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.

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.

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.

This study was conducted to investigate the impacts of chlorogenic acid (CGA) on growth performance, intestinal permeability, intestinal digestion and absorption-related enzyme activities, immune responses, antioxidant capacity and cecum microbial composition in weaned rabbits. One hundred and sixty weaned rabbits were allotted to four treatment groups and fed with a basal diet or a basal diet supplemented with 400, 800, or 1,600 mg/kg CGA, respectively. After a 35-d trial, rabbits on the 800 mg/kg CGA-supplemented group had higher (p < 0.05) ADG and lower (p < 0.05) F/G than those in control (CON) group. According to the result of growth performance, eight rabbits per group were randomly selected from the CON group and 800 mg/kg CGA group to collect serum, intestinal tissue samples and cecum chyme samples. Results showed that compared with the CON group, supplementation with 800 mg/kg CGA decreased (p < 0.05) levels of D-lactate, diamine oxidase, IL-1β, IL-6, and malondialdehyde (MDA), and increased IL-10 concentration in the serum; increased (p < 0.05) jejunal ratio of villus height to crypt depth, enhanced (p < 0.05) activities of maltase and sucrase, increased (p < 0.05) concentrations of IL-10, T-AOC, MHCII and transforming growth factor-α, and decreased (p < 0.05) levels of TNF-α and MDA in the jejunum of weaned rabbits. In addition, results of high-throughput sequencing showed that CGA supplementation elevated (p < 0.05) microbial diversity and richness, and increased (p < 0.05) the abundances of butyrate-producing bacteria (including genera V9D2013_group, Monoglobus, Papillibacter, UCG-005, and Ruminococcus). These results indicated that dietary supplementation with 800 mg/kg CGA could improve the growth performance of weaned rabbits by enhancing intestinal structural integrity, improving the intestinal epithelium functions, and modulating the composition and diversity of gut microbiota.

Diets containing higher levels of fat can lead to obesity, which is potentially harmful to health. Endogenous butyric acid is produced by intestinal microbial fermentation and participates in lipid metabolism. However, there is less butyric acid produced in the body, butyric acid has a shorter half-life in the blood. We used intraperitoneal injection of sodium butyrate to study the mechanism of butyrate involved in body lipid metabolism. Triglycerides in adipose tissue and liver were significantly reduced by butyrate. The content of triglyceride in plasma in butyrate group was also significantly decreased. In adipose tissue, butyrate up-regulated gene expression of hormone-sensitive lipase (HSL), carnitine palmitoyl transferase (CPT)1 and CPT2, and increased protein expression of G protein-coupled receptor (GPR)41, phosphorylated extracellular-signal-regulated kinase (P-ERK), adenosine 5’-monophosphate (AMP)-activated protein kinase (AMPK) and P-AMPK. Gene expression of lipoprotein lipase (LPL), differentiation-dependent factor 1 (ADD1) and fatty acid synthase (FAS) was down-regulated. In liver, butyrate up-regulated protein expression of GPR41, ERK, P-ERK, P-AMPK. Gene expression of ADD1 and FAS was down-regulated. In muscle tissue, butyrate significantly up-regulated the expression of gene LPL, fatty acid transport protein (FATP) and fatty acid-binding protein (FABP) and protein GPR41, GPR43. Thus, butyrate is involved in body lipid metabolism mainly through the GPR41-mediated ERK-AMPK pathway. Inhibits lipid synthesis in adipose tissue and the liver and promotes lipolysis, avoiding obesity caused by diets with higher fat content.

Weanling rabbits frequently exhibit diarrhea or flatulence. Our experiment was conducted to investigate the effect of garlic straw on the performance and intestinal barrier of rabbits. Hyla rabbits (60 d, n=160) with similar body weight were divided into 4 groups (4 replicates per group and 10 rabbits per replicate): fed a basal diet (control) or fed an experimental diet with 5%, 10%, or 15% garlic straw powder supplement. The results showed that the dietary addition of garlic straw increased significantly the average daily gain and average daily feed intake. Compared with the control, dietary addition of 10-15% garlic straw decreased significantly the death rate of rabbit. Rabbits in 10% garlic straw group had a higher secretory immunoglobulins A and immunoglobulins G concentration in jejunum and ileum than control, while lower tumour necrosis factor α (TNFα) concentration in jejunum. Compared with the control, dietary addition of 10% garlic straw increased significantly genes expression of zonula occluden protein 2 (ZO2) in jejunum and ileum and mucin4 in ileum, while did not alter the genes expression of junctional adhesion molecule 2 (JAM2), JAM3, ZO1, occluding, claudin1, mucin1, mucin6 and toll-like receptor 4 in jejunum and ileum and mucin4 in jejunum. In conclusion, dietary supplement of garlic straw modulates immune responses and enhances intestinal barrier, meanwhile inhibits the synthesis of pro-inflammatory cytokine of TNFα. Besides, our experiment offers positive evidence in improving rabbit health of garlic instead of antibiotics.