Short-chain fatty acids (SCFAs) (a microbial fermentation production in the rabbit gut) have an important role in many physiological processes, which may be related to the reduced body fat of rabbits. In the present experiment, we study the function of acetate (a major SCFA in the rabbit gut) on fat metabolism. Ninety rabbits (40 days of age) were randomly divided into three groups: a sham control group (injection of saline for four days); a group experiencing subcutaneous injection of acetate for four days (2 g/kg BM per day, one injection each day, acetate); and a pair-fed sham treatment group. The results show that acetate-inhibited lipid accumulation by promoting lipolysis and fatty acid oxidation and inhibiting fatty acid synthesis. Activated G protein-coupled receptor 41/43, adenosine monophosphate activated protein kinase (AMPK) and extracellular-signal-regulated kinase (ERK) 1/2 signal pathways were likely to participate in the regulation in lipid accumulation of acetate. Acetate reduced hepatic triglyceride content by inhibiting fatty acid synthesis, enhancing fatty acid oxidation and lipid output. Inhibited peroxisome proliferator-activated receptor α (PPARα) and activated AMPK and ERK1/2 signal pathways were related to the process in liver. Acetate reduced intramuscular triglyceride level via increasing fatty acid uptake and fatty acid oxidation. PPARα was associated with the acetate-reduced intracellular fat content.

Deoxynivalenol (DON) is commonly detected in cereals, and is a threat to human and animal health. The effects of microbiological detoxification are now being widely studied. A total of 24 pigs (over four months) were randomly divided into three treatments. Treatment A was fed with a basal diet as the control group. Treatment B was fed with naturally DON-contaminated wheat as a negative control group. Treatment C was fed with a contaminated diet that also had Clostridium sp. WJ06, which was used as a detoxicant. Growth performance, relative organ weight, intestinal morphology, and the intestinal flora of bacteria and fungi were examined. The results showed that after consuming a DON-contaminated diet, the growth performance of the pigs decreased significantly (p < 0.05), the relative organ weight of the liver and kidney increased significantly (p < 0.05), and the integrity of the intestinal barrier was also impaired, though the toxic effects of the contaminated diets on growing pigs were relieved after adding Clostridium sp. WJ06. The data from MiSeq sequencing of the 16S ribosomal ribonucleic acid (rRNA) gene and internal transcribed spacer 1 (ITS1) gene suggested that the abundance of intestinal flora was significantly different across the three treatments. In conclusion, the application of Clostridium sp. WJ06 can reduce the toxic effects of DON and adjust the intestinal microecosystem of growing pigs.

The present study was conducted to investigate the effect of copper supplementation on lipidmetabolism in rabbits. Our study showed dietary copper addition (5-45 mg/kg) increased bodymass gain, but decreased fat and liver weights compared with those in the control group (P <0.05). Copper (45 mg/kg) addition significantly increased the skeletal muscle weight, but inhibitedcytoplasmic lipid accumulation in liver, skeletal muscle and adipose tissue (P < 0.05). Comparedwith the control group, dietary copper addition (45 mg/kg) significantly increased plasmatriglyceride levels but decreased very low density lipoprotein levels (P < 0.05). Copper treatmentsignificantly increased gene expression of carnitine palmitoyltransferase (CPT) 1, CPT2 andperoxisome proliferator-activated receptor (PPAR) a in liver (P < 0.05). In skeletal muscle, CPT1,CPT2, fatty acid transport protein, fatty acid-binding protein, and PPARa mRNA as well asphosphorylated AMP-activated protein kinase (AMPK) levels were significantly up-regulated bycopper treatment (P < 0.05). Rabbits receiving copper supplementation had higher CPT1, CPT2,PPARa and hormone-sensitive lipase mRNA levels in adipose tissue (P < 0.05). In conclusion,copper promoted skeletal muscle growth and reduced fat accretion. PPARa signaling in liver,skeletal muscle and adipose tissues and AMPK signaling in skeletal muscle tissue were involved inthe regulation of lipid metabolism by copper.

The present study was conducted to investigate the effect of Artemisia argyi on the production performance and intestinal barrier of rabbits. Weaned Hyla rabbits (30 d, n=160) of similar body weight were divided into 4 groups (40 rabbits per treatment), and they were fed a control diet or fed an experimental diet supplemented with 3%, 6%, or 9% Artemisia argyi. The results showed that the dietary supplementation with Artemisia argyi did not affect the rabbits’ food intake and body weight gain regardless of the inclusion level but decreased the diarrhea rate and diarrhea index (p < 0.05). Dietary addition of Artemisia argyi increased the small intestine length and villus height/crypt depth, regardless of the inclusion level (p < 0.05). Compared with the control, the Artemisia argyi supplementation increased the gene expression of zonula occludens 1 (ZO-1) and claudin 1 in all segments of the small intestine and regardless of the level of Artemisia argyi (p < 0.05). In the duodenum, a dietary supplementation with 6% and 9% Artemisia argyi increased the immunoglobulins A (IgA) content (p < 0.05). In the jejunum, the Artemisia argyi supplementation decreased interleukin 2 (IL2) and IL6 content regardless of the inclusion level (p < 0.05). In the ileum, a 3% Artemisia argy addition decreased IL2 content while a 6% Artemisia argy addition decreased IL6 content (p < 0.05). Furthermore, 6-9% Artemisia argyi supplementation increased the IgA content in the ileum (p < 0.05). In conclusion, dietary addition of Artemisia argyi reduces diarrhea and modulates the gut immune function without impacting growth performances of rabbits.

Wnt signaling plays an important role in the growth and development of hair follicles (HFs). Among the signaling molecules, Wnt10b was shown to promote the differentiation of primary skin epithelial cells toward the hair shaft and inner root sheath of the HF cells in mice in vitro. Whisker HFs were isolated from Rex rabbits and cultured in vitro to measure hair shaft growth. Meanwhile, dermal papilla cells (DPCs) were isolated and cultrued in vitro. Treatment with AdWnt10b or the Wnt/β-Catenin Pathway inhibitor, XAV939, assessed the DPCs proliferation by CCK-8 assay. And the cell cycle was also analyzed by flow cytometry. We found that Wnt10b could promote elongation of the hair shaft, whereas XAV-939 treatment could eliminated this phenomenon. AdWnt10b treatment promoted the proliferation and induced G1/S transition of DPCs. AdWnt10b stimulation upregulated β-Catenin protein in DPCs. Inhibition of Wnt/β-Catenin signaling by XAV-939 could decreased the basal and Wnt10b-enhanced proliferation of DPCs. And could also suppress the cell cycle progression in DPCs. In summary, our study demonstrates that Wnt10b could promote HFs growth and proliferation of DPCs via the Wnt/β-Catenin signaling pathway in Rex rabbits.

Copper serves as a co-factor for a host of metalloenzymes, particularly cytochrome c oxidase (COX). Although it is known that impaired COX function can lead to the excessive accumulation of reactive oxygen species (ROS), the mechanisms underlying how copper depletion leads to cell damage are poorly understood. Here, we have investigated the role of copper depletion during ferroptosis. The bathocuproinedisulfonic (BCS) treatment depolarized the mitochondrial membrane potential, increased the total cellular ROS levels, stimulated oxidative stress, and reduced the glutathione levels. Moreover, the depletion of copper limited the protein expression of glutathione peroxidase 4 (GPX4), which is the only enzyme that is known to prevent lipid peroxidation. Furthermore, we found that copper depletion decreased the sensitivity of the dermal papilla cells (DPCs) to erastin (an inducer of ferroptosis), and the ferroptosis inhibitor ferrostatin-1 (Fer-1) partially prevented BCS-mediated cell death. Overall, these findings establish a direct link between copper and ferroptosis; BCS-mediated copper depletion strongly enhances ferroptosis via mitochondrial perturbation and a reduction in antioxidative mechanisms.