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Leydig cells produce testosterone in response to luteinizing hormone (LH) via the cyclic adenosine monophosphate (cAMP)/protein kinase A pathway. Additionally, these cells are responsible for producing insulin-like peptide 3 (INSL3), a peptide hormone that is essential for testicular descent. The insl3 promoter in Leydig cells can be activated by cAMP through the transcription factor Nur77, which has also been shown to regulate the promoters of the steroidogenic enzymes, cyp17 and 3b-hsd. While the mechanism of LH action on testosterone production is well characterized, the effect of LH on insl3 abundance has yet to be shown directly. The MA-10 Leydig cells treated with hCG exhibited a transient and robust increase in nur77 mRNA, while insl3 mRNA abundance remained unchanged. Further, cAMP failed to affect insl3 mRNA, though nur77 mRNA abundance was significantly increased. Inhibition of LH-receptor-linked signal transduction pathways in the presence of hCG implicated multiple signaling networks in the regulation of both insl3 and nur77. Treatment with hCG or cAMP did not affect the abundance of 3b-hsd mRNA. Interestingly, though the MA-10 cell line has been reported to lack CYP17 activity and mRNA and so produce progesterone instead of testosterone, cyp17 mRNA was present and inducible by hCG and cAMP. The addition of hCG, testosterone, nor the combination of hCG and testosterone affected insl3 mRNA abundance. Though hCG consistently increased nur77 mRNA abundance, the addition of testosterone did not enhance the effects of hCG. Collectively, these results indicate that insl3 is regulated by factors other than LH/CG and cAMP in the MA-10 cell line.