Morphological effects of long-term consumption of energy drinks on the intracranial visual relay centres of adult wistar rats.

Morphological effects of long-term consumption of energy drinks on the intracranial visual relay centres namely superior colliculus and lateral geniculate body of adult wistar rats were carefully studied. The study included rats of both sexes (N = 20), with average weight of 200g randomly assigned into treated (n1=10) and control (n2=10) groups. The rats in the treated group received energy drinks and distilled water alternatively on a daily basis for 10hrs and 14hrs liberally in thirty days, while the control group received distilled water liberally for the thirty days. The rats were sacrificed by cervical dislocation on the thirty-first day of the experiment and the superior colliculus and lateral geniculate body were carefully dissected out, weighed using the Mettler Toledo weighing balance, and quickly fixed in 10% formal saline for further histological study. The findings indicated that there was a significant (p < 0.05) increase in the weight (g) and relative weight (%) of the treated superior colliculus and a significant (p < 0.05) decrease in the weight (g) and relative weight (%) of the treated lateral geniculate body as compared to their corresponding control group. The microanatomy of the superior colliculus and lateral geniculate body of the rats treated with energy drinks revealed cellular degenerative changes, sparse cellular population, hypertrophy, pyknotic nuclei with microcystic changes and vacuolation in the stroma of the superior colliculus and lateral geniculate body as compared to the control group. It was therefore concluded that long-term consumption of energy drinks might have an adverse effect on the intra cranial visual sensibilities by affecting the microanatomy of the superior colliculus and lateral geniculate body of adult wistar rats. We therefore recommended that further studies aiming at corroborating these findings be done.Key words: Morphological effects, Energy drink, Superior colliculus, Lateral geniculate body, Wistar rats

The Concept of Male Reproductive Anatomy

The human reproductive system is made up of the primary and secondary organs, which helps to enhances reproduction. The male reproductive system is designed to produce male gametes and convey them to the female reproductive tract through the use of supportive fluids and testosterone synthesis. The paired testis (site of testosterone and sperm generation), scrotum (compartment for testis localisation), epididymis, vas deferens, seminal vesicles, prostate gland, bulbourethral gland, ejaculatory duct, urethra, and penis are the parts of the male reproductive system. The auxiliary organs aid in the maturation and transportation of sperm. Semen is made up of sperm and the secretions of the seminal vesicles, prostate, and bulbourethral glands (the ejaculate). Ejaculate is delivered to the female reproduc¬tive tract by the penis and urethra. The anatomy, embryology and functions of the male reproductive system are discussed in this chapter

Endocrine Functions of the Testes

The testes, also known as the male gonads are found in the scrotal sacs. In addition to their spermatogenic functions, they also secrete steroids and protein hormones. The steroid hormones are the androgens, testosterone and dihydrotestosterone as well as estrogen, while the protein hormones are inhibins, activins, and anti-Mullerian hormone (AMH). This chapter therefore discusses the role of the testis in the production and functions of the testicular androgens as well as testicular protein hormones

Testosterone: The Male Sex Hormone

Males primarily use testosterone as a sex hormone. Through its effects on the androgen receptor, it is released by the interstitial cells of the testes and is in charge of the male external genitalia development as well as the internal reproductive glands and ducts during adolescence and maturity. Additionally, testosterone is required for the descent of testes via the inguinal canal in the last 2 months of fetal development. When a Y chromosome and consequently the SRY gene are missing from an embryo, ovaries form. The Wolffian ducts do not mature because the fetal ovaries do not release enough testosterone. It is mostly used to treat male hypogonadism. Notably, this chapter addresses the following context: historical view of testosterone research, biosynthesis, secretion, metabolism, transport mechanism, biological actions, health benefit of testosterone, factors that promote and inhibit testosterone secretion, therapeutic implication as well as pathophysiology of testosterone secretion

Possible mechanisms involved in the protective effect of lutein against cyclosporine-induced testicular damage in rats

Oxidative stress and aberrant inflammatory response have important implications in cyclosporin-induced reproductive functions. Previous studies have shown that agents with antioxidant and anti-inflammatory activities might be beneficial in reversing cyclosporin-induced reproductive impairment. Lutein is a naturally occurring compound with antioxidant and anti-inflammatory properties. However, the effect of lutein against cyclosporin-induced reproductive impairment remains in complete. Hence, we investigated the protective effect of lutein, specifically focusing on the role of nuclear factor erythroid 2 related factor-2 (Nrf2)/heme-oxygenase-1 (HO-1)/connexin-43 (Cx-43) upregulation system against cyclosporine-induced reproductive impairment. Six male Wistar rats were allotted into 5 groups and given daily gavage of cyclosporine (40 mg/kg) and/or lutein (30 mg/kg) for four (4) weeks or in combination, respectively. The testicular antioxidant scaffolds: superoxide dismutase (SOD), catalase (CAT), reduced glutathione (GSH), add to sulfhydryl (T-SH), non-protein sulfhydryl (NP-SH), glutathione reductase (GR), glutathione-S -transferase (GST), glutathione peroxidase (GSH-Px), thiobarbituric acid reactive substances (TBARS), myeloperoxidase (MPO), testicular proinflammatory cytokines, apoptotic related protein, nucleic acids, sialic acid, testicular proton pump ATPase, stress responsive protein, BTB-related protein and total protein levels in the testes were assayed thereafter. Cyclosporin significantly increased NOX-1, TNF-α, IL-1β, MPO, caspase-3 and -9 levels, which were reversed by lutein. Lutein reversed cyclosporin-induced decreases in Nrf2, HO-1, BCL-2, cytochrome C, with corresponding increase in CAT, SOD, GSH, T-SH, NP-SH, GST, GR, GSH-Px, and Cx-43 levels compared to cyclosporin groups. Lutein also abates cyclosporin-induced alterations Na + -K + -ATPase activities. Our findings showed that lutein's protective effect against cyclosporin-induced reproductive impairment might be associated with mechanisms linked to its antioxidant, anti-apoptotic, and anti-inflammatory properties, notably through up-regulation of Nrf2/HO-1/Cx-43 signaling and down-regulation of NOX-1 signaling

Intermittent fasting and exercise therapy abates STZ‐induced diabetotoxicity in rats through modulation of adipocytokines hormone, oxidative glucose metabolic, and glycolytic pathway

Abstract Diabetes is a global, costly, and growing public health issue. Intermittent fasting (IF) and exercise therapy have been shown to improve insulin sensitivity (IS) in large studies, although the underlying processes are still unknown. The goal of this study, which included both nondiabetic and diabetic rats, was to look at the mechanisms of intermittent fasting and exercise in the management of diabetotoxicity. The effects of starvation and honey on the oral glucose tolerance test, insulin tolerance test, adipocytokines, oxidative glucose metabolic enzymes, glycolytic enzymes, food intake, and body weight in rats with streptozotocin‐induced diabetes were also investigated. In the nondiabetic phase, rats were administered an oral regimen of distilled water (0.5 ml/rat), honey (1 g/kg body weight), and interventions with IF, and starvation for 4 weeks while in the diabetic phase, after STZ or citrate buffer injections, interventions with IF, exercise, starvation, and honey treatment began for 4 weeks. At all OGTT and ITT points, there was a substantial rise in glucose in the STZ group. Adipocytokines hormone, oxidative glucose metabolic enzymes, glycolytic enzymes, and body weight were all affected by STZ when compared to starvation and honey, however, IF and exercise significantly reduced these alterations. In diabetic rats, intermittent fasting and exercise enhanced serum adipocytokines levels. These findings imply that adipokines modulate glycolytic/nonmitochondrial enzymes and glucose metabolic/mitochondrial dehydrogenase to mediate the antidiabetic effects of intermittent fasting and exercise