| First Author | Salker MS | Year | 2017 |
| Journal | Sci Rep | Volume | 7 |
| Issue | 1 | Pages | 12612 |
| PubMed ID | 28974690 | Mgi Jnum | J:255764 |
| Mgi Id | MGI:6109856 | Doi | 10.1038/s41598-017-11674-3 |
| Citation | Salker MS, et al. (2017) Loss of Endometrial Sodium Glucose Cotransporter SGLT1 is Detrimental to Embryo Survival and Fetal Growth in Pregnancy. Sci Rep 7(1):12612 |
| abstractText | 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. |
