Faculty of Medicine and Health Sciences

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The vision of the Faculty of Medicine and Health Sciences is to be a dynamic, people-centred and inclusive environment, internationally recognised for its excellence in research, education and clinical training in medicine and health sciences, and for the contribution it makes to improving health and health care in South Africa, the African continent and beyond.

This faculty was known as the Faculty of Health Sciences until 30 April 2012.

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Browsing Faculty of Medicine and Health Sciences by browse.metadata.advisor "Aboua, Yapo Guillaume"

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    The effects of a green rooibos extract on the reproductive function of obesity-induced insulin resistant or hypertensive male wistar rats
    (Stellenbosch : Stellenbosch University, 2019-12) Manirafasha, Claudine; Du Plessis, S. S.; Huisamen, Barbara; Aboua, Yapo Guillaume; Stellenbosch University. Faculty of Medicine and Health Sciences. Dept. of Biomedical Sciences: Medical Physiology.
    ENGLISH ABSTRACT: Diet-induced obesity (DIO) due to a high caloric diet (HCD) predisposes an individual to the development of diabetes and cardiovascular diseases, with high prevalence in young populations. Existing evidence supports the sentiment that insulin resistance and hypertension (HT) affect male reproduction. A greater understanding of the influence of insulin resistance and/or HT on male reproduction is required in order to prevent or treat male infertility. Due to the limitations of orthodox drugs, there is currently a strong movement towards and support for studies on phytomedicine. Rooibos (Aspalathus linearis) has been used in several studies and is known to have natural antioxidant effects and anti-obesogenic, antidiabetic, anti-hypertensive and anti-infertility activities. Currently, the company Afriplex (Pty) Ltd is producing an aspalathin-rich laboratory standardized extract prepared from green rooibos called Afriplex GRTTM (GRT). However, there is very little knowledge regarding the use of GRT in obesity-related insulin resistance and/or HT, and specifically, its effects on male reproductive health. Aim This study aimed to explore the effect of GRT on the reproductive function in obesity-induced insulin resistant and hypertensive male Wistar rats. Methods A prospective randomized control and experimental animal study design was used. Two different diets were used to induce obesity-related insulin resistance with or without HT in male Wistar rats. Subsequently, the possible protective properties of GRT on the male reproductive system were evaluated. Animals (weighing 120 ±10 g, approximately 7 weeks old) were randomly assigned to seven groups with seven rats each. All rats had unrestricted access to their respective diets and water for 16 weeks. At baseline (week 0–10), we had three groups: 1) lean control (LC) – animals that received standard rat chow; 2) obese (OB) – animals that received a diet to induce obesity associated with insulin resistance; and 3) obese with hypertension (OBHT) – animals were placed on a slightly modified DIO and additionally developed HT. From weeks 11 to 16, one LC, OB and OBHT group were each treated with GRT (prepared and supplied by Afriplex (Pty) Ltd) at 60 mg/kg/day as a dietary supplement in the form of jelly blocks. An additional group of OBHT animals was treated during the same period for 6 weeks with Captopril, an angiotensin-converting-enzyme (ACE) inhibitor (positive control for HT) at 60 mg/kg per day. Food and water intake were monitored on a daily basis. An oral glucose tolerance test was performed during the 10th week after the onset of the respective diets and during the 16th week, after which the animals were sacrificed. Blood pressure measurements were taken once per week throughout the experimental period. After the 16-week period, animals were killed and blood, testis and epididymal tissue were harvested for further analysis. Body weight, intra-peritoneal fat, non-fasting glucose levels, IL-1β, IL-6, IL-12, IL-18 and TNFα, oxidative stress (OS) markers (superoxide dismutase and catalase activity, malondialdehyde), testosterone and estradiol, sperm concentration, viability, morphology, total motility, progressive motility and various velocity parameters were measured. Results and conclusion Both diets successfully induced insulin resistance with or without hypertension and demonstrated detrimental effects on male reproductive function as evidenced by OS and hormone dysregulation. Treatment with GRT reversed OS and balanced the androgens. This study provided insight into the pharmacological effects of GRT in the treatment of pathophysiological changes that occur in DIO associated with insulin resistance or HT. These findings will hopefully inspire further research into the clinical setting related to the GRT and could possibly lead to the development of new drugs from this compound.
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    An investigation of obesity as an etiology of male infertility in a rat model
    (Stellenbosch : Stellenbosch University, 2021-03) Skosana, Bongekile Trisha; Du Plessis, Stefan S.; Aboua, Yapo Guillaume; Van der Horst, Gerhard; Marais, Erna; Stellenbosch University. Faculty of Medicine and Health Science. Dept. of Biomedical Sciences: Medical Physiology.
    ENGLISH ABSTRACT: Until recent decades, the inability to produce offspring has been seen as a female-related issue, but better understanding has made it evident that male fertility is l ikewise an essential determinant of couple fertility. Infertility in males has numerous causative factors, including lifestyle factors and obesity. Obesity has been shown to compromise fertility through changes in several aspects of reproductive function, including dysregulation ofhormones (the HPG axis) and changes in the structure of the reproductive organs. There is, however, a great deal that is still unknown about how obesity and infertility interchangeably affect each other. New molecular techniques such as proteomics have been shown to provide insights into disease-causing mechanisms. These techniques may provide an avenue to discover more intrinsic changes that obesity may give rise to; it can also aid in the discovery of mechanisms through which obesity can act to bring about changes in male fertility. The overall aims of this study were: (1) To examine the effects of obesity on male fertility by observing specific macroscopic (anthropometric), microscopic (sperm parameters, histology of the testis and epididymis) and molecular (antioxidant enzyme, reproductive hormones) changes in a diet-induced obesity animal model; (2) To examine changes in protein expression within the reproductive tissues of obese animals, quantify these changes, and identify the affected molecular pathways. This study made use of an animal model of diet-induced obesity (DIO) to assess the effects of obesity on male reproductive organs and sperm parameters. Male Wistar rats (n=40) were randomly and equally divided into control (age-matched) and DIO groups and received standard rat chow or a high caloric diet ad libitum for 54 weeks, respectively. A long-term diet was chosen to mimic the gradual and chronic onset of obesity. At 60 weeks of age, rats were sacrificed by euthanasia. Each animal had their body weight measured and immediately examined post-mortem to determine visceral fat weight, testis weight and non-fasting blood glucose. Blood was collected from the thoracic cavity and used for plasma extraction and haematocrit analysis. Testis and epididymides were excised, weighed and preserved appropriately for subsequent sperm parameter evaluations (morphology and viability), histological analysis (H & E staining), protein determination, antioxidant evaluation (catalase, superoxide dismutase, glutathione, lipid peroxidation), and proteomics analysis (Liquid Chromatography Mass Spectrometry (LC-MS/MS)). The chronic diet elevated body and visceral fat weights significantly in the DIO group compared to controls. Sperm morphology and viability, as well as estradiol production were negatively altered in the DIO group. These changes were associated with alterations in several macroscopic, microscopic and molecular changes including changes in relative testicular weight, histological aberrations, and a reduction in antioxidant enzymes within the testis and epididymis respectively. Interestingly, testosterone was not significantly reduced, as seen in experiments with a shorter DIO feeding duration. This points towards a compensatory mechanism to counteract chronically increased testosterone concentrations. Protein expression profiles of the DIO and control groups suggest that the predominant molecular pathways affected by th treatment were related to metabolism. These seem to be the possible driver of changes in other proteins including those involved in the production of reactive oxygen species (ROS). Some lesser researched antioxidant proteins were increased in expression to counteract ROS. The negative histological changes observed in the DIO group were linked to the underexpression of structural proteins involved in cell-to-cell adhesion. Reproductive proteins including those involved in sperm production, fertilization and the early stages of embryonic development were reduced in expression in the DIO group. These negative changes were possibly instigated by the observed increases in stress proteins, redox and inflammatory proteins. It is therefore evident that long-term obesity can impair male reproductive parameters and could be a contributing factor to the decline in male fertility by affecting sperm and reproductive parameters. Proteomic analysis of the epididymis and sperm showed that proteins essential in metabolism, ROS production, stress, inflammation and in the regulation of reproductive function as well as sperm and epididymis structure were negatively affected. In addition, long-term obesity can mask detrimental changes in physiology due to compensatory mechanisms, making changes in reproductive parameters difficult to explain.