc5a1 -/- mice. In humans, SLC5A1 expression was upregulated upon decidualization of primary endometrial stromal cells. Endometrial SLC5A1 expression during the implantation window was attenuated in patients with recurrent pregnancy loss when compared with control subjects. Our findings reveal a novel mechanism establishing adequate endometrial glycogen stores for pregnancy. Disruption of this histiotrophic pathway leads to adverse pregnancy outcome.
journal_name
Sci Repjournal_title
Scientific reportsauthors
Salker MS,Singh Y,Zeng N,Chen H,Zhang S,Umbach AT,Fakhri H,Kohlhofer U,Quintanilla-Martinez L,Durairaj RRP,Barros FSV,Vrljicak P,Ott S,Brucker SY,Wallwiener D,Vrhovac Madunić I,Breljak D,Sabolić I,Koepsell H,Brosensdoi
10.1038/s41598-017-11674-3subject
Has Abstractpub_date
2017-10-03 00:00:00pages
12612issue
1issn
2045-2322pii
10.1038/s41598-017-11674-3journal_volume
7pub_type
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