Effect of Prediabetes on Membrane Bicarbonate Transporters in Testis and Epididymis

Effect of Prediabetes on Membrane Bicarbonate Transporters in Testis and Epididymis The formation of competent spermatozoa is a complex event that depends on the establishment of adequate environments throughout the male reproductive tract. This includes the control of bicarbonate (HCO3 −) concentration, which plays an essential role in the maintenance of extracellular and intracellular pH (pHi) values. Diabetes mellitus alters pHi regulation in mammalian cells, mainly by altering the activity of ion transporters, particularly HCO3 −-dependent mechanisms. Yet, little is known about the effects of this pathology and its prodromal stage, prediabetes, on the membrane transport mechanisms of male reproductive tract cells. Herein, we analyzed protein and mRNA levels of the most relevant HCO3 − transporters of the SLC4 family [anion exchanger 2 (AE2), Na+-driven Cl−/HCO3 − exchanger (NDCBE), electrogenic Na+/HCO3 − cotransporter 1 (NBCe1), electroneutral Na+/HCO3 − cotransporter 1 (NBCn1)] in the testis and epididymis of a prediabetic animal model. Firstly, we identified the HCO3 − transporters of the SLC4 family, in both testicular and epididymal tissue. Secondly, although no alterations were detected in protein expression, mRNA levels of NBCe1, NBCn1 and NDCBE were significantly increased in the testis of prediabetic rats. On the other hand, in the epididymis, prediabetes caused an increase of AE2 and a decrease of NDCBE protein levels. These alterations may be translated into changes of HCO3 − transepithelial epididymal fluxes in vivo, which may represent a threat for sperm survival. Moreover, these results provide evidence of the molecular mechanism that may be responsible for the significant increase in abnormal sperm morphology already reported in prediabetic rats. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png The Journal of Membrane Biology Springer Journals

Effect of Prediabetes on Membrane Bicarbonate Transporters in Testis and Epididymis

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Publisher
Springer US
Copyright
Copyright © 2013 by Springer Science+Business Media New York
Subject
Life Sciences; Biochemistry, general; Human Physiology
ISSN
0022-2631
eISSN
1432-1424
D.O.I.
10.1007/s00232-013-9601-4
Publisher site
See Article on Publisher Site

Abstract

The formation of competent spermatozoa is a complex event that depends on the establishment of adequate environments throughout the male reproductive tract. This includes the control of bicarbonate (HCO3 −) concentration, which plays an essential role in the maintenance of extracellular and intracellular pH (pHi) values. Diabetes mellitus alters pHi regulation in mammalian cells, mainly by altering the activity of ion transporters, particularly HCO3 −-dependent mechanisms. Yet, little is known about the effects of this pathology and its prodromal stage, prediabetes, on the membrane transport mechanisms of male reproductive tract cells. Herein, we analyzed protein and mRNA levels of the most relevant HCO3 − transporters of the SLC4 family [anion exchanger 2 (AE2), Na+-driven Cl−/HCO3 − exchanger (NDCBE), electrogenic Na+/HCO3 − cotransporter 1 (NBCe1), electroneutral Na+/HCO3 − cotransporter 1 (NBCn1)] in the testis and epididymis of a prediabetic animal model. Firstly, we identified the HCO3 − transporters of the SLC4 family, in both testicular and epididymal tissue. Secondly, although no alterations were detected in protein expression, mRNA levels of NBCe1, NBCn1 and NDCBE were significantly increased in the testis of prediabetic rats. On the other hand, in the epididymis, prediabetes caused an increase of AE2 and a decrease of NDCBE protein levels. These alterations may be translated into changes of HCO3 − transepithelial epididymal fluxes in vivo, which may represent a threat for sperm survival. Moreover, these results provide evidence of the molecular mechanism that may be responsible for the significant increase in abnormal sperm morphology already reported in prediabetic rats.

Journal

The Journal of Membrane BiologySpringer Journals

Published: Oct 9, 2013

References

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