The objective of this experiment was to determine whether changing the dietary neutral detergent fiber (NDF)/starch ratio affected caecal microbiota when 4 different diets (diet A: 2.3 NDF/starch, diet B: 1.9, diet C: 1.4, diet D: 1.0) were formulated. A total of 200 weaned rabbits (35 days old, 50 per group) were used for the experiment, which started after an adaptation period of 7 days (i.e., day 42). Caecal contents were obtained from rabbits fed different NDF/starch diets at 52, 62, 72, and 82 days of life. The bacterial community structure was characterized by high-throughput 16S rRNA sequencing. Firmicutes, Actinobacteria, Synergistetes, and Tenericutes did not significantly change with diet or age. However, Bacteroidetes (P < 0.05), Proteobacteria (P < 0.01), and Verrucomicrobia (P < 0.05) reads were significantly affected by diet, and Proteobacteria (P < 0.01) and Verrucomicrobia (P < 0.05) reads were significantly influenced by age. At the genus level, Escherichia/Shigella (P < 0.01) was overrepresented in diet A (high fiber) relative to diet D (high starch) in 52- and 62-day-old rabbits. Venn diagrams and heat map plot analyses revealed that the number of gut species shared between animals with different diet treatments increased with age. These results suggest that dietary fiber per starch ratios and age significantly alter the composition of caecal microbiota in growing rabbits.

Simple SummaryLots of short-chain fatty acids (SCFAs) are produced in the rabbit cecum after dietary fiber fermentation. In addition to supplying energy, SCFAs could regulate lipid metabolism, but the related mechanism is still unknown. In our experiment, we study the effect of acetate (major SCFAs, 70–80%) on rabbit lipid metabolism. The present study found that acetate alters the process of lipid metabolism in rabbit liver, skeletal muscle and adipose tissue, and inferred some signaling pathways related to the process. A mechanism of acetate-regulating lipid metabolism is useful to identify the function in fat metabolism of microbiological products from rabbit and rabbit processes for nutrition metabolism.AbstractShort-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.

Exogenous CAT derived from microorganisms has been widely used in food, medicine, and other industries. Recent study also found that exogenous CAT supplementation could improve growth performance and antioxidant capacity of weaned pigs.

The present study was conducted to investigate the effect of copper supplementation on lipid metabolism in rabbits. Our study showed dietary copper addition (5-45 mg/kg) increased body mass 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 inhibited cytoplasmic lipid accumulation in liver, skeletal muscle and adipose tissue (P < 0.05). Compared with the control group, dietary copper addition (45 mg/kg) significantly increased plasma triglyceride levels but decreased very low density lipoprotein levels (P < 0.05). Copper treatment significantly increased gene expression of carnitine palmitoyltransferase (CPT) 1, CPT2 and peroxisome 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 as phosphorylated AMP-activated protein kinase (AMPK) levels were significantly up-regulated by copper 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 in the regulation of lipid metabolism by copper.

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 cultured 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 up-regulated 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.