Two experiments were conducted to evaluate the effects of chromium (Cr) on the growth performance, bone trait, serum traits, and immune responses in broilers. The broilers were fed corn-soybean meal basal diet supplemented with Cr at level of 0 (control), 200, 400, or 800 ppb in the form of chromium picolinate (CrPic). The broilers were fed treated diets for 6 weeks in Exp. 1, but the Cr supplement was removed for the last 3 weeks in Exp. 2. Exp. 1 showed that dietary supplement of Cr did not affect growth performance of the broiler, though improved feed efficiency (p<0.05) was observed during 0 to 3 weeks. Moreover, serum total (p<0.05) and HDL cholesterols (p<0.06) were significantly higher in pooled Cr added group at 6 weeks of age, however, the difference was not significant in Exp. 2. The pooled Cr added group in Exp.1 had significantly lower (p<0.05) alkaline phosphatase activity and higher (p<0.09) calcium at 3 weeks. Significantly lower phosphorus was also observed in Exp. 2. With continued supplement of Cr as in Exp. 1, the alkaline phosphatase activity maintained higher at 6 weeks, as opposed to significantly lower in Exp. 2, which had no further Cr supplement. Higher bone breaking strength was observed in 400 ppb Cr supplemented in Exp. 1, though not significantly different. Serum glucose and triglyceride were not affected by Cr supplement. Antibody against Infectious Bronchitis (IB) was significantly (p<0.05) higher with 400 ppb Cr supplemented, and anti-Newcastle disease (ND) antibody also tended to be higher (p<0.06) in pooled Cr added group at 6 weeks of age in Exp. 1. Peripheral blood blastogenesis activity was not different among the treatments. The results suggest that diet supplemented with 400 ppb CrPic may be beneficial to the broilers.

Two experiments were conducted to investigate the effect of dietary glutamine (Gln) supplement on the performance and villus morphology of weaned pigs. In Exp. 1, 48 pigs were fed diets supplemented with 0, 0.5, 1.0, or 1.5% Gln for 28 days. Dietary Gln supplemented levels did not influence performance and plasma Gln concentration of weaned pigs. In Exp. 2, 48 weaned pigs were fed the same treatment diets of Exp. 1 for 7 or 14 days. Dietary Gln supplement reduced the ratio of small intestine weight to empty carcass weight at d 14 postweaning. However, the villus height and villus height/crypt depth ratio at the duodenum were increased. IgA and protein in the bile from d 7 and d 14 postweaning were higher in the pigs fed the diet supplemented with 0.5% Gln. Plasma IgA concentration was not influenced by dietary Gln levels. In conclusion, dietary Gln supplement might benefit the development of the small intestine and bile IgA production in weaned pigs.

This study attempted to determine ingested porcine epidermal growth factor (pEGF) on the gastrointestinal tract development of early-weaned piglets. Thirty-two piglets (14-day weaned) were randomly allotted to supplemented with 0 (control), 0.5, 1.0, or 1.5 mg pEGF/kg diet. Each treatment consisted of four replicates with two pigs per pen for a 14 days experimental period. Piglets were sacrificed and gastrointestinal tract samples were collected to measure mucosa morphology, mRNA expression and activities of digestive enzymes in the gastrointestinal tract of piglets at the end of the experiment. Diets supplemented with pEGF failed to influence growth performance but tended to increase jejunal mucosa weight (p < 0.09) and protein content (p < 0.07). Piglets supplemental pEGF induced incrementally the gastric pepsin activity (p < 0.05) and stimulated jejunal alkaline phosphatase (ALP) and lactase activities accompanied with the increase of jejunal ALP and maltase mRNA expression. No effect of pEGF on the activities of all enzymes in ileum except the stimulation of ileal aminopeptide N mRNA expression. These results reveal that dietary pEGF supplementation might enhance gene expression and activities of digestive enzymes in the stomach and jejunum of piglets.

Ganoderma lucidum polysaccharides (GLP) have renal protection effect but there was no study on the diabetic nephropathy. This study was designed to investigate its effect and mechanism using a diabetic rat model induced by streptozotocin (50 mg/kg, i.p.). The diabetic rats were treated with GLP (300 mg/kg/day) for 10 weeks. The blood glucose, glycated hemoglobin, body weight, and the levels of blood creatinine, urea nitrogen, and urine protein were assessed. And renal pathologies were assessed by the tissue sections stained with hematoxylin-eosin, Masson’s trichome, and periodic acid-Schiff. The expression of phosphorylated phosphoinositide 3 kinase (p-PI3K), phosphorylated protein kinase B (p-Akt), and phosphorylated mammalian target of rapamycin (p-mTOR), the autophagy proteins beclin-1, LC3-II, LC3-I, and P62; the apoptosis-related proteins caspase-3 and caspase-9; and the inflammation markers IL-6, IL-1β, and TNF-ɑ were assessed. Results showed that GLP alleviated the impairment of renal function by reducing urinary protein excretion and the blood creatinine level and ameliorated diabetic nephropathy. The expression of p-PI3K, p-Akt, and p-mTOR in the diabetic kidney were significantly reduced in the GLP treatment group compared to the without treatment group. GLP treatment activated the autophagy indicators of beclin-1 and the ratio of LC3-II/LC3-I but reduced p62 and also inhibited the expression of caspase-3, caspase-9 and IL-6, IL-1β, and TNF-ɑ. In conclusion, the effect of GLP amelioration diabetic nephropathy may be via the PI3k/Akt/mTOR signaling pathway by inhibition of the apoptosis and inflammation and activation of the autophagy process.