Q. Liu,C. Wang,Y. L Zhang,C. X. Pei,S. L Zhang,G. Guo,W. J. Huo,W. Z. Yang
The present study evaluated the effects of isovalerate supplementation on the development of the small intestinal mucosa in dairy calves. Forty-eight Chinese Holstein bull calves at 15 days of age and 45.1 ± 0.36 kg of body weight were assigned randomly to four groups. The treatments were control, low-isovalerate, moderate-isovalerate and high-isovalerate with 0, 3, 6 and 9 g isovalerate per calf per day, respectively. The study comprised 75 days with a 15-day adaptation period followed by a 60-day sampling period. Calves were weaned at 60 days of age. Six calves were chosen from each treatment at random and slaughtered at 30 and 90 days of age. The small intestine morphology and activities of amylase and trypsin improved significantly with increasing age. No interaction between treatments and age was observed. The small intestine length, mucosa layer thickness, villus height and crypt depth increased linearly with increasing isovalerate supplementation. However, the ratio of villus height to crypt depth was not affected by treatment. Activities of amylase and trypsin increased linearly. The lactase activity increased linearly during the 75-day period and for pre-weaned calves but was unaltered for post-weaned calves. The relative mRNA expressions of growth hormone receptor, insulin-like growth factor-1 receptor and sodium-glucose co-transporter-1 in the small intestine mucosa increased linearly, and a similar pattern was observed for the expression of peptide transporter-1 in the duodenum and proximal jejunum. The results suggested that small intestine development was promoted by isovalerate in a dose-dependent manner.
Short-chain fatty acids (SCFAs) can enhance the growth of aquatic animals and improve flesh quality through the gut-muscle axis. However, the effects of valeric acid, one of the SCFAs, on aquatic animals remain unreported. This study sought to explore the effects of valeric acid on Nile tilapia ( Oreochromis niloticus ). A total of 360 Juvenile tilapia (mean weight, 1.820 ± 0.007 g) with 3 tanks for each treatment were randomly assigned to 12 rectangular acrylic tanks and fed with four isolipidic (6 % lipid) and isonitrogenous (37 % protein) diets for 60 days, including a control diet (CK) and three experimental diets supplemented with 500 mg/kg (CK + LV), 1000 mg/kg (CK + MV), and 2000 mg/kg (CK + HV) of sodium valerate. The results discovered that the enhanced flesh hardness ( p < 0.01) of tilapia caused by valerate was attributed to decreased myofiber size ( p < 0.001). Transcriptome analysis revealed significant enrichment of the Forkhead box O (FOXO) signaling pathway in the valerate-treated group ( p < 0.001). Subsequent qPCR, western blot, immunohistochemistry, and immunofluorescence analyses demonstrated that valerate inhibited muscle cell proliferation by activating the FOXO signaling pathway, suppressing FOXO nuclear export, and consequently downregulating cyclins and cyclin-dependent kinases (CDKs) ( p < 0.01). Furthermore, valerate suppressed muscle differentiation by inhibiting the transcription and protein levels expression of myogenic regulatory factors (MRFs) ( p < 0.001). Additional validation in C2C12 myoblasts and myotubes confirmed that valerate indeed inhibited myoblasts proliferation and myotubes differentiation ( p < 0.001). These findings indicated that valerate reduced myofiber size by suppressing myoblasts proliferation and myotubes differentiation. This study elucidated the effects and mechanisms of valerate on skeletal muscle and introduced a novel approach to enhance fish flesh hardness.
危险品化学品经营许可证（带存储）