In this study we aimed to investigate the role of tomato seed oil (TSO) in the alleviation of hyperlipidemia and the regulation of gut microbiota in C57BL/6J mice. Mice were divided into the following four diet-based groups: low-fat diet (LF, n = 8), high-fat diet (HF, n = 6), HF diet with TSO replacing one-third of lard (TL, n = 8), and HF diet with TSO replacing two-thirds of lard (TH, n = 8). The results showed that TH significantly reduced weight gain, relative adipose tissue weights, plasma cholesterol, triacylglycerol, low-density lipoprotein cholesterol (LDL-C), ratio of LDL-C to high-density lipoprotein cholesterol (HDL-C), hepatic cholesterol, and total fatty acids, and markedly increased plasma HDL-C. TSO supplementation also dose-dependently increased fecal cholesterol excretion and reduced fecal total fatty acids. This was accompanied by upregulation of the gene expression of hepatic PPARα, ACADL, CYP7A1, LXRα, ABCA1, and SR-B1. Metagenomic analyses demonstrated that TSO tended to reduce the Firmicutes/Bacteroidetes ratio, significantly increased the relative abundance of the genus Lactobacillus, and reduced the relative abundance of the genera Rikenella, Enterorhabdus, unclassified_o_Clostridiales and Ruminococcaceae_UCG-009. These results proved that TSO was effective in attenuating hyperlipidemia in C57BL/6J mice by enhancing fatty acid β-oxidation, reducing cholesterol absorption, promoting cholesterol efflux, and favorably modulating the gut microbiota.

TPSO stands out not only for its abundance of n-3 PUFAs but also for the presence of various important minor components that offer diverse health benefits. TPSO holds great potential as a superior oil that deserves global recognition and promotion.

Ursolic acid (UA) is a triterpenoid acid widely abundant in fruits and vegetables such as apple, blueberry and cranberry. The present study was carried out to investigate the effect of UA supplementation in diet on blood cholesterol, intestinal cholesterol absorption and gut microbiota in hypercholesterolemic hamsters. A total of thirty-two hamsters were randomly assigned to four groups and given a non-cholesterol diet (NCD), a high-cholesterol diet containing 0.1% cholesterol (HCD), an HCD diet containing 0.2% UA (UAL), or an HCD diet containing 0.4% UA (UAH) for 6 weeks. Results showed that UA supplementation reduced plasma cholesterol by 15–16% and inhibited intestinal cholesterol absorption by 2.6–9.2%. The in vitro micellar cholesterol solubility experiment clearly demonstrated that UA could displace 40% cholesterol from micelles. In addition, UA decreased the ratio of Firmicutes to Bacteroidetes, whereas it enhanced the growth of short chain fatty acid (SCFA)-producing bacteria in the intestine. In conclusion, UA possessed a cholesterol-lowering activity and could favorably modulate the gut microbiota.