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During the fermentation of ripened pu-erh tea (RPT), the composition of lipids and other compounds changes significantly. In this study, we conducted industrial fermentation of RPT and observed that the levels of water extract, tea polyphenols, free amino acids, catechins, caffeine, rutin, theophylline, luteolin, and myricetin decreased, while the level of soluble sugar increased. Additionally, the levels of gallic acid, quercetin, ellagic acid, and kaempferol first increased and then decreased during fermentation. We identified a total of 731 lipids, which were classified into seven categories using a lipomics method. Among these lipids, 85 with relatively high contents decreased, while 201 lipids with low contents increased after fermentation. This led to an overall decrease in the sum contents of lipids and dominant lipids, including glycerophospholipids and saccharolipids. We also detected 33 medium- and long-chain fatty acids, with α-linolenic acid (881.202 ± 12.13–1322.263 ± 19.78 μg/g), palmitic acid (797.275 ± 19.56–955.180 ± 30.49 μg/g), and linoleic acid (539.634 ± 15.551–706.869 ± 12.14 μg/g) being the predominant ones. Coenzymes Q9 (62.76–63.57 μg/g) and Q10 (50.82–59.33 μg/g) were also identified in the fermentation process. Our findings shed light on the changes in lipids during the fermentation of RPT and highlight the potential bio-active compounds, such as α-linolenic acid, linoleic acid, Coenzymes Q9, and Q10, in ripened pu-erh tea. This contributes to a better understanding of the fermentation mechanism for RPT.

Probiotics have been proved to have beneficial effects in improving hyperlipidemia. The purpose of the current research was to investigate the ameliorative effects of Pediococcus acidilactici FZU106, isolated from the traditional brewing of Hongqu rice wine, on lipid metabolism and intestinal microbiota in high-fat diet (HFD)-induced hyperlipidemic rats. Results showed that P. acidilactici FZU106 intervention obviously inhibited the abnormal increase of body weight, ameliorated serum and liver biochemical parameters related to lipid metabolism and oxidative stress. Histopathological evaluation also showed that P. acidilactici FZU106 could significantly reduce the excessive lipid accumulation in liver caused by HFD-feeding. Furthermore, P. acidilactici FZU106 intervention significantly increased the short-chain fatty acids (SCFAs) levels in HFD-fed rats, which was closely related to the changes of intestinal microbial composition and metabolism. Intestinal microbiota profiling by high-throughput sequencing demonstrated that P. acidilactici FZU106 intervention evidently increased the proportion of Butyricicoccus, Pediococcus, Rothia, Globicatella and [Eubacterium]_coprostanoligenes_group, and decreased the proportion of Corynebacterium_1, Psychrobacter, Oscillospira, Facklamia, Pseudogracilibacillus, Clostridium_innocuum_group, Enteractinococcus and Erysipelothrix in HFD-fed rats. Additionally, P. acidilactici FZU106 significantly regulated the mRNA levels of liver genes (including CD36, CYP7A1, SREBP-1c, BSEP, LDLr and HMGCR) involved in lipid metabolism and bile acid homeostasis. Therefore, these findings support the possibility that P. acidilactici FZU106 has the potential to reduce the disturbance of lipid metabolism by regulating intestinal microflora and liver gene expression profiles.