Estradiol stimulates glycogen synthesis whereas progesterone promotes glycogen catabolism in the uterus of the American mink (Neovison vison).

Glycogen synthesis by mink uterine glandular and luminal epithelia (GE and LE) is stimulated by estradiol (E ) during estrus. Subsequently, the glycogen deposits are mobilized to near completion to meet the energy requirements of pre-embryonic development and implantation by as yet undetermined mechanisms. We hypothesized that progesterone (P ) was responsible for catabolism of uterine glycogen reserves as one of its actions to ensure reproductive success. Mink were treated with E , P or vehicle (controls) for 3 days and uteri collected 24 h (E , P and vehicle) and 96 h (E ) later. To evaluate E priming, mink were treated with E for 3 days, then P for an additional 3 days (E →P ) and uteri collected 24 h later. Percent glycogen content of uterine epithelia was greater at E + 96 h (GE = 5.71 ± 0.55; LE = 11.54 ± 2.32) than E +24 h (GE = 3.63 ± 0.71; LE = 2.82 ± 1.03), and both were higher than controls (GE = 0.27 ± 0.15; LE = 0.54 ± 0.30; P < 0.05). Treatment as E →P reduced glycogen content (GE = 0.61 ± 0.16; LE = 0.51 ± 0.13), to levels not different from controls, while concomitantly increasing catabolic enzyme (glycogen phosphorylase m and glucose-6-phosphatase) gene expression and amount of phospho-glycogen synthase protein (inactive) in uterine homogenates. Interestingly, E →P increased glycogen synthase 1 messenger RNA (mRNA) and hexokinase 1mRNA and protein. Our findings suggest to us that while E promotes glycogen accumulation by the mink uterus during estrus and pregnancy, it is P that induces uterine glycogen catabolism, releasing the glucose that is essential to support pre-embryonic survival and implantation.