Reproductive dysfunction is often characterized by malfunction of the reproductive tissues, which may lead to disruption of the synergistic rhythm that should bring about a progression of sexual events and the conception of new life. This may therefore result in the sexual dysfunction and infertility that can be seen in couples having prolonged biological difficulty in reproducing their offspring after having unrestricted sexual intercourse for at least twelve months. Several factors have been implicated in the cause and progression of reproductive dysfunction, including poor nutrition, drug side effects, disease states, and toxicant ingestion. A well-known food additive that has been found to be potent at initiating reproductive anomalies in males is monosodium glutamate (MSG). This regular flavor enhancer is widely used as a taste enhancer in several diets. The different mechanisms by which it may induce reproductive dysfunctions include spermatogenic alteration resulting in a low sperm count, high sperm abnormality, reduced live sperm and decreased sperm pH, oxidative damage (increased lipid peroxidation and reduced antioxidant enzyme activities), histological alteration (blood hemorrhage, distorted germ and Sertoli cells), as well as gonadotropin imbalance (reduced testosterone, luteinizing hormone, and follicle-stimulating hormone concentrations). Therefore, this review discusses various established mechanisms through which MSG may induce reproductive dysfunction and the treatment strategies to ameliorate its toxic effects.

Monosodium glutamate (MSG) is one of the most popular food additives in the world and is often ingested with commercially processed foods. It can be described as a sodium salt of glutamic acid with the IUPAC name - Sodium 2-aminopentanedioate and is ionized by water to produce free sodium ions and glutamic acid. MSG use has significantly increased over the past 30 years, its global demand stands huge at over three million metric tons which is worth over $4.5 billion. Asia was responsible for more than three quarter of world MSG consumption with the country China also leading in global consumption as well as production and export to other countries. Prior to year 2020, global demand for MSG increased by almost four percent each year with the highest significant increase in demand for MSG predicted to rise in Thailand, Indonesia, Vietnam and China, followed by Brazil and Nigeria. However, several researches featured in this review has identified MSG consumption as a major contributor to the development and progression of some metabolic disorders such as obesity, which is a risk factor for other metabolic syndromes like hypertension, diabetes mellitus and cancer initiation. The mechanism by which MSG induce obesity involves induction of hypothalamic lesion, hyperlipidemia, oxidative stress, leptin resistance and increased expression of peroxisome proliferator-activated receptors (PPARs) Gamma and Alpha. Similarly for induction of diabetes mellitus, MSG consumption resulted in decreased pancreatic beta cell mass, increased oxidative stress and metabolic rates, reduced glucose and insulin transport to adipose tissue and skeletal muscles, insulin insensitivity, reduced insulin receptors and induced severe hyperinsulinemia. Dietary salt, an active component of MSG is also found to be a major risk factor for high blood pressure (which may lead to hypertension). MSG is used to enhance the taste of tobacco, causing smokers to consume the product in excess and thereby increasing the risk of cancer development. Depending on the amount consumed, MSG has both positive and negative effects. Despite the controversy surrounding MSG's safety and its probable contribution to risk of development and progression of metabolic disorders, its global consumption is still very high. Therefore, this article will sensitize the public on the need for cautious use of MSG in foods and also aid regulatory agencies to further review the daily MSG consumption limit based on metabolic toxicities observed at the varied dosages reported in this review.

Benign prostatic hyperplasia (BPH) is a urological disease characterized by proliferation of the stromal and epithelial cells of the prostate of older men. Ketogenic diet (KD) is a high fat, moderate protein and low carbohydrate diet which acts on metabolic systems through hormonal modulation and simulation amongst other mechanisms. This study investigated the effect of KD consumption in Testosterone Propionate (TP) induced BPH. Twenty-Five male rats were divided into five groups of five animals each; control and KD group were administered distilled water and KD respectively, while the remaining groups were given 30 mg/kg body weight of TP subcutaneously once daily for 28 days. Thereafter, the three groups, TP, TP + Finasteride, TP + KD were administered standard rat chow, finasteride (0.1 mg/kg) and KD respectively, for 42 days prior to sacrificing the rats and their serum and prostate glands obtained for analysis. Triglyceride, Total cholesterol, HMG CoA reductase, Follicle Stimulating Hormone, Luteinizing Hormones, Testosterone, Prostate Specific Antigen (PSA) concentration and Malondialdehyde levels were significantly increased (p ≤ 0.05) while superoxide dismutase, catalase and glutathione peroxidase activities were significantly (p ≤ 0.05) reduced in the TP group. These changes were reversed significantly (p ≤ 0.05) in the finasteride and KD treatment groups. The diet also caused significant (p ≤ 0.05) decrease in prostate weight and stromal glandular tissue. This study suggests that ketogenic diet consumption ameliorated prostatic hyperplasia in the rats and may be considered as an affordable and non-invasive management option for benign prostatic hyperplasia in men.