## 4 Discussion
Moreover, the organic BLS juice containing 77.5 mg of polyphenols prevented the increase in the activity of the enzyme GPx induced by the hyperlipidic diet 30 min after ingestion, compared with the placebo, after a high-fat meal. In addition, the hyperlipidic meal induced hypertriglyceridemia after 120 min and increased MDA after 30 min. The vitexin-2-O-rhamnoside is a vitexin derivative flavonoid glycoside derived from apigenin found in many food sources [36]. Studies has reported that vitexin is capable ofdonating electrons and acting as a good radical scavenger and being good for antioxidant enzyme-protecting activities, which could effectively prevent cells from oxidative damage [36; 37]. Considering the importance of reducing food waste, some studies [8; 19; 38] have characterized vitexin and its derivatives as the most prominent compounds in beet leaves and stalks, highlighting the use of unconventional parts of foods in an attempt to improve the effects of unregulated intake of fatty meals. The ingestion of high-fat meals is probably the most potent physiological factor in increasing the serum concentration of TG in the postprandial period [39]. Unlike meals rich in polyunsaturated fatty acids, meals rich in saturated fat such as the one used in the present study can stimulate transcription factors such as sterol response element-binding protein 1c (SREBP-1c), which stimulates the transcription of genes that encode multiple enzymes involved in the synthesis of fatty acids and their incorporation into TG [40]. Thus, TG and fatty acids accumulate mainly in the liver and plasma [41]. In order to assess the postprandial metabolic and hormonal response to different diets, [PERSON] et al. [42] conducted a randomized, controlled crossover clinical study with 10 participants and reported that a high-fat diet aggravated hypertriglyceridemia in obese individuals with dyslipidemia. Corroborating these results, [PERSON] et al. [43] showed an increase in the TG concentrations in 15 individuals who were overweight within 8 h of eating a high-fat meal. This increase in the serum TG concentration and a probable inefficiency in the removal of triglyceride-rich lipoproteins (LRTs) can increase the inflammatory process and intensify the increase of reactive species in the postprandial period, consequently leading to oxidative damage [44]. In the present study, the biomarker of inflammatory activity TNF\(\alpha\) was evaluated, which is closely associated with low-grade inflammation, systemic oxidative stress and the formation of atherosclerotic plaque in obese and dyslipidemic individuals [45; 46]. However, there were no changes in this biomarker in the study period. A systematic review conducted by [PERSON] et al. (2017) [47] analyzed the degree and duration of postprandial action of five relevant inflammation biomarkers, including TNF\(\alpha\). The authors reported that 70% of the studies that evaluated TNF\(\alpha\) after eating a high-fat diet did not observe changes in this biomarker. The authors concluded that while TNF\(\alpha\) is a good marker of low-grade inflammatory activity, it does not seem to be sufficiently responsive to a stimulus with hyperlipidic diets or might be too variable to be a reliable indicator of the inflammatory response in the immediate period after ingestion of a hyperlipidic diet. On the other hand, in our study, the high-fat diet caused an increase in oxidative damage, demonstrated by the increase in MDA in patients who ingested the placebo, similar to other studies conducted with dyslipidemia individuals [48; 49]. The increase in ROS production, evidenced by this increase in MDA, may lead to the activation of NF-E2-related factor 2 (Nrf2), which will promote the transcription of genes that encode antioxidant enzymes [50], increasing the activity of these enzymes. There was a significant increase in GPx activity in the placebo group (\(p\) = 0.026) and an attenuation of this increase in the high dose group (\(p\) = 0.045).