Impact of Dietary Sodium Butyrate and Salinomycin on Performance and Intestinal Microbiota in a Broiler Gut Leakage Model

Unfavorable alterations of the commensal gut microbiota and dysbacteriosis is a major health problem in the poultry industry. Understanding how dietary intervention alters the microbial ecology of broiler chickens is important for prevention strategies. A trial was conducted with 672 Ross 308 day-old male broilers fed a basic diet (no additives, control) or the basic diet supplemented with 500 mg/kg encapsulated butyrate or 68 mg/kg salinomycin. Enteric challenge was induced by inclusion of 50 g/kg rye in a grower diet and oral gavage of a 10 times overdose of a vaccine against coccidiosis. Compared to control and butyrate-supplemented birds, salinomycin supplementation alleviated growth depression. Compared to butyrate and non-supplemented control, salinomycin increased potentially beneficial Ruminococcaceae and reduced potentially pathogenic Enterobacteriaceae and counts of Lactobacillus salivarius and Clostridium perfringens. Further, salinomycin supplementation was accompanied by a pH decrease and succinic acid increase in ceca, while coated butyrate (0.5 g/kg) showed no or limited effects. Salinomycin alleviated growth depression and maintained intestinal homeostasis in the challenged broilers, while butyrate in the tested concentration showed limited effects. Thus, further investigations are required to identify optimal dietary inclusion rates for butyrate used as alternative to ionophore coccidiostats in broiler production.

Effects of Pantothenic Acid Supplementation on Growth Performance, Carcass Traits, Plasma Parameters of Starter White Pekin Ducks Fed a Corn–Soybean Meal Diet

This study aimed to evaluate the effects of different dietary pantothenic acid levels on growth performance, carcass traits, and plasma biochemical parameters of starter Pekin ducks from 1 to 21 days of age, as well as the pantothenic acid requirement of starter ducks. A total of 384 one-day-old male white Pekin ducklings were assigned randomly into 6 dietary treatments, each with 8 replicate pens of 8 ducks. Ducks were fed conventional basal corn–soybean diets containing 8.5, 10.5, 12.5, 14.5, 16.5, and 18.5 mg/kg pantothenic acid for 21 days. Growth depression, poor pantothenic acid status, fasting hypoglycemia, and elevated plasma uric acid (UA) content were observed in the ducks fed the pantothenic acid-deficient basal diet (p < 0.05), and these adverse effects were ameliorated by pantothenic acid supplementation. Among all ducks, the birds fed the basal diet with no supplementation of pantothenic acid had the lowest body weight, average daily weight gain (ADG), average daily feed intake (ADFI), breast meat yield, and plasma pantothenic acid and glucose contents (p < 0.05), and the greatest plasma UA content (p < 0.05). In addition, all these parameters showed a linear or quadratic response as dietary pantothenic acid levels increased (p < 0.05). According to broken-line regression, the pantothenic acid requirements of starter male white Pekin ducks for body weight, ADG, and plasma pantothenic acid content were 13.36, 13.29, and 15.0 mg/kg, respectively. The data potentially provides theoretical support for the utilization of pantothenic acid in duck production.

Molecular mechanisms of growth depression in broiler chickens (Gallus Gallus domesticus) mediated by immune stress: a hepatic proteome study

Background Immunological stress decreases feed intake, suppresses growth and induces economic losses. However, the underlying molecular mechanism remains unclear. Label-free liquid chromatography and mass spectrometry (LC-MS) proteomics techniques were employed to investigate effects of immune stress on the hepatic proteome changes of Arbor Acres broilers (Gallus Gallus domesticus) challenged with Escherichia coli lipopolysaccharide (LPS). Results Proteomic analysis indicated that 111 proteins were differentially expressed in the liver of broiler chickens from the immune stress group. Of these, 28 proteins were down-regulated, and 83 proteins were up-regulated in the immune stress group. Enrichment analysis showed that immune stress upregulated the expression of hepatic proteins involved in defense function, amino acid catabolism, ion transport, wound healing, and hormone secretion. Furthermore, immune stress increased valine, leucine and isoleucine degradation pathways. Conclusion The data suggests that growth depression of broiler chickens induced by immune stress is triggered by hepatic proteome alterations, and provides a new insight into the mechanism by which immune challenge impairs poultry production.

Abnormal TPM2 expression is involved in the regulation of atherosclerosis progression via mediating RhoA signaling in vitro

IntroductionOx-LDL (oxidized low densitylipoprotein)-induced endothelial cell injury and dysfunction of vascular smooth muscle cell played critical roles in the development of atherosclerosis (AS). Tropomyosin 2 (TPM2) was indicated to be implicated in cardiac diseases, but its critical role and regulation mechanism in AS progression had not yet been elucidated.Material and methodsThe expression of TPM2 was investigated in AS tissues. Ox-LDL was used to construct an AS in vitro model based on endothelial and vascular smooth muscle cells (HAEC and VSMC). Overexpression assay was performed to evaluate the role of TPM2 in AS. Meanwhile, Narciclasine treatment analysed the involvement of RhoA pathway.ResultsTPM2 was dramatically upregulated both in AS tissues and ox-LDL-induced HAEC cells. The overexpression of TPM2 attenuated ox-LDL-stimulated cell growth depression, inflammatory and adhesive responses in HAEC, as well as oxidative stress and mitochondrial dysfunction. Besides, VSMC, impacted by TPM2-overexpressed HAEC, showed alleviated cellular processes which was abnormally activation induced by ox-LDL. Furthermore, the depressed activation of RhoA pathway was found in TPM2-overexpressed HAEC and activating the signaling rescued these effects of TPM2 exerted on ox-LDL-stimulated HAEC and VSMC.ConclusionsTPM2 had an advantageous impact on ox-LDL-induced AS progression in vitro via mediating RhoA pathway. This evidence might be contributed to the therapy of AS.

Severe pantothenic acid deficiency induces alterations in the intestinal mucosal proteome of starter Pekin ducks

Background Pantothenic acid deficiency (PAD) results in growth depression and intestinal hypofunction of animals. However, the underlying molecular mechanisms remain to be elucidated. Mucosal proteome might reflect dietary influences on physiological processes. Results A total of 128 white Pekin ducks of one-day-old were randomly assigned to two groups, fed either a PAD or a pantothenic acid adequate (control, CON) diet. After a 16-day feeding period, two ducks from each replicate were sampled to measure plasma parameters, intestinal morphology, and mucosal proteome. Compared to the CON group, high mortality, growth retardation, fasting hypoglycemia, reduced plasma insulin, and oxidative stress were observed in the PAD group. Furthermore, PAD induced morphological alterations of the small intestine indicated by reduced villus height and villus surface area of duodenum, jejunum, and ileum. The duodenum mucosal proteome of ducks showed that 198 proteins were up-regulated and 223 proteins were down-regulated (> 1.5-fold change) in the PAD group compared to those in the CON group. Selected proteins were confirmed by Western blotting. Pathway analysis of these proteins exhibited the suppression of glycolysis and gluconeogenesis, fatty acid beta oxidation, tricarboxylic acid cycle, oxidative phosphorylation, oxidative stress, and intestinal absorption in the PAD group, indicating impaired energy generation and abnormal intestinal absorption. We also show that nine out of eleven proteins involved in regulation of actin cytoskeleton were up-regulated by PAD, probably indicates reduced intestinal integrity. Conclusion PAD leads to growth depression and intestinal hypofunction of ducks, which are associated with impaired energy generation, abnormal intestinal absorption, and regulation of actin cytoskeleton processes. These findings provide insights into the mechanisms of intestinal hypofunction induced by PAD.

Intestinal Health of Pigs Upon Weaning: Challenges and Nutritional Intervention

The primary goal of nursery pig management is making a smooth weaning transition to minimize weaning associated depressed growth and diseases. Weaning causes morphological and functional changes of the small intestine of pigs, where most of the nutrients are being digested and absorbed. While various stressors induce post-weaning growth depression, the abrupt change from milk to solid feed is one of the most apparent challenges to pigs. Feeding functional feed additives may be viable solutions to promote the growth of nursery pigs by enhancing nutrient digestion, intestinal morphology, immune status, and by restoring intestinal balance. The aim of this review was to provide available scientific information on the roles of functional feed additives in enhancing intestinal health and growth during nursery phase. Among many potential functional feed additives, the palatability of the ingredient and the optimum supplemental level are varied, and these should be considered when applying into nursery pig diets. Considering different stressors pigs deal with in the post-weaning period, research on nutritional intervention using a single feed additive or a combination of different additives that can enhance feed intake, increase weight gain, and reduce mortality and morbidity are needed to provide viable solutions for pig producers. Further research in relation to the feed palatability, supplemental level, as well as interactions between different ingredients are needed.

Severe pantothenic acid deficiency induces alterations in the intestinal mucosal proteome of starter Pekin ducks

Background: Pantothenic acid deficiency (PAD) results in growth depression and intestinal hypofunction of animals. However, the underlying mechanisms remain to be established. Mucosal proteome might reflect dietary influences on physiological processes.Results: A total of 128 one-day-old Pekin ducks were divided into two groups, with 8 replicates and 8 birds per replicate. All the ducks were fed either a PAD or a pantothenic acid adequate (control, CON) diet. After a 16-day feeding period, two ducks from each replicate were sampled to measure plasma parameters, intestinal morphology, and mucosal proteome. High mortality, growth retardation, fasting hypoglycemia, reduced plasma insulin, and oxidative stress were observed in the PAD group compared to the CON group. Furthermore, PAD induced morphological alterations of the small intestine indicated by reduced villus height and villus surface area of duodenum, jejunum, and ileum. The duodenum mucosal proteome of ducks showed that 198 proteins were upregulated and 223 proteins were downregulated (> 1.5-fold change) in the PAD group compared to those in the CON group. Selected proteins were confirmed by Western blotting. Pathway analysis of these proteins exhibited the suppression of glycolysis and gluconeogenesis, fatty acid beta oxidation, tricarboxylic acid cycle, oxidative phosphorylation, oxidative stress, and intestinal absorption in the PAD group, indicating impaired energy generation and abnormal intestinal absorption. We also show that nine out of eleven proteins involved in regulation of actin cytoskeleton were upregulated by PAD, probably indicates reduced intestinal integrity.Conclusion: PAD leads to growth depression and intestinal hypofunction of ducks, which are associated with impaired energy generation, abnormal intestinal absorption, and regulation of actin cytoskeleton processes. These findings provide insights into the mechanisms of intestinal mucosa metabolic disorders due to PAD.

Severe Pantothenic Acid Deficiency Induces Alterations in The Intestinal Mucosal Proteome of Starter Pekin Ducks

Background: Pantothenic acid deficiency (PAD) results in growth depression and intestinal hypofunction of animals. However, the underlying mechanisms remain to be established. We investigated intestinal mucosal proteome changes induced by PAD in ducks to explain its effects on growth and intestine. Results: A total of 128 one-day-old Pekin ducks were divided into two groups, with 8 replicates and 8 birds per replicate. All the ducks were fed either a PAD or a pantothenic acid adequate (control, CON) diet for 16 days. High mortality, growth retardation, fasting hypoglycemia, reduced plasma insulin, and oxidative stress were observed in the PAD group compared to the CON group. Furthermore, PAD induced morphological alterations of the small intestine indicated by reduced villus height and villus surface area of duodenum, jejunum, and ileum. The duodenum mucosal proteome of ducks showed that 198 proteins were upregulated and 223 proteins were downregulated (> 1.5-fold change) in the PAD group compared to those in the CON group. Pathway analysis of these proteins exhibited the suppression of glycolysis and gluconeogenesis, fatty acid beta oxidation, tricarboxylic acid cycle, oxidative phosphorylation, oxidative stress, and intestinal absorption in the PAD group, indicating impaired energy generation and abnormal intestinal absorption. We also show that nine out of eleven proteins involved in regulation of actin cytoskeleton were upregulated by PAD, probably indicates reduced intestinal integrity. Conclusion: PAD leads to growth depression and intestinal hypofunction of ducks, which are associated with impaired in energy generation, abnormal intestinal absorption, and regulation of actin cytoskeleton processes. These findings have important implications for understanding the effect of PAD on intestines.