c-peptide has been researched along with Infertility--Male* in 2 studies
2 other study(ies) available for c-peptide and Infertility--Male
| Article | Year |
|---|---|
Proinsulin C-peptide as an alternative or combined treatment with insulin for management of testicular dysfunction and fertility impairments in streptozotocin-induced type 1 diabetic male rats.
Diabetes mellitus (DM) is closely associated with male infertility and sexual dysfunction. Recent data indicate that the proinsulin C-peptide (CP) exerts important physiological effects and shows the characteristics of an endogenous peptide hormone. So, this study was done to investigate the effect of C-peptide with or without insulin treatment on testicular function and architecture in diabetic rats. Rats were divided into the following groups: control, diabetic, and diabetic groups treated with either CP alone or combined with insulin. Tested parameters included, estimation of serum follicle-stimulating hormone (FSH), luteinizing hormone (LH), testosterone, and glucose levels, testicular samples for histopathology and estimation of malondialdehyde (MDA), total antioxidant capacity (TAC), and B-cell leukemia/lymphoma-2 (BCL-2) levels as well as sperm count and motility. Results showed that DM caused a severe alteration in hormonal profile and reduced sperm parameters along with increased MDA and decrease in both TAC and BCL-2 levels. CP alone or with insulin treatment efficiently reversed all the negative effects of DM on rat testes, with maximum improvement in the combined regimen. Proposed mechanisms may involve its hypoglycemic, antioxidant, and antiapoptotic properties. Thus, CP could substitute for or better combined with insulin to prevent or retard diabetic-induced testicular dysfunction. Topics: Animals; Apoptosis; C-Peptide; Diabetes Mellitus, Experimental; Diabetes Mellitus, Type 1; Infertility, Male; Insulin; Male; Oxidative Stress; Rats; Sperm Count; Streptozocin; Testis | 2019 |
Directed overexpression of insulin in Leydig cells causes a progressive loss of germ cells.
The primary goal of this study was to determine the 5'region of the Insl3 gene that specifically targets the expression of human insulin to Leydig cells, and to explore whether the testicular proinsulin is efficiently processed to insulin that is able to rescue the diabetes in different mouse models of diabetes. We show here that the sequence between nucleotides -690 and +4 of mouse Insl3 promoter is sufficient to direct the Leydig cell-specific expression of the human insulin transgene (Insl3-hIns). We also found that the 3'untranslated region (3'UTR) of Insl3 was effective in enhancing transgene expression of the insulin in vivo. Expression analysis revealed that the temporal expression pattern of the hIns transgene in Leydig cells of transgenic testes is roughly the same as that of the endogenous Insl3. Despite the Leydig cells translate human proinsulin and secrete a significant level of free C-peptide into the serum, the Leydig cell-derived insulin is not able to overcome the diabetes in different mouse models of diabetes, suggesting a lack of glucose sensing mechanisms in the Leydig cells. A consequence of overexpression of the human proinsulin in Leydig cells was the decrease of fertility of transgenic males at older ages. Germ cells in transgenic males were able to initiate and complete spermatogenesis. However, there was a progressive and age-dependent degeneration of the germ cells that lead to male infertility with increasing age. Topics: 3' Untranslated Regions; Age Factors; Animals; Blood Glucose; C-Peptide; Diabetes Mellitus, Experimental; Homeodomain Proteins; Humans; Infertility, Male; Insulin; Leydig Cells; Male; Mice; Mice, Knockout; Mice, Transgenic; Paired Box Transcription Factors; Proinsulin; Promoter Regions, Genetic; Proteins; Spermatozoa; Time Factors; Up-Regulation | 2008 |