Epidermal growth factor (EGF) is a 53-amino acid peptide that plays an important role in regulating cell growth, survival, migration, apoptosis, proliferation, and differentiation. In addition, EGF has been established to be an effective intestinal regulator helping to protect intestinal barrier integrity, which was essential for the absorption of nutrients and health in humans and animals. Several researches have demonstrated that EGF via binding to the EGF receptor and subsequent activation of Ras/MAPK, PI3K/AKT, PLC-γ/PKC, and STATS signal pathways regulates intestinal barrier function. In this review, the relationship between epidermal growth factor and intestinal development and intestinal barrier is described, to provide a better understanding of the effects of EGF on intestine development and health.

Recently, industrial and agricultural by-products, resulting from crops, fruit and vegetable processing which can be used in animal diets have become a hot topic in the animal feed industry. This review focuses on the agro-industry by-products as feeds, not only for the nutritional values, but also for their nutricine contribution. In this review, we described the chemical composition of some by-products as feeds and their limiting factors in animal feeding.

The aim of the present study was to evaluate the effects of dietary supplementation with or without Bacillus subtilis (B. subtilis) on carcass traits, meat quality, amino acids, and fatty acids of broiler chickens. In total, 160 1-day-old Arbor Acres male broiler chicks were divided into two groups with eight replicates of 10 chicks each. Chickens received basal diets without (CN group) or with 500 mg/kg B. subtilis (BS group) for 42 days. Eight chickens from each group were slaughtered at the end of the trial, and carcass traits, meat quality, chemical composition, amino acid, and fatty acid profile of meat were measured. The results showed that the breast muscle (%) was higher in BS than in CN (p < 0.05), while abdominal fat decreased (p < 0.05). The pH_24h of thigh muscle was increased (p < 0.05) when supplemented with BS; however, drip loss, cooking loss of breast muscle, and shear force of thigh muscle decreased (p < 0.05). Lysine (Lys), methionine (Met), glutamic acid (Glu), and total essential amino acid (EAA) in breast muscle and Glu in thigh muscle were greater in BS than in CN (p < 0.05). C16:1, C18:1n9c, and MUFA in breast muscle and thigh muscle were greater in BS than in CN (p < 0.05). In conclusion, dietary supplementation with B. subtilis could improve the carcass traits and meat quality of broilers, which is beneficial for the consumers due to the improved fatty acid profile and amino acid composition.

The epidermal growth factor (EGF) has been widely used for protection of stress-induced intestinal mucosa dysfunction. However, whether EGF would alleviate oxidative injury and reduce apoptosis in porcine intestine is not yet known. Therefore, the aim of this study was to investigate the effect of EGF on lipopolysaccharides (LPS)-induced induction of oxidative stress and ensuing apoptosis in the porcine intestinal epithelial cell line, IPEC-J2. The present study showed that EGF significantly increased cell viability and decreased the LPS-induced induction of apoptosis, dehydrogenase (LDH) release and malonaldehyde (MDA) production. EGF also (i) decreased expression of the pro-apoptotic genes Fas, Bax, Cascase-3, Cascase-8, Cascase-9, and proteins such as P53, Fas, Bax, Caspase3; (ii) increased antiapoptotic protein B-cell lymphoma 2 (Bcl2) expression; (iii) increased mRNA levels of the nuclear factor erythroid 2-related factor 2 (Nrf2) related genes Nrf2, manganese superoxide dismutase (SOD2), catalase (CAT), glutathione peroxidase (GSH-Px), heme oxygenase (HO-1) and quinone oxidoreductase (NQO1); (iv) protein level of Nrf2-realeted proteins Nrf2, HO-1, NQO1; and (v) total antioxidant capacity (T-AOC), CAT, SOD, GSH-Px concentrations. Collectively, our results indicated that EGF enhanced Nrf2 protein expression, and upregulated the expression of phase II metabolizing enzymes (such as HO-1 and NQO1) and antioxidative enzymes (SOD, CAT and GSH-Px) to alleviate oxidative injury, and then protect IPEC-J2 cells from apoptosis induced by LPS.

The objective of this study was to compare the effect of sodium selenite (SS) and selenium yeast (SY) on performance, egg quality, and selenium concentration in eggs and serum biochemical indices in laying hens. Seven hundred twenty healthy Roman laying hens (21 weeks old, 18 weeks in lay) with a similar laying rate (90.27% ± 1.05%) were randomly divided into 5 groups with 6 replicates of 24 hens each. Five diets were prepared as a 1+2×2 factorial arrangement with control and two sources of Se at two levels. Control diet (control) was prepared without adding exogenous selenium (analyzed basal Se content of 0.178 mg/kg). The other four diets were prepared with the control diet supplemented with SY or SS at 0.3 mg/kg (low; L) or 0.5 mg/kg (high; H) to give 5 diets designated as control, SY-L, SY-H, SS-L, and SS-H. The analyzed selenium content in the SY-L, SY-H, SS-L, and SS-H diets were 0.362, 0.572, 0.323, and 0.533 mg/kg respectively. The pre-trial period lasted 7 d, and the experimental period lasted 56 d (30 weeks old), during which the egg production, egg quality, and hen serum parameters were measured. Results showed that selenium source and level had no effect (P > 0.05) on average daily egg weight and feed conversion ratio (FCR). However, the laying rate was different at the L and H levels of supplementation, regardless of source, such that hens that were supplemented had a higher performance than that of the control, and the H level of supplementation lead to a higher laying rate than that of the L level (P < 0.05). There was a difference in average daily feed intake (ADFI) with an interaction in selenium source and level (P < 0.05), such that SS-L was higher than other selenium supplemented treatment or control. There were no significant differences in egg quality (P > 0.05); at the high level, SY had higher egg yolk selenium compared with SS. However, within SY, adding 0.5 mg/kg selenium led to higher egg yolk selenium than 0.3 mg/kg selenium (P < 0.05). Moreover, adding 0.3 mg/kg SY, 0.3 mg/kg, or 0.5 mg/kg SS to the basal diet had no significant effect on the selenium content in the egg (P > 0.05). There were no significant differences in serum biochemical indices among the five groups (P > 0.05). In conclusion, adding a high level of selenium in the diet of laying hens significantly increased egg production, and addition of a high level of selenium in the form of SY led to a higher deposition of selenium in the yolk than that of SS. These results indicate that adding 0.5 mg/kg of SY in the diet of laying hens would result in Se-enriched eggs.

The aim of the present study was to investigate the effects of intrauterine growth retardation (IUGR) on the intestinal morphology, intestinal epithelial cell apoptosis, intestinal antioxidant capacity, intestinal glucose absorption capacity, and intestinal barrier function of piglets during the suckling period. A total of eight normal-birth-weight (NBW) piglets and eight IUGR newborn piglets (Duroc × Landrace × Yorkshire) were selected from eight litters, one NBW and one IUGR newborn piglet per litter. In each litter, piglets with birth weight of (within one SD of the mean birth weight) were selected as NBW piglets and piglets with birth weight of (two SD below the mean birth weight) were selected as IUGR piglets. At 21 days of age, all piglets were killed by exsanguinations for sampling. The results showed the body weight (BW) of IUGR piglets on day 0, day 7, day 14, and day 21, and the body weight gain (BWG) of IUGR piglets was significantly lower than that of NBW piglets. IUGR piglets exhibited impaired intestinal morphology, raised enterocyte apoptosis, and increased oxidative damage. It showed that IUGR leads to a lower antioxidant capacity and glucose absorption in the jejunum. In accordance, IUGR caused the intestinal barrier dysfunction by impairing tight junctions and increasing intestinal inflammatory injury. Collectively, these results add to our understanding that IUGR affects intestinal health of suckling piglets via altering intestinal antioxidant capacity, glucose uptake, tight junction, and immune responses, and the slow growth of piglets with IUGR may be associated with intestinal injury.