Corrigendum: Effects of essential oil extracted from Artemisia argyi leaf on lipid metabolism and gut microbiota in high-fat diet-fed mice.

[This corrects the article DOI: 10.3389/fnut.2022.1024722.].

Flavonoids, gut microbiota, and host lipid metabolism.

Flavonoids are widely distributed in nature and have a variety of beneficial biological effects, including antioxidant, anti-inflammatory, and anti-obesity effects. All of these are related to gut microbiota, and flavonoids also serve as a bridge between the host and gut microbiota. Flavonoids are commonly used to modify the composition of the gut microbiota by promoting or inhibiting specific microbial species within the gut, as well as modifying their metabolites. In turn, the gut microbiota extensively metabolizes flavonoids. Hence, this reciprocal relationship between flavonoids and the gut microbiota may play a crucial role in maintaining the balance and functionality of the metabolism system. In this review, we mainly highlighted the biological effects of antioxidant, anti-inflammatory and antiobesity, and discussed the interaction between flavonoids, gut microbiota and lipid metabolism, and elaborated the potential mechanisms on host lipid metabolism.

Effects of essential oil extracted from Artemisia argyi leaf on lipid metabolism and gut microbiota in high-fat diet-fed mice.

Artemisia argyi leaf is a well-known species in traditional Chinese medicine, and its essential oil (AAEO) has been identified to exert various physiological activities. The aim of this study was to investigate the effects of AAEO on lipid metabolism and the potential microbial role in high-fat diet (HFD)-fed mice. A total of 50 male mice were assigned to five groups for feeding with a control diet (Con), a high-fat diet (HFD), and the HFD plus the low (LEO), medium (MEO), and high (HEO) doses of AAEO. The results demonstrated that dietary HFD markedly increased the body weight gain compared with the control mice (p < 0.05), while mice in the HEO group showed a lower body weight compared to the HFD group (p < 0.05). The weight of fatty tissues and serum lipid indexes (TBA, HDL, and LDL levels) were increased in response to dietary HFD, while there was no significant difference in AAEO-treated mice (p < 0.05). The jejunal villus height was dramatically decreased in HFD-fed mice compared with the control mice, while HEO resulted in a dramatically higher villus height than that in the HFD group (p < 0.05). Microbial α-diversity was not changed in this study, but ß-diversity indicated that microbial compositions differed in control, HFD, and EO subjects. At the genus level, the relative abundance of Bacteroides was greater (p < 0.05) in the feces of the Con group when compared to the HFD and EO groups. On the contrary, the abundance of Muribaculum was lower in the Con group compared to the HFD and EO groups (p < 0.05). Although the Muribaculum in the EO group was lower than that in the HFD group, there was no statistically notable difference between the HFD and EO groups (p > 0.05). Simultaneously, the relative abundance of Alistipes (p < 0.05) and Rikenella (p < 0.05) was also dramatically higher in the Con group than in the HFD and EO groups. The abundance of norank_f__norank_o__Clostridia_UCG-014 was lower in the HFD or EO group than in the Con group (p < 0.05). In conclusion, the results suggested that HEO could affect body weight and lipid metabolism without gut microbes in ICR mice, and it was beneficial for the structure of the jejunal epithelial tissue.

Camellia (Camellia oleifera Abel.) Seed Oil Regulating of Metabolic Phenotype and Alleviates Dyslipidemia in High Fat-Fed Mice through Serum Branch-Chain Amino Acids.

Camellia (Camellia oleifera Abel.) seed oil (CO) has been shown to effectively reduce the blood lipid level of its host due to its fatty acid content, but the specific molecular mechanism associated with the metabolic phenotype after digestion is not clear. Here, we further investigated the relationship between branched-chain amino acids (BCAA) and the metabolic phenotype that may exhibit the anti-dyslipidemia effect of CO on mice fed a high-fat diet for 30 day C57BL/6J male mice were allocated to three groups: the control group (Cont), the high-fat feed group (HFD), and a high-fat feed group with CO treatment (CO). A serum sample was collected to detect lipid biomarkers and BCAA concentration. Notably, Low-density lipoprotein (LDL), Total Cholesterol (TC), and Triglycerides (TG) showed a significant decrease, whereas High-density lipoprotein (HDL) increased in CO mice but not in the HFD group. The concentration of Isoleucine (Ile), leucine (Leu), and valine (Val) was similar between the Cont and CO groups compared with the HFD group, exhibiting an inhibition induced by CO in mice fed with a high-fat diet. A metabolic phenotype from serum examined by non-targeted metabolite analysis using UHPLC/MS showed most metabolites exhibited lipid and BCAA metabolism. The results indicated that CO treatment notably regulated the metabolism of arachidonic acid and steroid biosynthesis in response to HFD-induced dyslipidemia. In addition, the expression of PPARγ genes that correlated with the BCAA and serum lipid biomarkers were compared, and significant inhibition was noticed, which might lead to the potential exposure of the anti-dyslipidemia mechanism of CO in HFD-fed mice. In conclusion, the expression of PPARγ genes, serum lipid level, BCAA concentration, and the metabolic phenotype was significantly positive in correlation with a high-fat diet, whereas oral CO improved the biomarkers and metabolism of some specific serum metabolites in HFD-fed mice.

Camellia (Camellia oleifera bel.) seed oil reprograms gut microbiota and alleviates lipid accumulation in high fat-fed mice through the mTOR pathway.

Camellia (Camellia oleifera bel.) seed oil (CO) is extensively used as an edible oil in China and Asian countries owing to its high nutritional and medicinal values. It has been shown that a high-fat diet enhances lipid accumulation and induces intestinal microbiota imbalance in mice. However, it is still to be learned whether CO prevents dyslipidemia through gut microbiota. Here, using 16S rRNA gene sequencing analysis of the gut microbiota, we found that oral CO relieved lipid accumulation and reversed gut microbiota dysbiosis. Compared to mice (C57BL/6J male mice) fed a high-fat diet, treatment with CO regulated the composition and functional profiling communities related to the lipid metabolism of gut microbiota. The abundances of Dubosiella, Lactobacillus, and Alistipes were markedly increased in CO supplementation mice. In addition, the colon levels of isobutyric acid, pentanoic acid, and isovaleric acid were similar between the control and CO supplementation mice. Besides, the results indicated that CO supplementation in mice alleviated lipid droplet accumulation in the hepatocytes and subcutaneous adipose tissue, although the liver index did not show a difference. Notably, CO supplementation for 6 weeks significantly reduced the levels of LDL, TC, and TG, while enhancing the level of HDL in serum and liver. Meanwhile, we also identified that CO supplementation suppressed the mammalian target of rapamycin (mTOR) signaling pathway in high fat-fed (HF-fed) mice. Taken together, our results suggest that CO improved dyslipidemia and alleviated lipid accumulation in HF-fed mice, the molecular mechanisms possibly associated with the reorganization of gut microbiota, in particular, Alistipes and Dubosiella, mediated the inhibition of the mTOR pathway.

Effects of melatonin on intestinal function and bacterial compositions in sucking piglets.

Melatonin has been reported to affect intestinal function by targeting microbiome, morphological structure, barrier integrity and nutrient absorptive system. While the effect of melatonin on intestinal development in newborn infants is obscure, thus, this study firstly attempted to investigate the hypothesis that melatonin treatment improves intestinal development in sucking piglets. 14 healthy newborn piglets received 10 ml melatonin solution (1 mg/ml) or drinking water (n = 7) for 21 days. The results showed that oral administration of melatonin increased liver relative weight (p < 0.05) but failed to affect growth performance in sucking piglets (p > 0.05). Immunostaining jejunal samples from melatonin group showed high expressions of nnos and claudin1, indicating that melatonin improved intestinal neural development and barrier integrity. Also, melatonin promoted intestinal absorptive function evidenced by the increased serum proline concentration in melatonin-treated piglets compared with the control (p < 0.05). Gut microbiota compositions were tested by 16S rDNA sequencing and the results showed that melatonin increased the relative abundance of Actinobacteria compared with the control (p < 0.05) at the phylum level. However, Selenomonadales was markedly reduced compared with the control at the order level (p < 0.05). Gut and faecal volatile fatty acids were tested to evaluate the microbiota metabolism, but no difference was noticed in volatile fatty acid concentrations (p > 0.05). Melatonin improved intestinal development by affecting neural development, barrier integrity, nutrient absorption and microbiota in sucking piglets.

Dietary resveratrol supplementation inhibits heat stress-induced high-activated innate immunity and inflammatory response in spleen of yellow-feather broilers.

The aim of this study was to investigate the effect of dietary resveratrol supplementation on innate immunity and inflammatory responses in the spleen of yellow-feather broilers under heat stress. A total of 288 yellow-feather broilers of 28-day-old were randomly assigned to 3 treatment groups with 6 replicates. A thermo-neutral group (TN) (24 ± 2°C) received a basal diet and another 2 heat-stressed groups (37 ± 2°C for 8 h/D and 24 ± 2°C for the remaining time) were fed the basal diet (HT) or basal diet with 500 mg/kg resveratrol (HT+Res) for 14 consecutive days. The results showed that heat stress decreased (P < 0.05) the growth index of thymus, spleen, and bursa of Fabricius, reduced (P < 0.05) the levels of complement C3 and C4 in serum. Heat stress also caused activation of inflammatory immune responses evidenced by increased (P < 0.05) the mRNA abundance of HSP (heat shock protein) 70, toll-like receptor (TLR)1, TLR4, TLR5, myeloid differentiation factor-88 (MyD88), nucleotide-binding oligomerization domain 1 (NOD1), Dectin-1, transforming growth factor-ß-activated kinase 1 (TAK1), interleukin (IL)-1, IL-4, IL-6, and tumor necrosis factor (TNF)-α, but decreased the mRNA abundance of interferon (IFN)-γ, activated nuclear factor kappa B (NF-κB), mitogen-activated protein kinases (MAPK), and phosphoinositide-3 kinases-protein kinase B (PI3K/AKT) signaling pathways. Dietary supplementation with resveratrol improved (P < 0.05) the growth index of thymus, spleen and bursa Fabricius, and increased (P < 0.05) the serum level of complement C3 under heat stress. In addition, resveratrol reduced (P < 0.05) the mRNA abundance of HSP70, TLR4, TLR5, NOD1, Dectin-1, and TAK1, and inhibited the NF-κB, MAPK and PI3K/AKT signaling pathway via down-regulated the phosphorylation of p65, extracellular signal-regulated kinases 1/2, c-Jun N-terminal protein kinase and AKT, as well as decreased the inflammatory cytokines expression, including IL-1, IL-4, IL-6, and TNF-α in the spleen under heat stress. Collectively, dietary resveratrol could have beneficial effects to regulate innate immunity and inflammatory response, via inhibiting the activation of NF-κB, MAPK, and PI3K/AKT signaling pathways induced by heat stress in the spleen.