Metabolomics is a branch of ‘omics’ sciences that utilises a couple of analytical tools for the identification of small molecules (metabolites) in a given sample. The overarching goal of metabolomics is to assess these metabolites quantitatively and qualitatively for their diagnostic, therapeutic, and prognostic potentials. Its use in various aspects of life has been documented. We have also published, howbeit in animal models, a few papers where metabolomic approaches were used in the study of metabolic disorders, such as metabolic syndrome, diabetes, and obesity. As the goal of every research is to benefit humankind, the purpose of this review is to provide insights into the applicability of metabolomics in medicine vis-à-vis its role in biomarker discovery for disease diagnosis and management. Here, important biomarkers with proven diagnostic and therapeutic relevance in the management of disease conditions, such as Alzheimer’s disease, dementia, Parkinson’s disease, inborn errors of metabolism (IEM), diabetic retinopathy, and cardiovascular disease, are noted. The paper also discusses a few reasons why most metabolomics-based laboratory discoveries are not readily translated to the clinic and how these could be addressed going forward.

All forms of life maintain a reducing environment (homeostasis) within their cells. Perturbations in the normal redox state can lead to an oxidative environment which has deleterious effects, especially in health. In biological systems, metabolic activities are dependent mainly on mitochondrial oxidative phosphorylation, a metabolic pathway that uses energy released by the oxidation of nutrients to produce ATP. In the process of oxidative phosphorylation, electrons are transferred from electron donors to electron acceptors such as oxygen in redox reactions and often results to the generation of reactive species. Reactive oxygen species consist of a class of radical and non-radical oxygen derivatives. The imbalance between the reactive oxygen species and antioxidant defence systems leads to oxidative burden and hence, damage biological molecules. Antioxidants help to prevent or fix the deleterious effects of reactive species. Sulfur is an important element in biological systems. This atom is usually integrated into proteins as the redox-active cysteine residue and in molecules such as glutathione, thioredoxin and glutaredoxin which are vital antioxidant molecules and are therefore essential for life. This review covers the role of sulfur containing antioxidant systems in oxidative environments.

Diabetes mellitus is a metabolic disease that can lead to high morbidity, mortality and long-term complications. Available treatment strategies, which are mainly based on treating hyperglycemia, with insulin and other pharmacological agents are not completely efficient and can even lead to development of unwanted side effects. Scientific evidence suggests that bioactive compounds from teas and other plant-based foods, which are known source of natural antioxidants, could be an attractive strategy to preferentially treat and manage type 2 diabetes mellitus (T2DM) and thus, have significant therapeutic implications. In this review, we attempt an in-depth analysis and discussion of the current progress in our understanding of the antidiabetic potential of two commercialized South Africa herbal tisanes—Rooibos and Honeybush and their polyphenols.

To investigate the role of red palm oil (RPO), rooibos tea extract (RTE) and their combined treatment (RPO + RTE) on antioxidant status in streptozotocin (STZ)-induced diabetic rats. Diabetes mellitus was induced by a single administration of streptozotocin (50 mg/kg) and the rats were treated for 7 weeks. Antioxidant enzymes [catalase (CAT), glutathione peroxidase (GPx), superoxide dismutase (SOD)], antioxidant capacity [trolox equivalence antioxidant capacity (TEAC), oxygen radical absorbance capacity (ORAC)] as well as total protein, albumin, globulin, total glutathione, conjugated diene and thiobarbituric acid reactive substances (TBARS) were investigated. Treatment with RPO, RTE and RPO + RTE significantly (p>0.05) improved liver SOD and plasma ORAC in the diabetic rats. Similarly, diabetic rats treated with RTE and RPO + RTE enhanced liver GPx. A significant (P<0.05) increase in the plasma TBARS in the diabetic control group was observed when compared with the normal control group. Treatment of diabetic rats with RTE and RPO + RTE reduced plasma TBARS to a level not significantly different at P<0.05 from the normal control group. The results revealed the anti-oxidative potentials of red palm oil, rooibos and their combination in diabetic conditions and hence, they could be useful in the management of diabetes and its complications.

This study was carried out to investigate thein vitroantioxidant potentials of the leaves and fruits ofNauclea latifolia, a straggling shrub or small tree, native to tropical Africa and Asia. Hot water extracts of the leaves and fruits ofNauclea latifoliawere assessed for their total polyphenolic, flavanol, and flavonol contents as well as 1-diphenyl-2-picrylhydrazyl (DPPH) scavenging ability, ferric reducing antioxidant power (FRAP), Trolox equivalence antioxidant capacity (TEAC), and oxygen radical absorbance capacity (ORAC) assays. The aqueous extract of the leaves was found to contain higher level of total polyphenols (11.63±0.023 mg GAE/g), flavanol (1.45±0.10 mg CE/g), and flavonol (2.22±0.37 mg QE/g) than the extract of the fruits with values of1.75±0.02 mg GAE/g (total polyphenol),0.15±0.01 mg CE/g (flavanol), and1.00±0.13 mg QE/g (flavonol). Similarly, the aqueous extract of the leaves also exhibited higher DPPH (IC₅₀20.64 mg/mL), FRAP (86.10±3.46 μmol AAE/g), TEAC (94.83±3.57 μmol TE/g), and ORAC (196.55±0.073 μmol TE/g) than the extract of the fruits with DPPH (IC₅₀120.33 mg/mL), FRAP (12.23±0.40 μmol AAE/g), TEAC (12.48±0.21 μmol TE/g), and ORAC (58.88±0.073 μmol TE/g). The present study showed thatNauclea latifoliahas strong antioxidant potentials with the leaves demonstrating higherin vitroantioxidant activities than the fruits.

AMP-activated protein kinase (AMPK) is known to regulate both glucose and lipid metabolism, which play vital roles in the development of metabolic syndrome. One way of regulating AMPK is through hormonal activation using adiponectin. Patients diagnosed with type-2 diabetes (T2D) and obesity exhibit low adiponectin concentration levels in their blood. Moreover, studies have also shown that inflammatory processes play a significant role in the etiology of these metabolic diseases. In this study, the long-term effects of neonatal intake of oleanolic acid (OA) on the AMPK gene, genes associated with glucose transport and lipid metabolism, adiponectin levels, and inflammatory biomarkers in rats fed with a high fructose diet were investigated. Seven day old pups were randomly divided into five groups and treated as follows; 0.5% dimethylsulphoxide v/v in distilled water vehicle control (CON), oleanolic acid (OA, 60 mg/kg), high fructose diet (HF, 20% w/v), high fructose diet combined with oleanolic acid (HF+OA), and high fructose diet combined with metformin (HF+MET, 500 mg/kg). The treatments were administered once daily until day 14. The rats were then weaned at day 21 and fed standard rat chow and had ad libitum access to plain drinking water until day 112. The quantitative polymerase chain reaction (qPCR) was used to analyze the gene expressions of AMPK, Glut-4, Cpt-1, AdipoR1, AdipoR2, TNF-α, and IL-6 in the skeletal muscles. Bio-Plex Pro magnetic bead-based assay was used to measure plasma levels of inflammatory markers (TNF-α, IL-6, VEGF, and MCP-1) while ELISA kits were used to measure adiponectin concentration in blood plasma. The results obtained in this study showed that neonatal supplementation with OA significantly increased AMPK gene expression approximately ~4-fold in OA fed rats compared to those that were fed with HF alone. In addition, glut-4 gene expression was also significantly higher in the OA treatment group compared to all the other experimental groups except the CON group whereas Cpt-1 gene was more expressed when OA was administered alone. Together, these results indicated that OA can play a role in glucose and lipid metabolism gene regulation. Furthermore, the results showed that the OA group had ~1.5-fold increase in adiponectin concentration when comparedto the HF group. Moreover, HF increased levels of inflammatory cytokines, which was attenuated by neonatal administration of OA. Plasma concentration and gene expression in the skeletal muscle for TNF-α and IL-6 were significantly increased in rats that were treated with HF alone when compared to all the other groups. On the contrary, the high levels of TNF-α and IL-6 were reduced when OA was administered. These findings suggest that intake of oleanolic acid during the neonatal stage of development could be a potential strategic intervention for the long-term prevention of metabolic diseases such as T2D and obesity.