Objective:

To synthesize current evidence into an integrated life-course framework explaining how obesogenic exposures, including maternal metabolic disease, postnatal adiposity, and endocrine disrupting chemicals, may interfere with testicular descent and gonadal maturation.

Approach:

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Key Findings:

• Maternal obesity and gestational metabolic disorders may be associated with impaired Leydig cell function and influence testicular development.
• Postnatal and adolescent obesity may alter sex steroid balance and affect gonadal maturation.
• Endocrine-disrupting chemicals may exacerbate disturbances in testicular descent and development.

Interpretation:

The findings suggest that cryptorchidism should be viewed within a broader developmental and metabolic context rather than as an isolated anomaly.

Limitations:

• Most available human data linking obesity, endocrine-disrupting chemicals, and cryptorchidism are observational.
• Proposed mechanisms should be interpreted as biologically plausible associations rather than established causal pathways.

Conclusion:

Integrating metabolic context into cryptorchidism management supports closer endocrine–urologic collaboration.