Zinc deficiency deteriorates ovarian follicle development and function by inhibiting mitochondrial function

Area of Science:

• Reproductive biology
• Trace element metabolism
• Cellular physiology

Background:

• Zinc (Zn) is vital for human growth, development, and reproductive health.
• Decreased serum zinc is observed with aging and in conditions like PCOS and diabetes.
• The precise impact of zinc deficiency on female ovarian function remains unclear.

Purpose of the Study:

• To investigate the effects of dietary zinc deficiency on female reproductive system, specifically ovarian function.
• To elucidate the underlying mechanisms of zinc deficiency-induced ovarian dysfunction.
• To evaluate the efficacy of zinc glycine supplementation in mitigating these effects.

Main Methods:

• Comparative study of zinc-deficient and control groups in a rodent model.
• Assessment of ovarian follicle count, anti-Mullerian hormone (AMH) levels, and gene expression.
• Analysis of mitochondrial dynamics, oxidative stress, autophagy, and apoptosis markers in ovarian tissue.
• Evaluation of oocyte meiotic progression (germinal vesicle breakdown - GVBD).
• Intervention with zinc glycine in deficient subjects.

Main Results:

• Zinc deficiency significantly reduced follicle numbers and AMH levels.
• Abnormal gene expression related to hormone secretion regulation was observed.
• Disrupted mitochondrial dynamics, increased oxidative stress, inhibited autophagy, and elevated apoptosis in ovaries.
• Impaired oocyte maturation, evidenced by failure of GVBD and reduced oocyte quality.
• Zinc glycine administration successfully reversed oocyte meiotic arrest.

Conclusions:

• Dietary zinc deficiency negatively impacts ovarian hormone secretion and follicle maturation.
• Impaired mitochondrial function and suppressed autophagy are key mechanisms in zinc deficiency-induced ovarian damage.
• Zinc glycine supplementation offers a potential therapeutic strategy for counteracting zinc deficiency-related reproductive issues.