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Sperm apoptosis signalling in diabetic men.

Claudia Roessner¹, Uwe Paasch, Jürgen Kratzsch

¹Universitätsklinikum Leipzig AöR, Klinik und Poliklinik für Dermatologie, Venerologie und Allergologie, EAA Training Centre, Germany.

Reproductive Biomedicine Online

|July 17, 2012

Summary

Diabetes significantly impacts male fertility by increasing sperm DNA fragmentation and apoptosis signaling. These cellular changes, particularly pronounced in type II diabetes, reduce sperm

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Area of Science:

Reproductive Biology
Endocrinology
Cellular Biology

Background:

Diabetes mellitus is linked to male subfertility.
Previous research indicates reduced sperm motility and DNA integrity in diabetic men, possibly due to oxidative stress.
The precise pathophysiology of diabetes-related male subfertility remains incompletely understood.

Purpose of the Study:

To investigate apoptosis signaling and sperm DNA fragmentation in men with type I and type II diabetes.
To elucidate the subcellular mechanisms underlying diabetes-associated male subfertility.

Main Methods:

Semen specimens from healthy donors (n=18) and diabetic patients (type I, n=13; type II, n=14) were analyzed.
Sperm subpopulations were assessed for apoptosis markers (disrupted mitochondrial potential, activated caspase 3), reactive oxygen species (ROS), and DNA fragmentation using flow cytometry.
Density gradient centrifugation was used for sperm preparation.

Main Results:

Diabetic men exhibited significantly higher concentrations of spermatozoa with disrupted mitochondrial potential, activated caspase 3, ROS, and fragmented DNA compared to healthy controls (P<0.05).
These detrimental effects on sperm parameters were more pronounced in men with type II diabetes.
All measured subcellular parameters were inversely correlated with sperm fertilizing potential.

Conclusions:

Apoptosis signaling, evidenced by disrupted mitochondrial potential and activated caspase 3, is significantly elevated in sperm of diabetic males (type I and II).
Disrupted mitochondrial potential is a key factor contributing to reduced sperm motility in diabetic individuals.
Increased ROS and sperm DNA fragmentation, alongside elevated apoptosis, provide a comprehensive subcellular explanation for male subfertility in diabetes.