A study of carbohydrate metabolism in 'delayed' and 'activated' mouse blastocyst and uterus

Sakhuja, Deepa; Sengupta, Jayasree; Manchanda, Smita

doi:10.1677/joe.0.0950283

Cited by 8 publications

(4 citation statements)

References 15 publications

(17 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…As found by Weitlauf & Kiessling (1980), our results show that metabolic activation in vitro is not accompanied by an increase in cell numbers, while activation in utero resulted in a significantly higher number of blastomeres. Our earlier study (Sakhuja et al, 1982) had shown that dormant blastocysts exhibited significantly higher levels of PFK and PK, in comparison to normal implanting or delayed and activated blastocysts. We have now observed that within 6 h after activation in utero and in vitro there was a sharp decline in PFK and PK levels and, thereafter, steady states were maintained during the next 18 h, the levels at this time being similar to those found in normally implanting embryos.…”

Section: Discussionmentioning

confidence: 89%

“…Studies on carbohydrate metabolism during delay of implantation suggest that there is a depression of metabolic functions in the quiescent blastocyst, with reduced C02 output (Menke & McLaren, 1970) and oxygen consumption (Nilsson, Magnusson, Widehn & Hillensjo, 1982). Nevertheless, there are elevated levels of phosphofructokinase, pyruvate kinase and low lactate dehydrogenase in delayed mouse blastocysts, which returned to normal preimplantation levels upon activation with oestradiol-17ß (Sakhuja, Sengupta & Manchanda, 1982). It is not clear whether this represents heightened function of glycolysis in the delayed blastocysts or whether the enzymes showed high levels but may not have been in an active state.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Carbohydrate metabolism in 'delayed implanting' mouse blastocysts undergoing activation in utero and in vitro

Sakhuja-Talwar¹,

Sengupta²,

Manchanda³

1984

Reproduction

Self Cite

View full text Add to dashboard Cite

Delayed blastocysts were activated by injecting oestradiol-17 beta to delayed implanting mice or by exposure to culture medium lacking serum. Four enzymes of carbohydrate metabolism (phosphofructokinase, pyruvate kinase, lactate dehydrogenase, malate dehydrogenase) were studied at different time periods and specific time-dependent changes were found during activation. A characteristic feature was a marked decline by 6 h in the activities of phosphofructokinase and pyruvate kinase. Blastocyst activation in vitro and in utero showed similar trends in metabolic patterns during the 24-h period studied.

show abstract

Section: Discussionmentioning

confidence: 89%

Section: Introductionmentioning

confidence: 99%

Carbohydrate metabolism in 'delayed implanting' mouse blastocysts undergoing activation in utero and in vitro

Sakhuja-Talwar¹,

Sengupta²,

Manchanda³

1984

Reproduction

Self Cite

View full text Add to dashboard Cite

show abstract

“…Lacto-N-Fucopentaose-1, a possible ligand of galectin-1 (Sparrow et al, 1987), is found on the surface of the uterine epithelium, when it becomes more abundant and restricted to specific areas immediately prior to implantation (Lindenberg et al, 1988). The levels of galectin-1 mRNA during pseudopregnant or delay of implantation were compatible with carbohydrate metabolism in the uterus which remained essentially unchanged during the delay period (Sakhuja et al, 1982). In addition, the secreted galectin-1 in the uterine lumen may bind a galactosecontaining cell surface epitope present on the embryonic surface.…”

Section: Discussionmentioning

confidence: 99%

Expression of galectin‐1 mRNA in the mouse uterus is under the control of ovarian steroids during blastocyst implantation

Choe

Choi

et al. 1997

Mol. Reprod. Dev.

View full text Add to dashboard Cite

Galectin-1 is a member of beta-galactoside-binding lectins expressed in a variety of mammalian tissues. We report here that galectin-1 mRNA is abundantly expressed in the mouse reproductive organs such as the uterus and ovary. Uterine expression of galectin-1 mRNA is specifically regulated in the embryonic implantation process. Its expression increased at a high level on the fifth day post coitum (dpc 5) when embryos hatched into the endometrial epithelial cells. In the absence of embryos, however, galectin-1 expression in the mouse uterus decreased on dpc 5. In the delayed implantation mice, galectin-1 mRNA levels was augmented by the termination of the delay of implantation. Ovarian steroids progesterone and estrogen differentially regulated galectin-1 mRNA level in uterine tissues. Treatment with RU486, a progesterone receptor antagonist, blocked progesterone-induced galectin-1 mRNA level in uterine tissues of ovariectomized mouse. ICI182780, a pure estrogen receptor antagonist, clearly blocked the estrogen effect. Taken together, galectin-1 gene expression in the uterine tissues was regulated by ovarian steroids and this regulation correlated with the implantation process.

show abstract

“…In contrast, glucose uptake remains basal until 16 h, but increases thereafter after activation of dormant blastocysts (14), suggesting that pyruvate is a major source of energy during the early stages of blastocyst activation. In contrast, evidence showing increased activity of phosphofructokinase and pyruvate kinase with decreased lactate dehydrogenase activity in dormant blastocysts (20) suggests that energy requirement during blastocyst activation is glucose dependent. Our results of significant increases in Pfkl (phosphofructokinase, liver, B-type), Eno1 (enolase 1␣, nonneuron), Pgk1 (phosphoglycerate kinase 1), Pkm2 (pyruvate kinase, muscle), and Ldh1 (lactate dehydrogenase 1, A chain) in activated blastocysts suggest that increased energy requirements during activation are satisfied by both glucose and pyruvate energy pathways.…”

Section: Carbohydrate Metabolic and Energy Pathways Are Differentiallymentioning

confidence: 93%

Global gene expression analysis identifies molecular pathways distinguishing blastocyst dormancy and activation

Hamatani

Daikoku

Wang

et al. 2004

Proc. Natl. Acad. Sci. U.S.A.

227

234

View full text Add to dashboard Cite

Delayed implantation (embryonic diapause) occurs when the embryo at the blastocyst stage achieves a state of suspended animation. During this period, blastocyst growth is very slow, with minimal or no cell division. Nearly 100 mammals in seven different orders undergo delayed implantation, but the underlying molecular mechanisms that direct this process remain largely unknown. In mice, ovariectomy before preimplantation ovarian estrogen secretion on day 4 of pregnancy initiates blastocyst dormancy, which normally lasts for 1-2 weeks by continued progesterone treatment, although blastocyst survival decreases with time. An estrogen injection rapidly activates blastocysts and initiates their implantation in the progesterone-primed uterus. Using this model, here we show that among Ϸ20,000 genes examined, only 229 are differentially expressed between dormant and activated blastocysts. The major functional categories of altered genes include the cell cycle, cell signaling, and energy metabolic pathways, particularly highlighting the importance of heparin-binding epidermal growth factor-like signaling in blastocyst-uterine crosstalk in implantation. The results provide evidence that the two different physiological states of the blastocyst, dormancy and activation, are molecularly distinguishable in a global perspective and underscore the importance of specific molecular pathways in these processes. This study has identified candidate genes that provide a scope for in-depth analysis of their functions and an opportunity for examining their relevance to blastocyst dormancy and activation in numerous other species for which microarray analysis is not available or possible due to very limited availability of blastocysts.S uccessful implantation results from reciprocal interactions between an implantation-competent blastocyst and a receptive uterus. Highly coordinated cellular and molecular events, directed by ovarian estrogen and progesterone (P 4 ), produce a favorable uterine environment, the receptive state, to support implantation. The blastocyst also functions as an active unit with its own molecular program of cell growth and differentiation (1, 2). It is difficult to distinguish embryonic and uterine events during normal pregnancy with respect to blastocyst activation and uterine receptivity because of the changing levels of ovarian hormones. Because estrogen is essential for on-time uterine receptivity and blastocyst activation in mice (3), ovariectomy before preimplantation estrogen secretion on the morning of day 4 results in implantation failure, initiating a state of blastocyst dormancy. This condition, referred as delayed implantation, can be maintained by continued P 4 treatment. However, implantation with blastocyst activation rapidly occurs by an estrogen injection in P 4 -primed mice (3, 4). Delayed implantation also occurs naturally (facultative) during lactation after postpartum ovulation and successful mating in mice; implantation occurs after termination of the suckling stimulus (5). Lactational delay ...

show abstract

A study of carbohydrate metabolism in 'delayed' and 'activated' mouse blastocyst and uterus

Cited by 8 publications

References 15 publications

Carbohydrate metabolism in 'delayed implanting' mouse blastocysts undergoing activation in utero and in vitro

Carbohydrate metabolism in 'delayed implanting' mouse blastocysts undergoing activation in utero and in vitro

Expression of galectin‐1 mRNA in the mouse uterus is under the control of ovarian steroids during blastocyst implantation

Global gene expression analysis identifies molecular pathways distinguishing blastocyst dormancy and activation

Contact Info

Product

Resources

About