| Mink uterine glycogen reserves are greatest during estrus and mobilized to near completion as pre-embryos develop into blastocysts and enter a state of dormancy or diapause, before implantation. Our findings suggest that during estrus, estradiol (E2) increases uterine glandular and luminal epithelial cell glycogen production, not directly, but by enhancing the actions of insulin on the cells. After ovulation, progesterone (P4) acts directly on uterine cells, promoting the rapid mobilization of glycogen reserves by increasing glycogen catabolism and inhibiting glycogen synthesis. We hypothesize that uterine intra-luminal glucose concentrations during pre-embryonic development to the blastocyst stage are determined by and perhaps correlated with circulating P4 concentrations. Because developing blastocysts, have an absolute requirement for glucose, our findings of increased insulin receptor expression by the glandular and luminal epithelium during diapause suggests to us that increased uterine sensitivity to insulin and glucose uptake at this time may be requisite to reactivation of the dormant blastocyst and implantation. |