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Decreased spermatogenesis, fertility, and altered Slc2A expression in Akt1-/- and Akt2-/- testes and sperm

Sung Tae Kim1, Kenan Omurtag, Kelle H Moley

  • 1Department of Obstetrics and Gynecology, Washington University in St. Louis, St. Louis, MO 63110, USA.

Reproductive Sciences (Thousand Oaks, Calif.)
|January 10, 2012
PubMed

Insights

The Akt1 and Akt2 genes are crucial for male reproductive health. Knockout mice lacking these genes show impaired sperm production, motility, and fertilization, highlighting their role in spermatogenesis and male fertility.

Area of Science:

  • Molecular Biology
  • Reproductive Biology
  • Biochemistry

Background:

  • Akt (protein kinase B) is a serine/threonine kinase with three isoforms (Akt1, Akt2, Akt3) involved in various cellular processes.
  • Dysregulation of Akt signaling pathways has been implicated in various diseases, but its specific role in male reproduction requires further elucidation.

Purpose of the Study:

  • To investigate the reproductive phenotype of male mice lacking Akt1 or Akt2.
  • To determine the impact of Akt1 and Akt2 deficiency on spermatogenesis, sperm function, and fertilization.

Main Methods:

  • Generation and analysis of Akt1 knockout (Akt1-/-) and Akt2 knockout (Akt2-/-) male mice.
  • Histological examination of testes, including seminiferous tubule diameter.
  • Assessment of protein expression (p-PTEN, p-GSK-3β) and glucose transporter (Slc2a) localization via Western blotting and immunohistochemistry.
  • Evaluation of sperm parameters: apoptosis, concentration, motility, and in vitro fertilization (IVF) success rate.

Main Results:

  • Akt1-/- testes exhibited reduced seminiferous tubule diameter compared to wild-type and Akt2-/- mice.
  • Elevated levels of phospho-phosphatase and tensin homologue deleted on chromosome 10 (p-PTEN) and phospho-glycogen synthase kinase 3β (GSK-3β) were observed in Akt1-/- testes.
  • Altered expression and plasma membrane localization of facilitative glucose transporters (Slc2a8, Slc2a9a, Slc2a9b) were detected in both Akt1-/- and Akt2-/- mice.
  • Increased sperm apoptosis and significantly lower sperm concentration and motility were found in both knockout groups.
  • Akt2-/- sperm showed markedly decreased fertilization rates in IVF, with resulting embryos exhibiting increased fragmentation and poor growth.

Conclusions:

  • Akt1 and Akt2 play critical roles in male reproductive function, including spermatogenesis, sperm maturation, and fertilization.
  • Altered SLC2A expression and increased PTEN and GSK3β activity may contribute to the observed reproductive deficits in Akt1-/- and Akt2-/- mice.
  • These findings underscore the importance of the Akt signaling pathway in maintaining male fertility.

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