Effects of excess corticosterone on NADPH generating enzymes and glucose oxidation in Leydig cells of adult rats

Abstract

<jats:p> Clinical and experimental studies have shown the adverse effects of excess glucocorticoid on testicular testosterone production. The NADPH co-enzyme has been recognized as an important factor that regulates several steps in steroidogenesis, while glucose oxidation acts as a limiting factor on testicular testosterone production. Nevertheless, the impact of excess corticosterone, the stress hormone on testicular NADPH availability and glucose oxidation is unknown. Therefore, the present study was designed to assess the specific effects of excess corticosterone on Leydig cell NADPH generating enzymes and glucose oxidation. Adult Wistar rats (200–250 g, b.w.) were treated with corticosterone-21-acetate (2 mg/100 g, b.w., i.m., twice daily) for 10 days and corticosterone-21-acetate plus luteinizing hormone (LH) (100 mg/kg b.w., i.m., daily) for 10 days. After the treatment period, experimental animals and controls were killed, blood was collected and the sera separated for testosterone assay. Testes were removed and Leydig cells were isolated, purified and used for estimating the specific activity of NADPH generating enzymes and <jats:sup>14</jats:sup>C-glucose oxidation. Serum testosterone, Leydig cellular <jats:sup>14</jats:sup>C-glucose oxidation and the specific activities of 6-phosphogluconate dehydrogenase (6-PGDH), NADP-iso-citrate dehydrogenase (ICDH) and malic enzyme were significantly decreased in corticosterone-treated rats. Coadministration of LH with corticosterone maintained the specific activities of 6-PGDH and ICDH and <jats:sup>14</jats:sup>C-glucose oxidation at control level. Nevertheless, serum testosterone and Leydig cellular malic enzyme activity showed a significant decrease in these rats. In conclusion, the inhibitory effects of excess corticosterone on Leydig cell steroidogenesis are mediated through impaired glucose oxidation and defective NADPH generation. Co-administration of LH with corticosterone failed to prevent the decrease in serum testosterone and Leydig cell malic enzyme activity, suggesting the dominant inhibitory effects of excess corticosterone. </jats:p>

Effects of Immobilization Stress on Kidneys of Wistar Male Rats: A Morphometrical and Stereological Analysis

“…In fact, such alterations have been shown to be related to chronic stress and high concentrations of GC [Welch, 1993;Porges et al, 1994;Almeida et al, 1998;Dallman et al, 2003;Kavitha et al, 2006]. For these parameters, significant differences were observed between the two groups ( table 1 ).…”

Corticosterone metabolism by chicken follicle cells does not affect ovarian reproductive hormone synthesis in vitro

“…Latif et al Latif et al (2011) suggested that 11β-HSD1 is enzymatically coupled to 17β-HSD3, utilizing NADPH and NADP in intermeshed regeneration systems. Kavitha et al Kavitha et al (2006) showed that the inhibitory effect of corticosterone on Leydig cell steroidogenesis is mediated through defective co-factor generation, resulting in NADPH shortage caused by the involvement of corticosterone on glucose oxidation.…”

Corticosterone impairs the mRNA expression and activity of 3β- and 17β-hydroxysteroid dehydrogenases in adult rat Leydig cells

“…that reduced glucose oxidation would have resulted in reduced ATP production, which in turn might have affected the activity of 17b-HSD. In addition to this, since corticosterone was shown to decrease the availability of NADPH (Kavitha et al 2006), the co-factor essential for optimal activity of 17b-HSD, the same may be responsible for the reduction in the activity of 17b-HSD.…”