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Paternal effect on embryo quality in diabetic mice is related to poor sperm quality and associated with decreased GLUT expression

S Kim, Obstetrics and Gynecology, Washington University School of Medicine, St.Louis, United States
K Moley, Obstetrics and Gynecology, Washington University School of Medicine, St.Louis, United States

Correspondence: Kelle Moley, Email: moleyk{at}wustl.edu

Abstract

The objective of this study was to determine if sperm quality, fertilization capacity, and subsequent embryo development are altered in diabetic male mice and if differences in facilitative glucose transporter (GLUT) expression in testis and sperm exist. Using two type 1 diabetic mouse models, GLUT expression in testis and sperm was determined by Western immunoblot and immunofluorescence staining. To address sperm quality and fertilization capacity, computer assisted sperm analysis (CASA) and in vitro fertilization (IVF) were performed. GLUT1, 3 and 5 did not change in expression in the testes or sperm between diabetic and non-diabetic mice. GLUT8 and GLUT9b were less expressed in testes of both diabetic models vs controls. GLUT9a was not expressed in the Akita testis or sperm as compared to strain-matched controls. 3β-HSD expression was significantly decreased in the Leydig cells from the diabetic mice. Sperm concentration and motility were significantly lower in both the diabetics as compared to the control. Theses parameters normalized in Akita diabetic males treated with insulin. In addition, fertilization rates were significantly lower in the Akita group (17.9%) and the streptozotocin (STZ)-injected male group (43.6%) as compared to the normal group (88.8%). Interestingly, of the fertilized zygotes, embryo developmental rates to the blastocyst stage were lower in both diabetic models (7.1%-Akita and 50.0%-STZ) as compared to controls (71.7%). Male diabetes may cause male subfertility by altering steroidogenesis, sperm motility and GLUT expression. This is the first study to link a paternal metabolic abnormality to a sperm effect on cell division and subsequent embryonic development.