Testicular endocrine function in GH receptor gene disrupted mice

Area of Science:

• Endocrinology
• Reproductive Biology
• Molecular Genetics

Background:

• Growth hormone (GH) is crucial for somatic growth and has known effects on reproductive organs.
• GH receptor (GHR) knockout mice provide a model to study the specific role of GH signaling in various physiological processes.
• Testicular function is regulated by complex hormonal interactions, including GH, IGF-I, and gonadotropins.

Purpose of the Study:

• To investigate the impact of GH receptor gene disruption on testicular function in mice.
• To evaluate the effects of LH administration on hormone levels and testicular parameters in GHR knockout mice.
• To elucidate the role of systemic IGF-I in modulating testicular endocrine function.

Main Methods:

• GH receptor knockout mice and wild-type littermates were used.
• Mice were treated with saline or ovine luteinizing hormone (LH).
• Plasma hormone levels (IGF-I, LH, FSH, PRL, androstenedione, testosterone), testicular receptor numbers (LH, PRL), mRNA levels (LHbeta-subunit, sulfated glycoprotein-2), and testicular morphometry were analyzed.

Main Results:

• GH receptor knockout mice lacked circulating IGF-I and had elevated PRL levels.
• LH administration stimulated testosterone production, but this response was attenuated in GH receptor knockout mice.
• Testicular LH and PRL receptor numbers were reduced, and Leydig cell volume was decreased in GH receptor knockout mice.

Conclusions:

• Disruption of the GH receptor gene significantly impairs testicular function, particularly LH-stimulated testosterone secretion.
• Reduced testicular LH and PRL receptor numbers, likely due to the absence of IGF-I, contribute to diminished steroidogenesis.
• Systemic IGF-I plays a critical modulatory role in maintaining normal testicular endocrine function.