(092) Leptin Increases T-cells in Testis to Modulate Leydig Stem Cell Function

Abstract Introduction Testis microenvironment which is comprised of cells like Sertoli and peritubular releases paracrine factors could potentially modulate testicular functions. In our previous studies, we identified Leptin as a key factor in the microenvironment, released by goes to bind its receptor Leydig cells. Once this association happens it further induces expression desert hedgehog signaling pathway, known play an important role Stem cell’s differentiation Adult Lydig Cells, are capable producing testosterone. However, one limitations study was that model used were from human extracted testes’ biopsies lacked intact immune microenvironment. present explored influence on Objective To explore Methods We 6-weeks old C57BL6 mice exposed two different concentrations Leptin, 10 100 mg/ml for seven days. After days treatment, these animals humanly sacrificed collected their blood testes. Blood subjected CBC differential profile performed using EDTA anti-coagulated samples with Hemavet Mascot Multispecies Hematology System Counter 1500R (CDC Technologies, Inc., Oxford, CT). Samples counted no longer than five minutes after drawn. addition that, testes comprehensive immunophenotyping allowed us evaluate detail impact treatment at doses cell types found within Results showed low dose (10mg/ml) increased levels serum Testosterone (13.20 + 0.37 ng/dl) but not significant, LH FSH (LH 0.016 0.02 ng/ml, 51.71 12.93 ng/ml) significant (p<0.05) increase. On contrary, received 100mg/ml changes hormone levels. profiling suggested amongst all compared, Lymphocytes Platelets significantly influenced specifically upon Leptin. Interestingly, highlighted had increase total number CD4+ (helper T cells) CD8+ (Cytotoxic lymphocytes) This pattern observed high Conclusions The observation made highlights unexplored aspects myoid modulating testis testosterone production. future studies will be exploring how correlated directly correlation can Cell into Cells. Disclosure No