Impaired sperm chromatin integrity in obese mice

Area of Science:

• Reproductive Biology
• Endocrinology
• Genetics

Background:

• Global obesity rates are rising, coinciding with declining male reproductive health.
• A potential link between obesity and male infertility, specifically reduced sperm quality, has been proposed.

Purpose of the Study:

• To investigate the impact of obesity on sperm chromatin integrity using diet-induced obesity (DIO) and leptin-deficient mouse models.
• To analyze the transcriptional changes in testicular marker genes in response to obesity.

Main Methods:

• Two mouse models of obesity were utilized: diet-induced obesity (HFD) and leptin deficiency.
• Sperm chromatin integrity was assessed using the sperm chromatin structure assay.
• Quantitative real-time PCR was employed to analyze the expression of selected testicular marker genes in DIO mice.

Main Results:

• Obese mice in both models exhibited significantly higher sperm DNA fragmentation compared to lean controls.
• Obesity did not lead to an increase in immature spermatozoa.
• In DIO mice, significant upregulation of Cyp2e1, Cyp19a1, Tnf, and Pparg genes was observed in the testes.

Conclusions:

• A positive correlation exists between body mass index and sperm DNA fragmentation in obese mouse models.
• High-fat diet-induced obesity may trigger local testicular responses impacting intratesticular signaling and spermatogenesis.
• These findings highlight obesity as a risk factor for male infertility due to impaired sperm chromatin integrity.