PARENT SESSION
SLIDE SESSION 13: GONADAL FUNCTION
Chairs: Robert Burghart, Francisco Moran (Trainee)
Univ Ottawa-Monpetit 203
1:30 PM-3:30 PM

EXPRESSION OF THE HUMAN GROWTH HORMONE-RELEASING HORMONE GENE ALTERS THE ENDOCRINE FUNCTION OF THE TESTIS.

Chandrashekar, V.¹, Panici, J. ¹, Fink , K. ¹, Bartke, A.¹, ¹

ABSTRACT- Growth hormone (GH) profoundly affects growth and development. However, the in vivo role of GH and insulin-like growth factor-I (IGF-I) in reproduction is poorly understood. Transgenic mice expressing the human GH-releasing hormone (hGHRH) gene secrete greatly increased amounts of GH. Since the major physiological effects of GH are via IGF-I, these mice are good experimental model to study the effects of IGF-I on testicular endocrine function. Therefore, adult male transgenic mice bearing the hGHRH gene and their normal siblings were injected with either saline or oLH (NIH-26, 0.3 g/g BW; N= 6-11 mice/group) in saline. One hour later, blood was obtained via heart puncture. Plasma IGF-I, LH, prolactin (PRL), androstenedione (A-Dione) and testosterone (T) levels were measured by RIAs. As expected, plasma IGF-I concentrations were significantly (P<0.001) higher in transgenic mice than in their normal siblings. Plasma LH and PRL levels were similar in saline-injected transgenic and normal mice. The basal plasma A-Dione and T levels were higher (A-Dione: P<0.001; T: P<0.02) in transgenic mice expressing the hGHRH gene relative to normal mice. Treatment with LH significantly (P<0.001) increased plasma A-Dione and T levels in both normal and hGHRH transgenic mice. However, these A-Dione and T responses to LH treatment were increased (A-Dione: P<0.01; T: P<0.001) in transgenic mice relative to their normal siblings. These results indicate that expression of hGHRH gene increase both A-Dione and T secretions. The increased secretions of androgens might have been due to the increased sensitivity of the Leydig cells to LH action. Thus, excess homologus, endogenously secreted IGF-I positively influences testicular steroidogenesis in adult transgenic mice expressing the hGHRH gene. Supported by NIH Grant HD37950

KEY WORDS: in vivo IGF-I effects, androgens, transgenic mice