Estradiol stimulates glycogen synthesis whereas progesterone promotes glycogen catabolism in the uterus of the American mink (<i>Neovison vison</i>)

Bowman, Kole; Rose, Jack

doi:10.1111/asj.12564

Cited by 21 publications

(28 citation statements)

References 33 publications

(31 reference statements)

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“…Uterine glycogen synthesis is stimulated by estradiol (E 2 ) in mink (Bowman & Rose, ; Rose, Hunt, Shelton, Wyler, & Mecham, ), which agrees with similar findings for rats, rabbits and guinea pigs (Demers & Jacobs, ; Demers et al, ). However, it is not known if E 2 acts directly to control uterine glycogen synthesis or has permissive actions that enhance glycogen synthesis in response to other hormones.…”

Section: Introductionsupporting

confidence: 74%

“…Although exogenous E 2 increased uterine glycogen synthesis in vivo in different mammals (Demers & Jacobs, ; Demers et al, ; Greenstreet & Fotherby, ) including mink (Bowman & Rose, ; Rose et al, ;) we show here that E 2 alone failed to increase glycogen synthesis by GMMe cells (Figure a). Interestingly, treatment of GMMe cells with insulin (50 µg/ml) alone, significantly increased glycogen content when compared to controls (Figure b).…”

Section: Discussionmentioning

confidence: 46%

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Activation of the IGF1 receptor stimulates glycogen synthesis by mink uterine epithelial cells

Dean

Rose

2018

Molecular Reproduction Devel

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Glycogen synthesis by mink uterine epithelial cells is stimulated by estradiol (E ) during estrus, although the mechanism/s through which the steroid promotes glycogen accumulation are unknown. Our aim was to determine if insulin is required for E induced glycogen synthesis by an immortalized mink uterine epithelial cell line (GMMe). We show that the cells expressed the genes for glycogen metabolizing enzymes (hexokinase 1, glucose-6-phosphatase 3, glycogen synthase 1, and glycogen phosphorylase-muscle), receptors for insulin, insulin-like growth factor 1 and E (Esr1). Interestingly, treatment of cells with E alone failed to stimulate glycogen production, whereas supraphysiological concentrations of insulin (50 μg/ml) only, significantly increased glycogen content. Moreover, insulin + E increased glycogen content when compared to insulin alone (p < 0.05), an affect that was blocked when cells were treated with the pure E receptor antagonist ICI 182,780. Glycogen synthesis in response to insulin was significantly inhibited when cells were pre-treated with picropodophyllotoxin, an IGF1R antagonist. Treatment of cells with LY294002, a phosphatidylinositol 3-kinase (PI3K) antagonist, blocked insulin's effects on glycogen production whereas treatment with U0126, an inhibitor of mitogen activated kinase-kinase (MEK1/2) was without effect. These findings suggest to us that the affects of E on glycogen synthesis by GMMe cells is mediated through Esr1 and increased responsiveness of the cells to insulin. Because picropodophylotoxin blocked the effects of insulin on glycogen production, and both insulin and IGF1 act through PI3K, it is possible that IGF1 plays a role in glycogen production by these cells.

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Section: Introductionsupporting

confidence: 74%

Section: Discussionmentioning

confidence: 46%

Activation of the IGF1 receptor stimulates glycogen synthesis by mink uterine epithelial cells

Dean

Rose

2018

Molecular Reproduction Devel

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“…In pigs and rabbits, reserves of glycogen in the oviducts were highest near ovulation and decreased during the following luteal phase [40,41]. Furthermore, the hormonal control of endometrial glycogen has been well studied in rats, rabbits, and mink, where P4 promotes glycogen catabolism while E2 stimulates uterine glycogen synthesis and storage [36,42,43]. Altogether, these data suggest that the products of glycogen catabolism in the oviduct epithelium are abundantly released in oEVs under P4 action during the luteal phase and that this process is inhibited by E2 during estrus.…”

Section: Discussionmentioning

confidence: 99%

Metabolomic Profile of Oviductal Extracellular Vesicles across the Estrous Cycle in Cattle

Gatien

Mermillod

Tsikis

et al. 2019

IJMS

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Oviductal extracellular vesicles (oEVs) have been proposed as key modulators of gamete/embryo maternal interactions. The aim of this study was to examine the metabolite content of oEVs and its regulation across the estrous cycle in cattle. Oviductal EVs were isolated from bovine oviducts ipsilateral and contralateral to ovulation at four stages of the estrous cycle (post-ovulatory stage, early and late luteal phases, and pre-ovulatory stage). The metabolomic profiling of EVs was performed by proton nuclear magnetic resonance spectroscopy (NMR). NMR identified 22 metabolites in oEVs, among which 15 were quantified. Lactate, myoinositol, and glycine were the most abundant metabolites throughout the estrous cycle. The side relative to ovulation had no effect on the oEVs' metabolite concentrations. However, levels of glucose-1-phosphate and maltose were greatly affected by the cycle stage, showing up to 100-fold higher levels at the luteal phase than at the peri-ovulatory phases. In contrast, levels of methionine were significantly higher at peri-ovulatory phases than at the late-luteal phase. Quantitative enrichment analyses of oEV-metabolites across the cycle evidenced several significantly regulated metabolic pathways related to sucrose, glucose, and lactose metabolism. This study provides the first metabolomic characterization of oEVs, increasing our understanding of the potential role of oEVs in promoting fertilization and early embryo development.

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“…They also represent a source of mink enzymes, for which few K m s have been determined under any conditions [24]. This also isolates the behavior of epithelial cells where most of the glycogen is stored [19,20], compared with the in vivo studies which work with homogenized uterine tissue containing both stromal and epithelial tissues. P 4 and E 2 affect enzymes involved in glucose and glycogen metabolism in the mink endometrium.…”

Section: Introductionmentioning

confidence: 92%

“…Mink exhibit an obligatory embryonic diapause, often having blastocysts suspended 50-60 days post-coitum. P 4 stimulates uterine glycogen catabolism in the mink endometrium, whereas E 2 promotes glycogen accumulation in vivo [19,20] and in cultured cells in the presence of insulin. The mechanisms by which E 2 and P 4 directly affect glycolysis and its enzymes in uteri have not been determined in mink and other mammals because of the confounding effect of hormones such as insulin.…”

Section: Introductionmentioning

confidence: 99%

Estradiol and progesterone affect enzymes but not glucose consumption in a mink uterine cell line (GMMe)

2020

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Cells lining the uterus are responsible for storage and secretion of carbohydrates to support early embryonic development. Histotrophic secretions contain glycogen and glycolytic products such as lactate and pyruvate. Insufficient carbohydrate storage as glycogen has been correlated with infertility in women. While it is clear that changes in estrogen (17-β-estradiol (E2)) and progesterone (P4) in vivo affect the distribution of glucose in the uterine cells and secretions, the biochemical mechanism(s) by which they affect this crucial allocation is not well understood. Furthermore, in cultured uterine cells, neither E2 nor P4 affect glycogen storage without insulin present. We hypothesized that P4 and E2 alone affect the activity of glycolytic enzymes, glucose and glycolytic flux to increase glycogen storage (E2) and catabolism (P4) and increase pyruvate and lactate levels in culture. We measured the rate of glucose uptake and glycolysis in a mink immortalized epithelial cell line (GMMe) after 24-h exposure to 10 μM P4 and 10 nM E2 (pharmacologic levels) at 5 mM glucose and determined the kinetic parameters (Vmax, Km) of all enzymes. While the activities of many glycolytic enzymes in GMMe cells were shown to be decreased by E2 treatment, in contrast, glucose uptake, glycolytic flux and metabolites levels were not affected by the treatments. The cellular rationale for P4- and E2-induced decreases in the activity of enzymes may be to prime the system for other regulators such as insulin. In vivo, E2 and P4 may be necessary but not sufficient signals for uterine cycle carbohydrate allocation.

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

Cited by 21 publications

References 33 publications

Activation of the IGF1 receptor stimulates glycogen synthesis by mink uterine epithelial cells

Activation of the IGF1 receptor stimulates glycogen synthesis by mink uterine epithelial cells

Metabolomic Profile of Oviductal Extracellular Vesicles across the Estrous Cycle in Cattle

Estradiol and progesterone affect enzymes but not glucose consumption in a mink uterine cell line (GMMe)

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