# A Narrative Review of Metabolomic Insights into Olive Oil's Nutritional Value
## 2 Olive Oil Metabolomics
### Oleic Acid  
About 70-80% of olive oil corresponds to oleic acid (OA), a monounsaturated fatty acid (MUFA). The main health benefits of olive oil have been attributed to OA for several years. For instance, it facilitates healing of cutaneous wounds by inhibiting early production of nitric oxide (NO). The lack of NO leads to the secretion of mediators by fibroblasts and inflammatory cells and a reduction in collagen deposition at the wound [17]. Furthermore, as an MUFA, OA regulates the structure of the cellular membrane, resulting in the regulation of adrenergic receptors and, consequently, a decrease in blood pressure, highlighting its important hypotensive effect [18]. The antioxidant effect of this metabolite is notable because it regulates the synthesis and activity of several antioxidant enzymes, which may contribute to its hypotensive effect by improving endothelial dysfunction. In general, supplementation with OA can reduce the levels of C-reactive protein (CRP), an inflammatory biomarker, thereby diminishing the risk of CVDs [19; 20]. Although a study analyzing data from several randomized trials concluded that there were no significant alterations in important pro-inflammatory mediators, such as interleukin (IL)-6 or tumour necrosis factor alpha (TNF-\(\alpha\)), following OA treatment [19], some authors described a reduction in the levels of these mediators [21; 22]. Even though several other anti-inflammatory effects of OA have been described, such as increased regulatory T cells and decreased nuclear factor kappa B (NF-\(\kappa\)B) levels in macrophages, some proinflammatory effects appear to be important. For instance, OA causes increased levels of reactive oxygen species (ROS) and matrix metalloproteinase (MMP)-9 in processes mediated by phospholipase C as well as increased granule release and phagocytosis in neutrophils. ROS production following OA supplementation can increase the killing capacity and phagocytosis of neutrophils, thereby contributing to the efficiency of the immune system. Moreover, OA enhanced lymphocyte proliferation [23]. OA plays a fundamental role in the development of insulin resistance and diabetes. Insulin resistance frequently leads to the development of diabetes, both of which are caused by decreased mitochondrial function [20]. This decreased mitochondrial function might result in incomplete oxidation of fatty acids, leading to the accumulation of lipid metabolites and lower generation of adenosine triphosphate (ATP). Normally, ATP regulates the exocytosis of insulin granules in pancreatic \(\beta\) cells, leading to the closure of ATP-sensitive K\({}^{+}\) channels and, consequently, the depolarization of these cells. Subsequently, calcium channels open, allowing the secretion of granules containing insulin. Insulin resistance occurs in the absence of high ATP levels [24; 25; 26]. OA upregulates the expression of genes responsible for fatty acid oxidation and improves insulin sensitivity. Furthermore, activation of nuclear respiratory factor 1 (NRF-1) by OA upgrades mitochondrial biogenesis, potentially contributing to decreased resistance [20]. There is a correlation between OA and a lower prevalence of neurodegenerative diseases [27]. This fatty acid has shown potential for therapeutic use because it can improve amyloidosis in cellular and mouse models of Alzheimer's disease [28]. Furthermore, both  
Figure 1: Graphical representation of olive oil components. MUFA = monounsaturated fatty acid; PUFA = polyunsaturated fatty acid. OA and linoleic acid, a polyunsaturated fatty acid (PUFA) that also constitutes olive oil, are associated with a decreased risk of [PERSON]'s disease. In fact, a complex containing camel \(\alpha\)-lactalbumin and OA has shown promising results as a potential therapeutic component by decreasing oxidative stress, improving dopamine levels, enhancing the expression of silent mating type information regulation 2 homolog (SIRT1), and preventing neurodegeneration [29].