Acetate Affects the Process of Lipid Metabolism in Rabbit Liver, Skeletal Muscle and Adipose Tissue

SIMPLE SUMMARY: Lots 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. ABSTRACT: 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.