Meiotic Induction in Cumulus Cell-Enclosed Mouse Oocytes: Involvement of the Pentose Phosphate Pathway1

Downs, Stephen M.; Humpherson, Peter G.; Leese, Henry J.

doi:10.1095/biolreprod58.4.1084

Cited by 127 publications

(89 citation statements)

References 68 publications

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“…Ovulation induction elicited large rises in the rates of glucose consumption and lactate production (2.0-and 1.8-fold respectively), a mechanism that could be explained by upregulation of hexokinase activity (Downs et al 1998). During ovulation induction in vitro, the actual proportion of glucose metabolised glycolytically decreased significantly and, in conjunction with a major increase in glucose consumption, this indicates that a substantial portion of glucose was being metabolised by pathways other than glycolysis.…”

Section: Discussionmentioning

confidence: 95%

“…Several energy-demanding processes requiring ATP are known to be triggered by ovulation induction, such as progesterone production (Peluso 2006) and luteal cell differentiation (Boos et al 1988). Glucose is also necessary for cumulus expansion (Sutton-McDowall et al 2004) and purine synthesis (Downs et al 1998). The predominance of glycolytic energy production in large follicles is well documented (Boland et al 1993, Gull et al 1999, and the enzymatic machinery for oxidative glucose metabolism is already present at preantral stages, including human follicles (Roy & Terada 1999).…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Carbohydrate metabolism by murine ovarian follicles and oocytes grown in vitro

Harris¹,

Adriaens²,

Leese³

et al. 2007

Reproduction

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Metabolic markers are potentially valuable for assessment of follicle development in vitro. Carbohydrate metabolism of murine preantral follicles grown to maturity over 13 days in vitro has been measured, and metabolism of resulting oocyte-cumulus complexes (OCCs) and denuded oocytes has been compared with in vivo ovulated control counterparts. Spent follicle culture media were analysed for glucose, lactate and pyruvate concentrations. During follicle in vitro growth, glycolysis accounted for a rise from w24 to 60% of all glucose consumed. Ovulation induction caused a significant increase in glucose uptake and lactate production by in vitrogrown follicles to 71.7G1.2 and 96.6G4.8 nmoles/day respectively. OCCs grown in vitro had significantly higher rates of glucose consumption and lactate and pyruvate production (110.1G3.5, 191.8G8.9 and 31.7G1.7 pmoles/h respectively) than in vivo ovulated controls (67.4G8.1, 113.9G17.1 and 20.2G4.0 pmoles/h respectively), but a reduced capacity for pyruvate consumption (1.13G0.06 vs 1.49G0.06 pmoles/h by in vivo ovulated oocytes). Metabolism of OCCs was affected by the quality of the original follicle. In vitro-grown oocytes had a reduced cytoplasmic volume when compared with controls (168.3G2.0 vs 199.0G3.2 proportionately respectively) but a similar rate of metabolism per unit volume. Meiotic status influenced metabolism of both OCCs and denuded oocytes. In conclusion, glucose consumption and lactate production by cultured follicles increased in tandem with developmental progression and were stimulated prior to ovulation. Additionally, the metabolic profiles of in vitro produced OCCs and the oocytes within them are affected by long-term exposure to the culture environment. Reproduction (2007) 134 415-424

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Section: Discussionmentioning

confidence: 95%

Section: Discussionmentioning

confidence: 99%

Carbohydrate metabolism by murine ovarian follicles and oocytes grown in vitro

Harris¹,

Adriaens²,

Leese³

et al. 2007

Reproduction

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“…Another route of glucose consumption that has been shown to play a large role in oocyte maturation is the pentose phosphate pathway (Downs & Utecht 1999, Downs et al 1998. Towards the end of maturation, the increase flux of glucose though the pentose phosphate pathway allows increased production of substrates involved in nuclear maturation (Sutton et al 2003).…”

Section: Discussionmentioning

confidence: 99%

Metabolic markers of developmental competence for in vitro-matured mouse oocytes

Preis¹,

Seidel²,

Gardner³

2005

Reproduction

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In vitro maturation of oocytes has enormous potential in assisted reproductive technology, but its use has been limited due to insufficient knowledge of oocyte physiology during this dynamic period and lack of an adequate maturation system. The aim of this study was to characterize the metabolic profiles of three groups of oocytes throughout maturation: cumulus -oocyte complexes (COCs), denuded oocytes, and denuded oocytes co-cultured with cumulus cells. Mouse oocytes were collected from 28-day-old unstimulated females and matured in a defined medium. Oocytes were matured individually and transferred into fresh 0.5 ml drops of medium at 4 h intervals until 16 h. Ultramicrofluorimetry was used to quantitate carbohydrate consumption from and metabolite release into the medium. Glucose consumption and lactate production of COCs increased (P < 0.001) over the maturation interval (0 -16 h). Glucose consumption by COCs that subsequently fertilized was higher between 8-12 h of maturation than by COCs that did not fertilize (38 versus 29 pmol/COC per h, respectively; P < 0.01). Lactate production by COCs that subsequently fertilized was higher between 8-16 h of maturation, than by oocytes that did not fertilize (8 -12 h, 66 versus 46 pmol/COC per h, P < 0.01; 12-16 h, 56 versus 40 pmol/COC per h, respectively; P < 0.05). These data indicate that the final hours of maturation may hold a unique marker of oocyte competence, as during this time fertilizable COCs take up more glucose and produce more lactate than those not subsequently fertilized.

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“…When metabolized to 6-amino-NAD and 6-amino-NADP, this nucleotide behaves as a competitive inhibitor of NAD(P ϩ )-requiring dehydrogenases that would include G6PDH, 6-PGDH, and glutathione reductase (32,33,(42)(43)(44)(45)(46)48). 6-Amino-NADP is an extremely potent competitive inhibitor of 6-PGDH, and concentrations that do not affect G6PDH may completely block 6-PGDH (43).…”

Section: Discussionmentioning

confidence: 99%

Regulation of the Glucose-6-phosphatase Gene by Glucose Occurs by Transcriptional and Post-transcriptional Mechanisms

Massillon¹

2001

Journal of Biological Chemistry

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To understand how glucose regulates the expression of the glucose-6-phosphatase gene, the effect of glucose was studied in primary cultures of rat hepatocytes. Glucose-6-phosphatase mRNA levels increased about 10-fold when hepatocytes were incubated with 20 mM glucose. The rate of transcription of the glucose-6-phosphatase gene increased about 3-fold in hepatocytes incubated with glucose. The half-life of glucose-6-phosphatase mRNA was estimated to be 90 min in the absence of glucose and 3 h in its presence. Inhibition of the oxidative and the nonoxidative branches of the pentose phosphate pathway blocked the stimulation of glucose-6-phosphatase expression by glucose but not by xylitol or carbohydrates that enter the glycolytic/gluconeogenic pathways at the level of the triose phosphates. These results indicate that (i) the glucose induction of the mRNA for the catalytic unit of glucose-6-phosphatase occurs by transcriptional and post-transcriptional mechanisms and that (ii) xylitol and glucose increase the expression of this gene through different signaling pathways.Glc-6-Pase 1 (EC 3.1.3.9) is a multicomponent protein complex comprising catalytic and transporting entities (1-5). The complex is tightly associated with the endoplasmic reticulum, and the enzymatic component catalyzes the hydrolysis of glucose 6-phosphate to glucose, a final common step to both the pathways of glycogenolysis and gluconeogenesis. Hepatic Glc-6-Pase activity is effectively regulated by hormonal and nutritional status. For example, fasting and hormones that increase cAMP concentration stimulate its gene expression while refeeding and insulin decrease it (1, 2, 6 -12).The expression of the genes for several other proteins is regulated by glucose; these include genes for L-type pyruvate kinase (13, 14), fatty-acid synthase (15, 16), PEPCK (17, 18), and the type 2 glucose transporter (GLUT-2) (19,20). The mechanism by which glucose regulates the expression of these genes remains largely unknown. Recently, Kahn and colleagues (21, 22) have proposed a signaling pathway model to explain the molecular mechanism by which glucose regulates the expression of the L-type pyruvate kinase. This model consists of the following details: (i) the presence of glucose is sensed in the cell; (ii) this information is transduced by intracellular messengers; (iii) a second messenger, presumably xylulose 5-phosphate, rises and then modulates the activity of protein kinase and protein phosphatase involved in a cascade of phosphorylation/dephosphorylation. This cascade then leads to a modification of the phosphorylation state of the glucoseresponsive complex, followed by an increase in the transcriptional rate of the target gene. In this model, the presence of an active glucokinase that phosphorylates glucose to glucose 6-phosphate (Glc-6-P) is paramount.The molecular mechanism by which glucose regulates the expression of the Glc-6-Pase gene is currently unknown. Here we show that glucose regulation of the expression of this gene involves metabolism of glucose...

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Meiotic Induction in Cumulus Cell-Enclosed Mouse Oocytes: Involvement of the Pentose Phosphate Pathway1

Cited by 127 publications

References 68 publications

Carbohydrate metabolism by murine ovarian follicles and oocytes grown in vitro

Carbohydrate metabolism by murine ovarian follicles and oocytes grown in vitro

Metabolic markers of developmental competence for in vitro-matured mouse oocytes

Regulation of the Glucose-6-phosphatase Gene by Glucose Occurs by Transcriptional and Post-transcriptional Mechanisms

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