Molecular characterization and expression patterns of two hormone-sensitive lipase genes in common carp Cyprinus carpio.

The hormone-sensitive lipase (HSL) gene plays an important role in mammals' lipid metabolism. Therefore, its function in fish is capturing increasing attention. In this study, two distinct cDNAs, designated HSL1 and HSL2, are firstly identified from common carp Cyprinus carpio. The full-length cDNA of HSL1 and HSL2 consists of 3379 bp and 2732 bp, encoding polypeptide of 693 and 847 amino acids, respectively, and shares 60.6% amino acid identity. Phylogenetic analysis suggests that HSL1 and HSL2 are derived from paralogous genes, which might have arisen during a teleost-specific genome duplication event. The two HSL mRNAs are differentially expressed, both in terms of distribution among tissues and in terms of abundance during embryogenesis. Moreover, both HSL mRNAs are expressed in various tissues, the highest in abdominal fat. Meanwhile, the two HSLs are detected at all stages of embryonic development, suggesting that they could be functional and involved in embryogenesis. In addition, the results show that the mRNA expression level of HSL2 in the high group of intramuscular fat content is significantly higher than that in the low group (P < 0.01). The research provides basic data for developing a further understanding of the function of HSL as well as molecular regulation mechanism in fat metabolism of common carp.

Ecofriendly Preparation of Cellulose Nanocrystal-Coated Polyimide Fiber: Strategy for Improved Wettability.

Polyimide (PI) fibers pose potential problems in applications. Their low surface activity causes poor interfacial wettability, easy agglomeration in aqueous solutions, and poor dispersibility. Therefore, this work proposes a method of surface modification of alkali-treated PI fibers with cellulose nanocrystals (CNCs) under the combined catalytic action of a Lewis acid and a crosslinker. The dispersion degree of PI fibers in aqueous solution before and after CNC modification and the contact angle of the PI fiber paper are measured. The results show that the wettability of the PI fibers improved. Furthermore, the structure and properties of PI fibers before and after CNC treatment are characterized via scanning electron microscopy, Fourier transform infrared spectroscopy, X-ray photoelectron spectroscopy, and thermogravimetric analysis. The pore-size distribution of the PI-fiber paper is measured by a porous-material pore-size analyzer. Compared with the original PI fibers, the oxygen content of the fiber surfaces increases after CNC treatment because of the esterification reaction and crosslinking that occur on the surfaces. The increase in the number of oxygen-containing polar groups and the increased surface roughness of the PI fiber improve its wettability. The contact angle of the PI fiber paper in deionized water is reduced by 14.9° and that in ethanol by 4.8°; the fiber dispersion degree is increased by 45%. These results indicate that the fibers have remarkably improved hydrophilicity and dispersion in the aqueous phase. Therefore, the method developed herein is to prepare high-performance organic fibers and corresponding composite materials.

Supplementation of Weizmannia coagulans BC2000 and Ellagic Acid Inhibits High-Fat-Induced Hypercholesterolemia by Promoting Liver Primary Bile Acid Biosynthesis and Intestinal Cholesterol Excretion in Mice.

The probiotic Weizmannia coagulans (W. coagulans) BC2000 can increase the abundance of intestinal transforming ellagic acid (EA) bacteria and inhibit metabolic disorders caused by hyperlipidemia by activating liver autophagy. This study aimed to investigate the inhibitory effects of W. coagulans BC2000 and EA on hyperlipidemia-induced cholesterol metabolism disorders. C57BL/6J mice (n = 10 in each group) were fed a low-fat diet, high-fat diet (HFD), HFD supplemented with EA, HFD supplemented with EA and W. coagulans BC77, HFD supplemented with EA, and W. coagulans BC2000. EA and W. coagulans BC2000 supplementation prevented HFD-induced hypercholesterolemia and promoted fecal cholesterol excretion. Transcriptome analysis showed that primary bile acid biosynthesis in the liver was significantly activated by EA and W. coagulans BC2000 treatments. EA and W. coagulans BC2000 treatment also significantly increased the intestinal Eggerthellaceae abundance and the liver EA metabolites, iso-urolithin A, Urolithin A, and Urolithin B. Therefore, W. coagulans BC2000 supplementation promoted the intestinal transformation of EA, which led to the upregulation of liver bile synthesis, thus preventing hypercholesterolemia.

Weizmannia coagulans BC2000 Plus Ellagic Acid Inhibits High-Fat-Induced Insulin Resistance by Remodeling the Gut Microbiota and Activating the Hepatic Autophagy Pathway in Mice.

(1) Background: Ellagic acid (EA) acts as a product of gut microbiota transformation to prevent insulin resistance, which is limited by high-fat diet (HFD)-induced dysbiosis. The aim of this study was to investigate the synergistic effects and mechanisms of supplementation with the probiotic Weizmannia coagulans (W. coagulans) on the prevention of insulin resistance by EA; (2) Methods: C57BL/6J mice were divided into five groups (n = 10/group): low-fat-diet group, high-fat-diet group, EA intervention group, EA + W. coagulans BC77 group, and EA + W. coagulans BC2000 group; (3) Result: W. coagulans BC2000 showed a synergistic effect on EA's lowering insulin resistance index and inhibiting high-fat diet-induced endotoxemia. The combined effect of BC2000 and EA activated the autophagy pathway in the mouse liver, a urolithin-like effect. This was associated with altered ß-diversity of gut microbiota and increased Eggerthellaceae, a potential EA-converting family. Ellagic acid treatment alone and the combined use of ellagic acid and W. coagulans BC77 failed to activate the hepatic autophagy pathway; (4) Conclusions: W. coagulans BC2000 can assist EA in its role of preventing insulin resistance. This study provides a basis for the development of EA-rich functional food supplemented with W. coagulans BC2000.

Prevention of High-Fat Diet-Induced Hypercholesterolemia by Lactobacillus reuteri Fn041 Through Promoting Cholesterol and Bile Salt Excretion and Intestinal Mucosal Barrier Functions.

Objectives: Lactobacillus reuteri Fn041 (Fn041) is a probiotic isolated from immunoglobulin A coated microbiota in the human breast milk of Gannan in China with a low incidence of hypercholesterolemia. This study aims to explore the role and mechanism of Fn041 in preventing hypercholesterolemia caused by a high-fat diet in mice. Methods: C57BL/6N mice were fed a low-fat diet or a high-fat diet and gavage with Fn041 and Lactobacillus rhamnosus GG (LGG) for 8 weeks. Results: Both Fn041 and LGG prevented the occurrence of hypercholesterolemia, liver and testicular fat accumulation. In addition, a high-fat diet causes intestinal dysbiosis and mucosal barrier damage, which is associated with hypercholesterolemia. Fn041 prevented the high-fat diet-induced reduction in alpha diversity of intestinal microbiota and intestinal mucosal barrier damage. Fn041 treatment significantly increased fecal total cholesterol and total bile acids. Conclusions: Fn041 prevented hypercholesterolemia by enhancing cholesterol excretion and mucosal barrier function.

Prevention of Atopic Dermatitis in Mice by Lactobacillus Reuteri Fn041 Through Induction of Regulatory T Cells and Modulation of the Gut Microbiota.

SCOPE: The development of atopic dermatitis (AD) in infants is closely related to the lagging development of intestinal microbiota, including that inoculated by breast milk bacteria, and immune development. Lactobacillus reuteri Fn041 is a secretory immunoglobulin A (sIgA) -coated bacterium derived from human milk. METHODS AND RESULTS: We intervene with L. reuteri Fn041 in maternal and offspring BALB/C mice during late gestation and lactation and after weaning of the pups, respectively. AD is then induced with MC903. L. reuteri Fn041 significantly suppresses AD symptoms such as skin swelling, mast cell, and eosinophil infiltration. This effect is attributed to the regulation of the systemic Th1 and Th2 cytokine ratios and the promotion of CD4+ CD25+ Foxp3+ regulatory T cell proliferation in mesenteric lymph nodes. It is also associated with the regulation of intestinal microbiota, particularly promoting Lactobacillus and Akkermansia. CONCLUSION: Our study strengthens the understanding that breast milk-derived sIgA coated potential probiotics are involved in the development of infant intestinal microbiota, thus promoting immune development and preventing allergic diseases, and expanding the knowledge of breast milk sIgA and bacterial interactions on infant immune development.

Depletion of gut secretory immunoglobulin A coated Lactobacillus reuteri is associated with gestational diabetes mellitus-related intestinal mucosal barrier damage.

Changes in secretory immunoglobulin A (SIgA) coated bacteria from early to late pregnancy were associated with the development of gestational diabetes mellitus (GDM). SIgA coated beneficial gut bacteria, which are depleted in GDM, are potential probiotics for the prevention of GDM. We investigated blood biochemistry, chronic inflammation, mucosal barrier biomarkers and faecal SIgA coated microbiota in healthy early pregnancy (T1H, n = 50), late pregnancy (T3H, n = 30) and women with GDM (T3D, n = 27). The "leaky gut" markers, zonulin and lipopolysaccharide (LPS), significantly increased in T3D compared to the T3H group. The Shannon index of SIgA coated microbiota was elevated in late pregnancy compared to early pregnancy and was the highest in the T3D group (p < 0.001). The T3D group was enriched in SIgA coated Escherichia and Streptococcus and depleted in Lactobacillus and Bifidobacterium. Blood glucose (BG) positively correlated with zonulin (p < 0.001) and LPS (p < 0.05). Lactobacillus reuteri negatively correlated with BG (p < 0.05), zonulin (p < 0.05) and LPS (p < 0.01). Lactobacillus reuteri QS01 isolated from the feces of T1H significantly reduced LPS released by the gut microbiota of GDM individuals in vitro. In conclusion, GDM may be related to intestinal mucosal damage and inflammation-induced dysbiosis of SIgA coated microbiota. SIgA coated L. reuteri can reduce the level of LPS of GDM in vitro.