Severe body condition loss lowers hepatic output of IGF1 with adverse effects on the dominant follicle in dairy cows.

The severe loss of body condition score (BCS) during the early lactation period has been associated with infertility in cows. However, the mechanisms are not fully understood. The aim of this study was to examine the effect of BCS loss on liver health, and ovarian functions in cows during early lactation. Retrospectively multiparous cows from two farms were categorized based on units of BCS (1-5 scale) loss as Moderate (MOD, <0.75 units; n = 11) or Severe (SEV, ≥0.75 units; n = 9) loss groups. From Weeks -3 to 7, relative to calving, MOD and SEV cows lost on average 0.4 and 1.0-unit BCS, respectively. All data except hepatic transcriptomes were analyzed with PROC MIXED procedure of SAS. The plasma concentration of non-esterified fatty acids at Week 0 and 1, ß-hydroxy butyrate at Week 1, and γ-glutamyl transferase at Weeks 1 and 7 relative to calving were higher in SEV cows. Hepatic transcriptome analysis showed that 1 186 genes were differentially expressed in SEV (n = 3) compared to MOD (n = 3) cows at Week 7 after calving. Pathway analysis revealed that significant DEGs in SEV cows enriched in lipid metabolisms including, lipid metabolic process, ether lipid metabolism, fatty acid beta-oxidation, fatty acid biosynthetic process, fatty acid metabolic process, fat digestion and absorption, linoleic acid metabolism, alpha-linolenic acid metabolism. The impaired liver function in SEV cows was associated with 1.5-fold reduction of hepatic IGF1 gene expression and lower serum IGF1 concentrations. At the ovarian level, SEV cows had lower IGF1 concentration in the follicular fluid of the dominant follicle of the synchronized follicular wave compared to that of MOD cows at 7 weeks after calving. Further, the follicular fluid concentration of estradiol-17ß was lower in SEV cows along with lower transcript abundance of genes from granulosa cells associated with dominant follicle competence, including CYP19A1, NR5A2, IGF1, and LHCGR. These data show that SEV loss of BCS during early lactation leading up to the planned start of breeding is associated with liver dysfunction, including lower IGF1 secretion, and impaired function of the dominant follicle in the ovary.

Effects of feeding extruded flaxseed on layer performance, total tract nutrient digestibility, and fatty acid concentrations of egg yolk, plasma and liver.

A study was conducted to determine the effects of graded levels of extruded flaxseed (EF) on laying hen performance, apparent total tract nutrient retention (ATTNR) and fatty acid concentrations of egg yolk, blood plasma and liver. Seventy-two White Leghorn layers (58 weeks old; three per cage) were randomly assigned to one of four dietary treatments: 0 (control), 3, 6 and 9% of EF-supplemented diets for 8 weeks. Results showed that feed intake, egg production, feed conversion ratio and egg weight were not affected by treatments. The ATTNR of dry matter (p = .001) and gross energy (p = .014) was lower for layers fed 9% EF than those fed the control diet, while ATTNR of organic matter (p = .001) and nitrogen-corrected apparent metabolizable energy (p = .003) were lower for birds fed 6% and 9% EF compared with those fed the control diet. Relative to the control diet, feeding EF increased (p < .001) egg yolk, plasma and liver n-3 polyunsaturated fatty acid (PUFA) concentrations. Birds fed 6% EF produced eggs > 300 mg of n-3 PUFA after two weeks of feeding, while the highest of n-3 PUFA concentrations were achieved for birds fed 9% EF. It was concluded that feeding EF up to 9% of the diet had no adverse effects on layer performance and increased n-3 PUFA concentrations in blood plasma, liver and egg yolk. However, moderate to high levels of EF (i.e., 6% and 9% of the diet) reduced nutrient ATTNR and nitrogen-corrected apparent metabolizable energy. Omega-3-enriched eggs can be achieved by feeding layers EF at 6% of the diet.

Temporal analysis of the effect of extruded flaxseed on the swine gut microbiota.

Flaxseed is a rich source of α-linolenic acid, an essential ω-3 fatty acid reported to have beneficial health effects in humans. Feeding swine a diet supplemented with flaxseed has been found to enrich pork products with ω-3 fatty acids. However, the effect of flaxseed supplementation on the swine gut microbiota has not been assessed to date. The purpose of this study was to investigate if extruded flaxseed has any impact on the bacterial and archaeal microbiota in the feces of growing-finishing pigs over a 51-day period, using denaturing gradient gel electrophoresis (DGGE) and real-time PCR. Bacterial DGGE profile analysis revealed major temporal shifts in the bacterial microbiota with only minor ones related to diet. The archaeal microbiota was significantly less diverse than that of Bacteria. The majority of bacterial DGGE bands sequenced belonged to the Firmicutes phylum while the archaeal DGGE bands were found to consist of only 2 species, Methanobrevibacter smithii and Methanosphaera stadtmanae. The abundance of Bacteroidetes decreased significantly from day 0 to day 21 in all diet groups while the abundance of Firmicutes was relatively stable across all diet cohorts and sampling times. There was also no significant correlation between pig mass and the ratio of Firmicutes to Bacteroidetes. While the addition of extruded flaxseed to the feed of growing-finishing pigs was beneficial for improving ω-3 fatty acid content of pork, it had no detectable impact on the fecal bacterial and archaeal microbiota, suggesting that extruded flaxseed may be used to improve meat quality without adverse effect on the swine gut microbiota or animal performance.

Effects of mannan oligosaccharide and virginiamycin on the cecal microbial community and intestinal morphology of chickens raised under suboptimal conditions.

There is an increasing movement against use of antibiotic growth promoters in animal feed. Prebiotic supplementation is a potential alternative to enhance the host's natural defense through modulation of gut microbiota. In the present study, the effect of mannan oligosaccharide (MOS) and virginiamycin (VIRG) on cecal microbial ecology and intestinal morphology of broiler chickens raised under suboptimal conditions was evaluated. MOS and VIRG induced different bacterial community structures, as revealed by denaturing gradient gel electrophoresis of 16S rDNA. The antibiotic treatment reduced cecal microbial diversity while the community equitability increased. A higher bacterial diversity was observed in the cecum of MOS-supplemented birds. Quantitative polymerase chain reaction results indicated that MOS changed the cecal microbiota in favor of the Firmicutes population but not the Bacteroidetes population. No difference was observed in total bacterial counts among treatments. MOS promoted the growth of Lactobacillus spp. and Bifidobacterium spp. in the cecum and increased villus height and goblet cell numbers in the ileum and jejunum. These results provide a deeper insight into the microbial ecological changes after supplementation of MOS prebiotic in poultry diets.

Cell walls of Saccharomyces cerevisiae differentially modulated innate immunity and glucose metabolism during late systemic inflammation.

BACKGROUND: Salmonella causes acute systemic inflammation by using its virulence factors to invade the intestinal epithelium. But, prolonged inflammation may provoke severe body catabolism and immunological diseases. Salmonella has become more life-threatening due to emergence of multiple-antibiotic resistant strains. Mannose-rich oligosaccharides (MOS) from cells walls of Saccharomyces cerevisiae have shown to bind mannose-specific lectin of Gram-negative bacteria including Salmonella, and prevent their adherence to intestinal epithelial cells. However, whether MOS may potentially mitigate systemic inflammation is not investigated yet. Moreover, molecular events underlying innate immune responses and metabolic activities during late inflammation, in presence or absence of MOS, are unknown. METHODS AND PRINCIPAL FINDINGS: Using a Salmonella LPS-induced systemic inflammation chicken model and microarray analysis, we investigated the effects of MOS and virginiamycin (VIRG, a sub-therapeutic antibiotic) on innate immunity and glucose metabolism during late inflammation. Here, we demonstrate that MOS and VIRG modulated innate immunity and metabolic genes differently. Innate immune responses were principally mediated by intestinal IL-3, but not TNF-α, IL-1 or IL-6, whereas glucose mobilization occurred through intestinal gluconeogenesis only. MOS inherently induced IL-3 expression in control hosts. Consequent to LPS challenge, IL-3 induction in VIRG hosts but not differentially expressed in MOS hosts revealed that MOS counteracted LPS's detrimental inflammatory effects. Metabolic pathways are built to elucidate the mechanisms by which VIRG host's higher energy requirements were met: including gene up-regulations for intestinal gluconeogenesis (PEPCK) and liver glycolysis (ENO2), and intriguingly liver fatty acid synthesis through ATP citrate synthase (CS) down-regulation and ATP citrate lyase (ACLY) and malic enzyme (ME) up-regulations. However, MOS host's lower energy demands were sufficiently met through TCA citrate-derived energy, as indicated by CS up-regulation. CONCLUSIONS: MOS terminated inflammation earlier than VIRG and reduced glucose mobilization, thus representing a novel biological strategy to alleviate Salmonella-induced systemic inflammation in human and animal hosts.

Distinct commensal bacteria associated with ingesta and mucosal epithelium in the gastrointestinal tracts of calves and chickens.

The primary aim of this study was to determine whether distinct gastrointestinal tract (GIT) microbial communities are established within ingesta and on mucosal surfaces of dairy calves and chickens to evaluate whether the principle of microbial segregation is of broad biological significance. Multivariate analysis of the predominant bacterial PCR-denaturing gradient gel electrophoresis profiles and estimated bacterial populations were compared in rumen, jejunum, ileum, cecum, and colon ingesta and matching mucosal tissues. Samples collected from 3-week old (n = 8) and 6-month old (n = 8) calves revealed that the predominant mucosa-associated bacteria were distinct from those inhabiting ingesta, and bacterial diversity varied significantly among the GIT regions. The estimated bacterial populations displayed significant regional differences for bovine mucosal (P = 0.05) and for ingesta (P = 0.03) only at 6 months of age. This indicates an established segregation of the enteric bacterial population throughout the GIT in weaned calves. Analysis of ileal and cecal bacterial profiles in chickens confirmed that the segregation of commensal bacteria between ingesta and the mucosal tissue was a common biological phenomenon. Our study provides some fundamental understanding of the impact of sample type (mucosa vs. ingesta), region, and host age on commensal bacterial establishment and segregation throughout the GIT.

Effects of Lactobacillus rhamnosus GG supplementation on cow's milk allergy in a mouse model.

BACKGROUND: Cow's milk allergy (CMA) is one of the most prevalent human food-borne allergies, particularly in infants and young children from developed countries. Our study aims to evaluate the effects of Lactobacillus rhamnosus GG (LGG) administration on CMA development using whole cow's milk proteins (CMP) sensitized Balb/C mice by two different sensitization methods. METHODS: LGG supplemented mice were either sensitized orally with CMP and cholera toxin B-subunit (CTB) as adjuvant, or intraperitoneally (IP) with CMP but without the adjuvant. Mice were then orally challenged with CMP and allergic responses were accessed by monitoring hypersensitivity scores, measuring the levels of CMP-specific immunoglobulins (IgG1, IgG2a and IgG) and total IgE from sera, and cytokines (IL-4 and IFN-γ) from spleen lysates. RESULTS: Sensitization to CMP was successful only in IP sensitized mice, but not in orally sensitized mice with CMP and CTB. Interestingly, LGG supplementation appeared to have reduced cow's milk allergy (CMA) in the IP group of mice, as indicated by lowered allergic responses. CONCLUSIONS: Adjuvant-free IP sensitization with CMP was successful in inducing CMA in the Balb/C mice model. LGG supplementation favourably modulated immune reactions by shifting Th2-dominated trends toward Th1-dominated responses in CMP sensitized mice. Our results also suggest that oral sensitization by the co-administration of CMP and CTB, as adjuvant, might not be appropriate to induce CMA in mice.