Glucose Transporter 8 Expression and Translocation Are Critical for Murine Blastocyst Survival1

Pinto, Anil; Carayannopoulos, Mary O.; Hoehn, Amanda; Dowd, Lia O.; Moley, Kelle H.

doi:10.1095/biolreprod66.6.1729

Cited by 84 publications

(68 citation statements)

References 35 publications

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“…On the other hand, GLUT8 is responsible for insulin-stimulated glucose transport in blastocysts [134] where it is crucial for embryonic development and survival. Embryos exposed to GLUT8 antisense oligo(deoxy)nucleotides demonstrated increased apoptosis in nuclei [140]. GLUT8 gene expression decreased following glucose deprivation or hypoxia in cultured, differentiated 3T3-L1 adipocytes; however, the conditions tested were beyond the physiologic range [137].…”

Section: Glut8mentioning

confidence: 96%

What we know about facilitative glucose transporters: Lessons from cultured cells, animal models, and human studies

Gorovits

Charron

2003

Biochem Molecular Bio Educ

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Glucose uptake by all cells in the organism by glucose transport proteins is among the most essential processes in life. The process of glucose uptake into tissues is performed by glucose transporters. This review focuses on the biology of facilitative glucose transporters (GLUTs). The knowledge that has accumulated for more than a decade with respect to the regulation of GLUT expression and function in various experimental conditions points to the great potential for GLUTs to be utilized as targets for designing therapies for treatment of diseases related to impaired regulation of glucose homeostasis including type 2 diabetes.Keywords: Glucose uptake, GLUT, insulin action, diabetes.The entry of glucose into cells is a crucial step in lifesupporting processes since glucose is the main monosaccharide in nature that provides carbon and energy for almost all cells. The passage of glucose into cells depends on different parameters, including expression of the appropriate glucose transporters in the target tissues and hormonal regulation of their function. Single cell eucaryotes such as Saccharomyces cerevisiae possess 20 genes encoding glucose or glucose-like transporters and express the glucose transporters most appropriate for the amount of glucose available [1]. In mammalian cells a tight regulation of blood glucose levels is needed to meet the energetic demands of the brain, a tissue that uses glucose as its primary energy source [2,3]. Adequate glucose flux into tissues provides maintenance of glucose homeostasis that is critical in well being. Transport of glucose across the plasma membrane is accomplished by two families of glucose transporters: sodium-glucose co-transporters (SGLT 1 1-3), mainly expressed in the apical membrane of renal and intestinal absorptive epithelial cells that transport glucose against its concentration gradient and utilize ATP (for a review, see Ref. 4), and facilitative glucose transporters (GLUTs) that are expressed in all cells that transport glucose down a concentration gradient [5][6][7]. Until now the search for the mammalian facilitative glucose transporters has yielded 12 carriers including GLUT1-5 and the recently discovered GLUT6 -12. GLUT1-4 share greater than 40% homology [8], and GLUT5, which is a fructose transporter, exhibits 42, 40, 38, and 41.6% identity with GLUT1, GLUT2, GLUT3, and GLUT4, respectively [9]. All GLUTs have been predicted to have 12 membrane-spanning domains (helices) connected by hydrophilic loops, the first of which is exofacial and contains an N-glycosylation site in GLUT1-5 (Fig. 1) [8,10]. Both the amino and carboxyl termini of GLUTs reside on the cytoplasmic side of the cell membrane [11]. The carboxyl termini of all GLUTs have unique amino acid sequences that have been utilized for development of reagents. The common sensitivity of the GLUT family to the inhibitory action of the fungal metabolite cytochalasin B has been reported widely and is utilized in studies of hexose transporters [12]. Substrate selectivity of GLUTs is dictated by conserve...

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Section: Glut8mentioning

confidence: 96%

What we know about facilitative glucose transporters: Lessons from cultured cells, animal models, and human studies

Gorovits

Charron

2003

Biochem Molecular Bio Educ

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“…KDMEM, which is commonly used for ES cell derivation and maintenance of mouse and human ES cell lines (Amit et al, 2000;Roach and Mcneish, 2002), contains high glucose (4500 mg/L). It has been reported that early preimplantation stage embryos (one-cell to morula stage embryos) differ from blastocysts in terms of their glucose consumption because glucose consumption increases dramatically after the morula stage, as the blastocoel forms within the blastocyst (Pinto et al, 2002). The lack of a significant effect of glucose levels for the efficiency of ES cell derivation in the present study may be due to the transition timing of development for glucose uptake.…”

Section: Preblastocyst- Blastocyst-derived Escs Are Highly Similarmentioning

confidence: 51%

Established Preblastocyst- and Blastocyst-Derived ES Cell Lines Have Highly Similar Gene Expression Profiles, Despite Their Differing Requirements for Derivation Culture Conditions

Kim

Park

Amano

et al. 2012

Cellular Reprogramming

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The efficiency of embryonic stem (ES) cell derivation relies on an optimized culture medium and techniques for treating preimplantation stage embryos. Recently, ES cell derivation from the preblastocyst developmental stage was reported by removing the zona pellucida from embryos of the most efficient strain for ES cell derivation (129Sv) during early preimplantation. Here, we showed that ES cells can be efficiently derived and maintained in a modified medium (MEMa), from preblastocysts of a low-efficiency mouse strain (a hybrid consisting of 50% B6, 25% CBA, and 25% DBA). Preblastocyst-derived ES cell lines were normal in terms of pluripotency-related protein expression, and chromosome number. Also, preblastocyst-derived ES cell lines from various culture conditions showed pluripotency in vivo through teratoma analysis. Interestingly, ES cell lines produced from preblastocysts and blastocysts, regardless of the derivation culture conditions, are nearly indistinguishable by their global gene expression profiles.

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“…We have previously shown that a decrease in glucose transport results in apoptosis at the blastocyst stage (Pinto et al 2002a). Because AMPK activation has been linked with glucose uptake (Ye et al 2006), we investigated whether activation of AMPK with the AMPK activator AICAR results in a change in 2-deoxyglucose uptake in TS cells transfected with Igf1r siRNA.…”

Section: Resultsmentioning

confidence: 99%

“…AMPK activators reverse Igf1r siRNA-induced decreases in 2-deoxyglucose uptake and SLC2A8 cell surface expression Insulin-regulated embryonic transporter SLC2A8 (GLUT8) is necessary for murine blastocyst survival (Pinto et al 2002a). We have previously shown that a decrease in glucose transport results in apoptosis at the blastocyst stage (Pinto et al 2002a).…”

Section: Resultsmentioning

confidence: 99%

Crosstalk between the AMP-activated kinase and insulin signaling pathways rescues murine blastocyst cells from insulin resistance

Louden¹,

Maggie²,

Moley³

2008

Reproduction

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Maternal insulin resistance results in poor pregnancy outcomes. In vivo and in vitro exposure of the murine blastocyst to high insulin or IGF1 results in the down-regulation of the IGF1 receptor (IGF1R). This in turn leads to decreased glucose uptake, increased apoptosis, as well as pregnancy resorption and growth restriction. Recent studies have shown that blastocyst activation of AMP-activated protein kinase (AMPK) reverses these detrimental effects; however, the mechanism was not clear. The objective of this study was to determine how AMPK activation rescues the insulin-resistant blastocyst. Using trophoblast stem (TS) cells derived from the blastocyst, insulin resistance was recreated by transfecting with siRNA to Igf1r and down-regulating expression of the protein. These cells were then exposed to AMPK activators 5-aminoimidazole-4-carboxamide riboside and phenformin, and evaluated for apoptosis, insulin-stimulated 2-deoxyglucose uptake, PI3-kinase activity, and levels of phospho-AKT, phospho-mTor, and phospho-70S6K. Surprisingly, disrupted insulin signaling led to decreased AMPK activity in TS cells. Activators reversed these effects by increasing the AMP/ATP ratio. Moreover, this treatment increased insulin-stimulated 2-deoxyglucose transport and cell survival, and led to an increase in PI3-kinase activity, as well as increased P-mTOR and p70S6K levels. This study is the first to demonstrate significant crosstalk between the AMPK and insulin signaling pathways in embryonic cells, specifically the enhanced response of PI3K/AKT/mTOR to AMPK activation. Decreased insulin signaling also resulted in decreased AMPK activation. These findings provide mechanistic targets in the AMPK signaling pathway that may be essential for improved pregnancy success in insulin-resistant states.

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Glucose Transporter 8 Expression and Translocation Are Critical for Murine Blastocyst Survival1

Cited by 84 publications

References 35 publications

What we know about facilitative glucose transporters: Lessons from cultured cells, animal models, and human studies

What we know about facilitative glucose transporters: Lessons from cultured cells, animal models, and human studies

Established Preblastocyst- and Blastocyst-Derived ES Cell Lines Have Highly Similar Gene Expression Profiles, Despite Their Differing Requirements for Derivation Culture Conditions

Crosstalk between the AMP-activated kinase and insulin signaling pathways rescues murine blastocyst cells from insulin resistance

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