Decreased spermatogenesis, fertility, and altered Slc2A expression in Akt1-/- and Akt2-/- testes and sperm.
Akt is serine/threonine protein kinase associated with various                    cellular processes and 3 different isoforms exist. This work describes the                    reproductive phenotype of Akt1-/- and Akt2-/-                    in male mice. The seminiferous tubule diameter in Akt1-/-                    testes was less than wild-type or Akt2-/- testes. The                    expression of phospho-phosphatase and tensin homologue deleted on chromosome 10                    (p-PTEN) and phospho-glycogen synthase kinase 3β (GSK-3β) was elevated in                        Akt1-/- testes. Alterations in expression and localization                    to the plasma membrane of several facilitative glucose transporters                        (Slc2a8, 9a and 9b) were                    detected in these knockout compared to wild-type mice. Apoptotic sperm were more                    prevalent in both null mice compared to wild-type mice, whereas sperm                    concentration and motility were significantly lower in the null sperm. Finally,                        Akt2-/- sperm had a markedly decreased fertilization rate                    by in vitro fertilization (IVF) and resulting embryos displayed increased                    fragmentation and poor growth. These results suggest that altered                        SLC2A expression and increased PTEN and GSK3β activity may                    be responsible for the decreased spermatogenesis, sperm maturation, and                    fertilization in the Akt1-/- and Akt2-/- male                    mice.
Department of Obstetrics and Gynecology, Washington University in St. Louis, St. Louis, MO 63110, USA.
Sung Tae
ST
Kim
Kenan
K
Omurtag
Kelle H
KH
Moley
D000818:Animals; D005260:Female; D005307:Fertilization in Vitro; D005786:Gene Expression Regulation; D051246:Glucose Transport Proteins, Facilitative / Q000378:metabolism*; D007248:Infertility, Male / Q000378:metabolism* / Q000473:pathology; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D051057:Proto-Oncogene Proteins c-akt / Q000378:metabolism*; D013091:Spermatogenesis / Q000502:physiology*; D013094:Spermatozoa / Q000378:metabolism*; D013737:Testis / Q000378:metabolism
D051246:Glucose Transport Proteins, Facilitative; C514862:Akt1 protein, mouse; C494922:Akt2 protein, mouse; D051057:Proto-Oncogene Proteins c-akt