The present study was conducted to investigate effects of rabbit meat extract on energy metabolism and muscle differentiation in C2C12 myotubes. Water extract of rabbit meat (10, 50, 100, and 200 μg/ml) was used to treat differentiated C2C12 cells. Reverse transcriptase polymerase chain reaction (RT-PCR) and western blot analysis were used to determine mRNA or protein levels of energy metabolism-related genes. Total adenosine triphosphate (ATP) content was also measured. Treatment with rabbit meat extract significantly increased expression levels of muscle differentiation markers (myogenin and myosin heavy chain) and mitochondrial biogenesis regulators (PGC1α, NRF1, and TFAM) in C2C12 myotubes compared to non-treated control. Additionally, rabbit meat extract activated phosphorylation of AMPK and acetyl-coA carboxylase (ACC). Rabbit meat extract significantly increased ATP contents in myotubes. These results suggest that rabbit meat extract has the potential to improve energy metabolism in skeletal muscles.

Background: Aflatoxin B1 (AFB1) is a toxic metabolite generated by Aspergillus species and is commonly detected during the processing and storage of food; it is considered a group I carcinogen. The hepatotoxic effects, diseases, and mechanisms induced by AFB1 owing to chronic or acute exposure are well documented; however, there is a lack of research on its effects on the intestine, which is a crucial organ in the digestive process. Dogs are often susceptible to chronic AFB1 exposure owing to lack of variation in their diet, unlike humans, thereby rendering them prone to its effects. Therefore, we investigated the effects of AFB1 on canine small intestinal epithelial primary cells (CSIc). Methods: We treated CSIc with various concentrations of AFB1 (0, 1.25, 2.5, 5, 10, 20, 40, and 80 μM) for 24 h and analyzed cell viability and transepithelial-transendothelial electrical resistance (TEER) value. Additionally, we analyzed the mRNA expression of tight junction-related genes (OCLN, CLDN3, TJP1, and MUC2), antioxidant-related genes (CAT and GPX1), and apoptosis-related genes (BCL2, Bax, and TP53). Results: We found a significant decrease in CSIc viability and TEER values after treatment with AFB1 at concentrations of 20 μM or higher. Quantitative polymerase chain reaction analysis indicated a downregulation of OCLN, CLDN3, and TJP1 in CSIc treated with 20 μM or higher concentrations of AFB1. Additionally, AFB1 treatment downregulated CAT , GPX1, and BCL2. Conclusions: Acute exposure of CSIc to AFB1 induces toxicity, and exposure to AFB1 above a certain threshold compromises the barrier integrity of CSIc.