This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Riley, J. K Articles by Moley, K. H Search for Related Content PubMed PubMed Citation Articles by Riley, J. K Articles by Moley, K. H

Glucose utilization and the PI3-K pathway: mechanisms for cell survival in preimplantation embryos

¹ Department of Obstetrics and Gynecology and the ² Department of Cell Biology and Physiology, Washington University School of Medicine, 4911 Barnes-Jewish Hospital Plaza, St Louis, Missouri 63110, USA

Correspondence should be addressed to KH Moley; Email: moleyk{at}wustl.edu

The maintenance of optimal glucose utilization during the preimplantation period is critical for embryo survival. A decrease in glucose transport during preimplantation development has been linked to the early steps of programmed cell death in these embryos. Decreased glucose transport is not thought to be simply a consequence of cell death, rather it is thought to be a trigger that can initiate the apoptotic cascade. Extensive apoptosis during the preimplantation period may manifest later in pregnancy as a malformation – or miscarriage, if cell loss is excessive. Phosphatidylinositol 3-kinase (PI3-K) is a known regulator of a number of physiologic responses including cellular proliferation, growth, and survival as well as glucose metabolism. Studies performed in other cell systems have demonstrated that the PI3-K pathway plays a critical role in maintaining glucose transport and metabolism. This review will present the current evidence that suggests that PI3-K is vital for preimplantation embryo survival and development. In addition, data demonstrating that PI3-K activity is important for glucose metabolism during this early developmental period will be discussed.

This article has been cited by other articles:

				S. T. Kim and K. H. Moley Regulation of Facilitative Glucose Transporters and AKT/MAPK/PRKAA Signaling via Estradiol and Progesterone in the Mouse Uterine Epithelium Biol Reprod, July 1, 2009; 81(1): 188 - 198. [Abstract] [Full Text] [PDF]

				H. Gao, G. Wu, T. E. Spencer, G. A. Johnson, X. Li, and F. W. Bazer Select Nutrients in the Ovine Uterine Lumen. I. Amino Acids, Glucose, and Ions in Uterine Lumenal Flushings of Cyclic and Pregnant Ewes Biol Reprod, January 1, 2009; 80(1): 86 - 93. [Abstract] [Full Text] [PDF]

				H. Gao, G. Wu, T. E. Spencer, G. A. Johnson, and F. W. Bazer Select Nutrients in the Ovine Uterine Lumen. II. Glucose Transporters in the Uterus and Peri-Implantation Conceptuses Biol Reprod, January 1, 2009; 80(1): 94 - 104. [Abstract] [Full Text] [PDF]

				E. Louden, M. M Chi, and K. H Moley Crosstalk between the AMP-activated kinase and insulin signaling pathways rescues murine blastocyst cells from insulin resistance Reproduction, September 1, 2008; 136(3): 335 - 344. [Abstract] [Full Text] [PDF]

				J. Adjaye, R. Herwig, T. C. Brink, D. Herrmann, B. Greber, S. Sudheer, D. Groth, J. W. Carnwath, H. Lehrach, and H. Niemann Conserved molecular portraits of bovine and human blastocysts as a consequence of the transition from maternal to embryonic control of gene expression Physiol Genomics, October 19, 2007; 31(2): 315 - 327. [Abstract] [Full Text] [PDF]

				Sung Tae Kim and K. H. Moley The Expression of GLUT8, GLUT9a, and GLUT9b in the Mouse Testis and Sperm Reproductive Sciences, July 1, 2007; 14(5): 445 - 455. [Abstract] [PDF]