The consumption of carotenoids has beneficial effects on health, reducing the risk of certain forms of cancer, cardiovascular diseases, and macular degeneration, among others. The mechanism of action of carotenoids has not been clearly identified; however, it has been associated with the antioxidant capacity of carotenoids, which acts against reactive oxygen species and inactivating free radicals, although it has also been shown that carotenoids modulate gene expression. Dietary carotenoids are absorbed and accumulated in the liver and other organs, where they exert their beneficial effects. In recent years, it has been described that the intake of carotenoids can significantly reduce the risk of suffering from liver diseases, such as non-alcoholic fatty liver disease (NAFLD). This disease is characterized by an imbalance in lipid metabolism producing the accumulation of fat in the hepatocyte, leading to lipoperoxidation, followed by oxidative stress and inflammation. In the first phases, the main treatment of NAFLD is to change the lifestyle, including dietary habits. In this sense, carotenoids have been shown to have a hepatoprotective effect due to their ability to reduce oxidative stress and regulate the lipid metabolism of hepatocytes by modulating certain genes. The objective of this review was to provide a description of the effects of dietary carotenoids from fruits and vegetables on liver health.

The objective of this work was to identify the effect of tomato juice on the expression of genes and levels of metabolites related to steatosis in rats. Male Sprague Dawley rats (8 weeks-old) were grouped (6 rats/group) in four experimental groups: NA (normal diet and water), NL (normal diet and tomato juice), HA (high-fat diet and water), and HL (high-fat diet and tomato juice). After an intervention period of 5 weeks, rats were sacrificed and biochemical parameters, biomarkers of oxidative stress, liver metabolites, and gene expression were determined. Although the H diet provoked dislipemia related to steatosis, no changes in isoprostanes or liver malondialdehyde (MDA) were observed. Changes in the gene expression of the HA group were produced by the high consumption of fat, whereas the consumption of tomato juice had different effects, depending on the diet. In the NL group, the genes involved in β-oxidation were upregulated, and in groups NL and HL upregulation of CD36 and downregulation of APOB and LPL were observed. In addition, in the HL group the accumulation of lycopene upregulated the genes FXR and HNF4A, which have been suggested as preventive factors in relation to steatosis. Regarding the metabolomics study, intake of tomato juice stimulated the biosynthesis of glutathione and amino acids of the transulfurization pathway, increasing the levels of metabolites related to the antioxidant response.

The purpose of this work was to evaluate the effect of dietary carotenoids from spinach on the inflammation and oxidative stress biomarkers, liver lipid profile, and liver transcriptomic and metabolomics profiles in Sprague–Dawley rats with steatosis induced by a high-fat diet. Two concentrations of spinach powder (2.5 and 5%) were used in two types of diet: high-fat (H) and standard (N). Although rats fed diet H showed an accumulation of fat in hepatocytes, they did not show differences in the values of adiponectin, tumor necrosis factor alpha (TNF-α), and oxygen radical absorption (ORAC) in plasma or of isoprostanes in urine compared with animals fed diet N. The consumption of spinach and the accumulation of α and β carotenes and lutein in the liver was inversely correlated with serum total cholesterol and glucose and the content of hepatic cholesterol, increasing monounsaturated fatty acids (MUFA), polyunsaturated fatty acids (PUFA) and reducing cholesterol in the livers of rats fed diet H and spinach. In addition, changes in the expression of genes related to the fatty liver condition occurred, and the expression of genes involved in the metabolism of fatty acids and cholesterol increased, mainly through the overexpression of peroxisome proliferator activated receptors (PPARs). Related to liver metabolites, animals fed with diet H showed hypoaminoacidemia, mainly for the glucogenic aminoacids. Although no changes were observed in inflammation and oxidative stress biomarkers, the consumption of spinach modulated the lipid metabolism in liver, which must be taken into consideration during the dietary treatment of steatosis.

In rats with hepatic steatosis, spinach intake increased gut Lactobacillus and lowered cholesterol and glucose.