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Arhin SK, Zhao J, Ji X, et al. Multiple facilitated glucose transporters SLC2As are required for normal mouse preimplantation embryo development. Am J Transl Res. 2019;11(6):3412-3425
Arhin, S. K., Zhao, J., Ji, X., Shi, C., Tang, J., Gu, Y., Xi, H., Cheng, J., Qu, X., Shi, H., Jin, X., & Lv, J. (2019). Multiple facilitated glucose transporters SLC2As are required for normal mouse preimplantation embryo development. American journal of translational research, 11(6), 3412-3425.
Arhin, Samuel Kofi, et al. "Multiple facilitated glucose transporters SLC2As are required for normal mouse preimplantation embryo development." American journal of translational research vol. 11,6 (2019): 3412-3425.
Arhin SK, Zhao J, Ji X, Shi C, Tang J, Gu Y, Xi H, Cheng J, Qu X, Shi H, Jin X, Lv J. Multiple facilitated glucose transporters SLC2As are required for normal mouse preimplantation embryo development. Am J Transl Res. 2019 Jun 15;11(6):3412-3425. eCollection 2019. PMID: 31312354; PMCID: PMC6614635.
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Am J Transl Res. 2019 Jun 15;11(6):3412-3425. eCollection 2019.

Multiple facilitated glucose transporters SLC2As are required for normal mouse preimplantation embryo development.

American journal of translational research

Samuel Kofi Arhin, Junzhao Zhao, Xu Ji, Changgeng Shi, Jianan Tang, Yihua Gu, Haitao Xi, Jing Cheng, Xianqin Qu, Huijuan Shi, Xingliang Jin, Jieqiang Lv

Affiliations

  1. Reproductive Medicine Center, Department of Obstetrics and Gynecology, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University Wenzhou 325027, Zhejiang, China.
  2. Key Laboratory of Contraceptive Drugs and Devices, Shanghai Institute of Planned Parenthood Research Shanghai 200032, China.
  3. Sydney Center for Regenerative and Developmental Medicine, Kolling Institute for Medical Research, Sydney Medical School, University of Sydney St. Leonards 2065, NSW, Australia.

PMID: 31312354 PMCID: PMC6614635

Abstract

BACKGROUND: Glucose metabolism is an essential energy source for mammalian preimplantation embryonic development. Therefore, we aimed to analyze the expression of all 12 known glucose transporters (facilitated solute carrier family 2, Slc2a) during early mouse embryo development.

METHODS: Gene and protein expression of Slc2a transporters in oocytes and embryos were assessed by the TaqMan gene expression assay and confocal immunofluorescence, respectively.

RESULTS: Except for Slc2a2, the other 11 Slc2a transcripts were detected in oocytes. Transcripts of Slc2a1, Slc2a3, Slc2a4, and Slc2a8 were the most enriched and detected in preimplantation embryos. The transcription of other Slc2a isoforms was barely detectable or absent after fertilization; however, they were detected in blastocysts, except for Slc2a10 and Slc2a13. Embryo culture in the simple defined medium caused a reduction in transcription of Slc2a1, Slc2a3, Slc2a4, and Slc2a8 in blastocyst; yet, amino acids partially reversed this impaired transcription of Slc2a1 and Slc2a4. SLC2A1 and SLC2A4 proteins were detected at all embryonic stages with nuclear accumulation in the embryos at the early cleavage stage. SLC2A3 and SLC2A8 were not detected in embryos until the eight-cell stage. The cellular membrane localization of SLC2A1, SLC2A3, and SLC2A8 occurred after compaction and was characterized in blastocysts. SLC2A4 was evenly distributed in the cytoplasm and nuclei without its characteristic membrane localization. Indinavir sulfate (a SLC2A4 inhibitor) decreased the rate of development and prevented glucose utilization in embryos after compaction. These inhibitory activities were partially reversed by exogenous insulin.

CONCLUSION: The results unveil distinct expression patterns of individual Slc2a glucose transporters during early embryo development. Taken together, they provide novel insights into the understanding and management of glucose metabolic infertility in assisted-reproductive technologies (ART).

Keywords: Assisted reproductive technology; SLC2A; gene expression; glucose transporters; preimplantation embryo

Conflict of interest statement

None.

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