The developmental pattern related to fatty acid uptake and oxidation in the yolk sac membrane and jejunum during embryogenesis in Muscovy duck.

This study aimed to investigate the developmental change of body growth and gene expression related to fatty acid uptake and oxidation in the yolk sac membrane (YSM) and jejunum during embryogenesis in Muscovy ducks. The weights of embryos and yolk sac (YS) (5 embryos per replicate, n = 6) were recorded on embryonic days (E)16, E19, E22, E25, E28, E31, and the day of hatch (DOH). The fat and fatty acid contents in YSM, jejunal histology, and gene expression related to fatty acid metabolism in YSM and jejunum were determined in each sampling time. Among the nonlinear models, the maximum growth is estimated at 2.83 (E22.5), 2.67 (E22.1), and 2.60 (E21.3) g/d using logistic, Gompertz, and Von Bertalanffy models, respectively. The weight of YS, and ether extract-free YS as well as the amounts of fat and fatty acids in YS decreased (P < 0.05) linearly, whereas the villus height, crypt depth, villus height/crypt depth, and musculature thickness in jejunum increased (P < 0.05) linearly during embryogenesis. The mRNA expression of CD36, SLC27A4, and FABP1 related to fatty acid uptake as well as the mRNA and protein expressions of PPARα and CPT1 related to fatty acid oxidation increased in a quadratic manner (P < 0.05) in both YS and jejunum, and the maximum values were achieved during E25 to E28. In conclusion, the maximum growth rate of Muscovy duck embryos was estimated at 2.60 to 2.83 g/d on E21.3 to E23.5, while the accumulations of lipid and fatty acid in YS were decreased in association with the increased absorptive area of morphological structures in jejunum. The gene and protein expression involved in fatty acid metabolism displayed a similar enhancement pattern between YSM and jejunum during E25 to E28, suggesting that fatty acid utilization could be strengthened to meet the energy demand for embryonic development.

ACE2 mediates tryptophan alleviation on diarrhea by repairing intestine barrier involved mTOR pathway.

The membrane-delimited receptor for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), angiotensin-converting enzyme 2 (ACE2), which is expressed in the intestine, collaborates with broad neutral amino acid transporter 1 (B0AT1). Tryptophan (Trp) is transported into intestinal epithelial cells by ACE2 and B0AT1. However, whether ACE2 and its binding protein B0AT1 are involved in Trp-mediated alleviation of intestinal injury is largely unknown. Here, we used weaned piglets and IPEC-J2 cells as models and found that ACE2/B0AT1 alleviated lipopolysaccharide (LPS)-induced diarrhea and promoted intestinal barrier recovery via transport of Trp. The levels of the aryl hydrocarbon receptor (AhR) and mechanistic target of rapamycin (mTOR) pathways were altered by ACE2. Dietary Trp supplementation in LPS-treated weaned piglets revealed that Trp alleviated diarrhea by promoting ACE2/B0AT1 expression, and examination of intestinal morphology revealed that the damage to the intestinal barrier was repaired. Our study demonstrated that ACE2 accompanied by B0AT1 mediated the alleviation of diarrhea by Trp through intestinal barrier repair via the mTOR pathway.

In-house ammonia induced lung impairment and oxidative stress of ducks.

Ammonia (NH3) is a toxic gas that in intensive poultry houses, damages the poultry health and induces various diseases. This study investigated the effects of NH3 exposure (0, 15, 30, and 45 ppm) on growth performance, serum biochemical indexes, antioxidative indicators, tracheal and lung impairments in Pekin ducks. A total of 288 one-day-old Pekin male ducks were randomly allocated to 4 groups with 6 replicates and slaughtered after the 21-d test period. Our results showed that 45 ppm NH3 significantly reduced the average daily feed intake (ADFI) of Pekin ducks. Ammonia exposure significantly reduced liver, lung, kidney, and heart indexes, and lowered the relative weight of the ileum. With the increasing of in-house NH3, serum NH3 and uric acid (UA) concentrations of ducks were significantly increased, as well as liver malondialdehyde (MDA), superoxide dismutase (SOD), and glutathione peroxidase (GPX-Px) contents. High NH3 also induced trachea and lung injury, thereby increasing levels of tumor necrosis factor-α (TNF-α) and interleukin-4 (IL-4) in the lung, and decreasing the mRNA expressions of zonula occludens 1 (ZO-1) and claudin 3 (CLDN3) in the lung. In conclusion, in-house NH3 decrease the growth performance in ducks, induce trachea and lung injuries and meanwhile increase the compensatory antioxidant activity for host protection.

Lactobacillus rhamnosus GG ameliorates hyperuricemia in a novel model.

Hyperuricemia (HUA) is a metabolic syndrome caused by abnormal purine metabolism. Although recent studies have noted a relationship between the gut microbiota and gout, whether the microbiota could ameliorate HUA-associated systemic purine metabolism remains unclear. In this study, we constructed a novel model of HUA in geese and investigated the mechanism by which Lactobacillus rhamnosus GG (LGG) could have beneficial effects on HUA. The administration of antibiotics and fecal microbiota transplantation (FMT) experiments were used in this HUA goose model. The effects of LGG and its metabolites on HUA were evaluated in vivo and in vitro. Heterogeneous expression and gene knockout of LGG revealed the mechanism of LGG. Multi-omics analysis revealed that the Lactobacillus genus is associated with changes in purine metabolism in HUA. This study showed that LGG and its metabolites could alleviate HUA through the gut-liver-kidney axis. Whole-genome analysis, heterogeneous expression, and gene knockout of LGG enzymes ABC-type multidrug transport system (ABCT), inosine-uridine nucleoside N-ribohydrolase (iunH), and xanthine permease (pbuX) demonstrated the function of nucleoside degradation in LGG. Multi-omics and a correlation analysis in HUA patients and this goose model revealed that a serum proline deficiency, as well as changes in Collinsella and Lactobacillus, may be associated with the occurrence of HUA. Our findings demonstrated the potential of a goose model of diet-induced HUA, and LGG and proline could be promising therapies for HUA.

Evidence from an Avian Embryo Model that Zinc-Inducible MT4 Expression Protects Mitochondrial Function Against Oxidative Stress.

BACKGROUND: Metallothioneins (MTs) have a strong affinity for zinc (Zn) and remain at a sufficiently high level in mitochondria. As the avian embryo is highly susceptible to oxidative damage and relatively easy to manipulate in a naturally closed chamber, it is an ideal model of the effects of oxidative stress on mitochondrial function. However, the protective roles and molecular mechanisms of Zn-inducible protein expression on mitochondrial function in response to various stressors are poorly understood. OBJECTIVES: The study aimed to investigate the mechanisms by which Zn-induced MT4 expression protects mitochondrial function and energy metabolism subjected to oxidative stress using the avian embryo and embryonic primary hepatocyte models. METHODS: First, we investigated whether MT4 expression alters mitochondrial function. Then, we examined the effects of Zn-induced MT4 overexpression and MT4 silencing on embryonic primary hepatocytes from breeder hens fed a normal Zn diet subjected to a tert-butyl hydroperoxide (BHP) oxidative stress challenge during incubation. In vivo, the avian embryos from hens fed the Zn-deficient and Zn-adequate diets were used to determine the protective roles of Zn-induced MT4 expression on the function of mitochondria exposed to oxidative stress induced by in ovo BHP injection. RESULTS: An in vitro study revealed that Zn-induced MT4 expression reduced reactive oxygen species accumulation in primary hepatocytes. MT4 silencing exacerbated BHP-mediated mitochondrial dysfunction whereas Zn-inducible MT4 overexpression mitigated it. Another in vivo study disclosed that maternal Zn-induced MT4 expression protected mitochondrial function in chick embryo hepatocytes against oxidative stress by inhibiting the peroxisome proliferator-activated receptor γ coactivator-1α (PGC-1α)/peroxisome proliferators-activated receptor-γ (PPAR-γ) pathway. CONCLUSION: This study underscores the potential protective roles of Zn-induced MT4 expression via the downregulation of the PGC-1α/PPAR-γ pathway on mitochondrial function stimulated by the stress challenge in the primary hepatocytes in an avian embryo model. Our findings suggested that Zn-induced MT4 expression could provide a new therapeutic target and preventive strategy for repairing mitochondrial dysfunction in disease.

Ochratoxin A induces abnormal tryptophan metabolism in the intestine and liver to activate AMPK signaling pathway.

BACKGROUND: Ochratoxin A (OTA) is a mycotoxin widely present in raw food and feed materials and is mainly produced by Aspergillus ochraceus and Penicillium verrucosum. Our previous study showed that OTA principally induces liver inflammation by causing intestinal flora disorder, especially Bacteroides plebeius (B. plebeius) overgrowth. However, whether OTA or B. plebeius alteration leads to abnormal tryptophan-related metabolism in the intestine and liver is largely unknown. This study aimed to elucidate the metabolic changes in the intestine and liver induced by OTA and the tryptophan-related metabolic pathway in the liver. MATERIALS AND METHODS: A total of 30 healthy 1-day-old male Cherry Valley ducks were randomly divided into 2 groups. The control group was given 0.1 mol/L NaHCO3 solution, and the OTA group was given 235 µg/kg body weight OTA for 14 consecutive days. Tryptophan metabolites were determined by intestinal chyme metabolomics and liver tryptophan-targeted metabolomics. AMPK-related signaling pathway factors were analyzed by Western blotting and mRNA expression. RESULTS: Metabolomic analysis of the intestinal chyme showed that OTA treatment resulted in a decrease in intestinal nicotinuric acid levels, the downstream product of tryptophan metabolism, which were significantly negatively correlated with B. plebeius abundance. In contrast, OTA induced a significant increase in indole-3-acetamide levels, which were positively correlated with B. plebeius abundance. Simultaneously, OTA decreased the levels of ATP, NAD+ and dipeptidase in the liver. Liver tryptophan metabolomics analysis showed that OTA inhibited the kynurenine metabolic pathway and reduced the levels of kynurenine, anthranilic acid and nicotinic acid. Moreover, OTA increased the phosphorylation of AMPK protein and decreased the phosphorylation of mTOR protein. CONCLUSION: OTA decreased the level of nicotinuric acid in the intestinal tract, which was negatively correlated with B. plebeius abundance. The abnormal metabolism of tryptophan led to a deficiency of NAD+ and ATP in the liver, which in turn activated the AMPK signaling pathway. Our results provide new insights into the toxic mechanism of OTA, and tryptophan metabolism might be a target for prevention and treatment.

Notch mediates the glycolytic switch via PI3K/Akt signaling to support embryonic development.

BACKGROUND: Energy metabolism disorder or insufficient energy supply during incubation will affect the development and survival of avian embryos. Especially, ß-oxidation could not provide the continuous necessary energy for avian embryonic development due to the increasing energy demand under hypoxic conditions during the mid-late embryonic stages. The role and mechanism of hypoxic glycolysis replacing ß-oxidation as the main source of energy supply for avian embryonic development in the mid-late stages is unclear. RESULTS: Here, we found that in ovo injection with glycolysis inhibitor or γ-secretase inhibitor both decreased the hepatic glycolysis level and impaired goose embryonic development. Intriguingly, the blockade of Notch signaling is also accompanied by the inhibition of PI3K/Akt signaling in the embryonic primary hepatocytes and embryonic liver. Notably, the decreased glycolysis and impaired embryonic growth induced by the blockade of Notch signaling were restored by activation of PI3K/Akt signaling. CONCLUSIONS: Notch signaling regulates a key glycolytic switch in a PI3K/Akt-dependent manner to supply energy for avian embryonic growth. Our study is the first to demonstrate the role of Notch signaling-induced glycolytic switching in embryonic development, and presents new insight into the energy supply patterns in embryogenesis under hypoxic conditions. In addition, it may also provide a natural hypoxia model for developmental biology studies such as immunology, genetics, virology, cancer, etc.

Effects of Dietary Tryptophan on Growth Performance, Plasma Parameters, and Internal Organs of 1-28-Day-Old Sichuan White Geese.

Although the nutrient requirements of geese during the growing stage are known, the dietary requirement of amino acids during the starting period remains unclear. Optimum nutrient supplementation during the starting period is crucial for improved survival rates, body-weight gain, and marketing weight in geese. Our study focused on the effect of dietary tryptophan (Trp) supplementation on the growth performance, plasma parameters, and internal-organ relative weights in 1-28-day-old Sichuan white geese. A total of 1080 1-day-old geese were divided randomly into six Trp-supplemented (0.145%, 0.190%, 0.235%, 0.280%, 0.325%, and 0.370%) groups. Average daily feed intake (ADFI), average daily gain (ADG), and duodenal relative weight were highest in the 0.190% group, brisket protein level and jejunal relative weight in the 0.235% group, and plasma total protein and albumin levels in the 0.325% group (P < 0.05). Dietary Trp supplementation did not significantly affect the relative weights of the spleen, thymus, liver, bursa of Fabricius, kidneys, and pancreas. Moreover, the 0.145% - 0.235% groups showed significantly decreased liver fat (P < 0.05). Based on the non-linear regression analysis of ADG and ADFI, the dietary Trp levels between 0.183% and 0.190% were estimated to be optimal for 1-28-day-old Sichuan white geese. In conclusion, optimal dietary Trp supplementation in 1-28-day-old Sichuan white geese resulted in increased growth performance (0.180% - 0.190%) along with improved proximal intestinal development and brisket protein deposition (0.235%). Our findings provide basic evidence and guidance for optimal levels of Trp supplementation in geese.

Maternal zinc alleviates tert-butyl hydroperoxide-induced mitochondrial oxidative stress on embryonic development involving the activation of Nrf2/PGC-1α pathway.

BACKGROUND: Mitochondrial dysfunction induced by excessive mitochondrial reactive oxygen species (ROS) damages embryonic development and leads to growth arrest. OBJECTIVE: The purpose of this study is to elucidate whether maternal zinc (Zn) exert protective effect on oxidative stress targeting mitochondrial function using an avian model. RESULT: In ovo injected tert-butyl hydroperoxide (BHP) increases (P < 0.05) hepatic mitochondrial ROS, malondialdehyde (MDA) and 8-hydroxy-2-deoxyguanosine (8-OHdG), and decreases (P < 0.05) mitochondrial membrane potential (MMP), mitochondrial DNA (mtDNA) copy number and adenosine triphosphate (ATP) content, contributing to mitochondrial dysfunction. In vivo and in vitro studies revealed that Zn addition enhances (P < 0.05) ATP synthesis and metallothionein 4 (MT4) content and expression as well as alleviates (P < 0.05) the BHP-induced mitochondrial ROS generation, oxidative damage and dysfunction, exerting a protective effect on mitochondrial function by enhancing antioxidant capacity and upregulating the mRNA and protein expressions of Nrf2 and PGC-1α. CONCLUSIONS: The present study provides a new way to protect offspring against oxidative damage by maternal Zn supplementation through the process of targeting mitochondria involving the activation of Nrf2/PGC-1α signaling.

Developmental changes in lipid and fatty acid metabolism and the inhibition by in ovo feeding oleic acid in Muscovy duck embryogenesis.

Hepatic lipid and fatty acid (FA) metabolism are critical for regulating energetic homeostasis during embryogenesis. At present, it remains unclear how an exogenous FA intervention affects embryonic development in an avian embryo model. In Exp. 1, 30 fertilized eggs were sampled on embryonic days (E) 16, 19, 22, 25, 28, 31 and the day of hatch (DOH) to determine the critical period of lipid metabolism. In Exp. 2, a total of 120 fertilized eggs were divided into two groups (60 eggs/group) for in ovo feeding (IOF) procedures on E25. Eggs were injected into the yolk sac with PBS as the control group and with oleic acid (OA) as the IOF-OA treatment group. Samples were collected on E28 and E31. In Exp. 1, hepatic triacylglycerol (TG) and cholesterol (CHO) contents increased while serum TG content decreased from E16 to DOH (P < 0.05). Both serum and liver displayed an increase in unsaturated FA and a decrease in saturated FA (P < 0.05). There was a quadratic increase in the target gene and protein expression related to hepatic FA de novo synthesis and oxidation (P < 0.05), whose inflection period was between E22 and E28. In Exp. 2, compared with the control embryos, IOF-OA embryos had an increased yolk sac TG content on E28 and E31, and a decreased serum TG and CHO content on E28 (P < 0.05). The IOF-OA embryos had less OA in the yolk sac and liver on E28, and less unsaturated FA in the serum and liver on E31 than did the control embryos (P < 0.05). Hepatic gene mRNA expression related to FA uptake, synthesis, and oxidation on E28 was lower in IOF-OA than in control embryos (P < 0.05), not on E31 (P > 0.05). Maximal metabolic changes in lipid and FA metabolism occurred on E22-E28 in Muscovy duck embryogenesis, along with the altered target gene and protein expression related to lipogenesis and lipolysis. IOF-OA intervention on E25 could inhibit the target gene expression related to FA uptake, synthesis, and oxidation, which may influence the normal FA metabolism on E28 during embryogenesis.

Predicting the metabolizable energy and metabolizability of gross energy of conventional feedstuffs for Muscovy duck using in vitro digestion method.

In total, two experiments were conducted to evaluate the effectiveness of an in vitro digestion method for predicting the metabolizable energy (ME) and metabolizability of gross energy (ME/GE) values using in vitro digestible energy (IVDE) and the digestibility of gross energy (IVDE/GE) content, respectively, of conventional feedstuffs for Muscovy ducks. In experiment 1, the apparent metabolizable energy (AME), true metabolizable energy (TME), AME/GE, and TME/GE of eight-grain feedstuff samples (two corn samples, three sorghum samples, and three barley samples) and eight protein feedstuff samples (two soybean meal samples, three cottonseed meal samples, and three rapeseed meal samples) were determined by the tube-feeding method with six different ducks for each sample. In experiment 2, a computer-controlled simulated digestion system (CCSDS) contain simulated digestive fluid was used to determine the enzymatic hydrolysis energy value of feedstuffs, which was defined as IVDE in our study. The simulated gastric fluid containing pepsin and simulated small intestinal fluid containing amylase, trypsin, and chymotrypsin for the in vitro gastric and intestinal digestion, respectively. The IVDE and in vitro digestibility of GE (IVDE/GE) of 16 feedstuff samples were determined using the CCSDS with five replicates per sample. The results showed that the IVDE and IVDE/GE were positively correlated with ME and ME/GE of feedstuffs, respectively. The coefficient of determination of eight regression models in predicting ME (grain feedstuffs: AME = 1.050 × IVDE- 0.9293, TME = 1.032 × IVDE + 0.6478; protein feedstuffs: AME = 1.331 × IVDE- 6.685, TME = 1.269 × IVDE-3.490) and ME/GE (grain feedstuffs: AME/GE = 1.069 × IVDE/GE- 6.516, TME/GE = 1.068 × IVDE/GE + 0.7764; protein feedstuffs: AME/GE = 1.093 × IVDE/GE -19.21, TME/GE = 1.196 × IVDE/GE - 13.25) of feedstuffs for Muscovy ducks ranged from 0.8610 to 0.9921. The accuracy of the regression model was acceptable as the difference between measured and predicted ME and ME/GE values was less than 0.45 MJ/kg (100 kcal/kg) and 2.62% for 14 of the 16 feed samples, respectively. In conclusion, the in vitro digestion method can be used to predict the ME and ME/GE of conventional feedstuffs for Muscovy ducks with acceptable accuracy.

Metabolizable energy (ME) is one of the major factors in formulating diets for ducks and most studies on the ME values of ingredients have been conducted on Peking ducks, with limited research on Muscovy ducks. Compared with the time-consuming in vivo digestion method, in vitro simulating digestion as a rapid and reliable method has been performed to predict ME and metabolizability of gross energy. Therefore, the precision of the in vitro digestion method was evaluated for Muscovy duck feed in our study.

In vitro evaluation of efficacy of nonstarch polysaccharides enzymes on wheat by simulating the avian digestive tract.

In this study, the efficacy of different nonstarch polysaccharide (NSP) enzyme sources on wheat ingredients and wheat basal diets in vitro were evaluated by simulating the avian digestive tract. In Exp. 1, pH level was increased from 2.0 to 8.0 by simulating the avian digestive tract. The relative enzyme activities of xylanase A, B, and C and ß-glucanase X at pH 3.0-3.5 were higher (P < 0.05) than those at pH 2.0 or 7.0-8.0. The optimal pH levels of 3.5 and 7.0 were screened by simulating the proventriculus and small intestine, respectively to evaluate the efficacy of NSP enzyme on wheat sources. In Exp. 2, wheat 1 contained the highest content of NSP fractions and the lowest digestibility in vitro dry matter (IVDMD) and energy (IVED) in wheat samples. Therefore, wheat 1 was selected for hydrolysis research under different NSP enzyme sources and levels (1,500, 4,500, 13,500, 40,500, 121,500 U xylanase/kg and 250, 500, 1,000, 2,000, 4,000 U ß-glucanase/kg) in vitro. The hydrolysis of wheat on the basis of the released reducing sugar content was determined by xylanase sources A > B > C (P < 0.05) and ß-glucanase sources of X > Y (P < 0.05). On the basis of the hydrolysis, the optimum dose of xylanase A and ß-glucanase X were 40,500 U/kg and 2,000 U/kg, respectively. Subsequently, the completely randomized designs involving 2 NSP enzymes treatments × 2 endogenous digestive enzymes treatments (Exp. 3), as well as 2 wheat basal diets × 2 NSP enzymes treatments (Exp. 4) were used to evaluate the efficacy of NSP enzymes on dietary nutrient digestibility. The addition of NSP enzymes (40,500 U xylanase A/kg and 2,000 U ß-glucanase X/kg) increased the IVDMD and IVED of wheat 1 without endogenous enzymes (P < 0.05), while the IVDMD and IVED of wheat 1 with endogenous enzyme were only slightly increased (P > 0.05). The addition of NSP enzymes could increase the IVDMD and IVED of corn-wheat-soybean meal diet (P < 0.05), but had no effect on those of wheat-cottonseed meal rapeseed meal diet (P > 0.05). In conclusion, xylanase and ß-glucanase additions could effectively eliminate the adverse effects on wheat and wheat basal diets at the optimal pH levels of 3.5 and 7.0 by simulating the proventriculus and small intestine parts, respectively. The efficacy of NSP enzymes was influenced by the enzyme sources, dietary type, and the interaction of endogenous enzymes.

The inclusion level of wheat in poultry feeds is limited by nonstarch polysaccharides (NSP). Feeding NSP will increase the intestinal viscosity and residence time of the digesta, reduce nutrient digestion, and absorption of nutrients by birds, thereby damaging the intestinal function and growth performance. The degradation of NSP in feed by supplementing NSP enzymes has a positive effect on nutrient availability and growth performance. Therefore, there is a need for a quick and reliable method to assess the efficacy of NSP enzymes from different types, sources, and processing techniques. Compared with the expensive and time-consuming in vivo method for animal feeding experiments, in vitro digestion has been proved to be a rapid method for predicting the efficacy of exogenous enzymes in various parts of the avian digestive tract. Therefore, in this study, the efficacy of different NSP enzyme sources on wheat ingredients and wheat basal diets were evaluated in vitro by simulating the avian digestive tract.

Crosstalk between Mycotoxins and Intestinal Microbiota and the Alleviation Approach via Microorganisms.

Mycotoxins are secondary metabolites produced by fungus. Due to their widespread distribution, difficulty in removal, and complicated subsequent harmful by-products, mycotoxins pose a threat to the health of humans and animals worldwide. Increasing studies in recent years have highlighted the impact of mycotoxins on the gut microbiota. Numerous researchers have sought to illustrate novel toxicological mechanisms of mycotoxins by examining alterations in the gut microbiota caused by mycotoxins. However, few efficient techniques have been found to ameliorate the toxicity of mycotoxins via microbial pathways in terms of animal husbandry, human health management, and the prognosis of mycotoxin poisoning. This review seeks to examine the crosstalk between five typical mycotoxins and gut microbes, summarize the functions of mycotoxins-induced alterations in gut microbes in toxicological processes and investigate the application prospects of microbes in mycotoxins prevention and therapy from a variety of perspectives. The work is intended to provide support for future research on the interaction between mycotoxins and gut microbes, and to advance the technology for preventing and controlling mycotoxins.

Bacterial Signatures of Cerebral Thrombi in Large Vessel Occlusion Stroke.

It is important to understand the microbial features of the cerebral thrombus and its clinical relevance in stroke patients, of which data were scarce. We aimed to investigate the microbial features of cerebral thrombi retrieved via thrombectomy in stroke patients with large vessel occlusion (LVO) and their correlations with 3-month mortality. In a prospective cohort study, thrombus samples were collected during mechanical thrombectomy in LVO stroke patients with successful revascularization at a tertiary hospital. Oral, fecal, and isolated plasma samples were collected within 12 h of admission. The microbial compositions of all samples were compared using 16S rRNA gene amplicon next-generation sequencing. Fluorescent in situ hybridization (FISH) was used to detect bacteria in thrombus samples. The primary outcome was 3-month mortality. Perioperative adverse events (AEs) within 48 h were also recorded. Bacterial DNA was detected in 96.2% of thrombus samples from 104 patients, and clusters of bacterial signals were seen in the thrombi with FISH. Compared with fecal and oral samples, the thrombus microbiota was mainly characterized by excessive enrichment of Proteobacteria, mainly originating from plasma. The bacterial concentrations, dominant bacteria, and distribution patterns differed in thrombi obtained from cardioembolic and large-artery atherosclerotic strokes. Higher abundances of Acinetobacter and Enterobacteriaceae were associated with a higher risk of perioperative AEs, and a higher abundance of Acinetobacter was independently associated with a higher risk of 90-day mortality. This study demonstrated the presence of bacteria in cerebral thrombi retrieved with thrombectomy in LVO strokes, with some bacteria associated with patients' prognoses. IMPORTANCE In this study, we (i) checked for the presence of bacteria in cerebral thrombi in over 95% of the LVO stroke patients using 16S rRNA sequencing, in contrast with periprocedural control samples that are bacteria negative; (ii) visualized clusters of bacterial signals in the thrombi using FISH; and (iii) cultivated Lactobacillus vaginalis, Bacillus cereus, and Kocuria marina in the bacterial culture of the tissue fragment solution of thrombus aspirates. We found excessive enrichment of Proteobacteria in the thrombi, mainly originating from plasma, as indicated with fast expectation-maximization microbial source tracking (FEAST). Different bacterial concentrations, dominant bacteria, and distribution patterns were found in thrombi obtained from cardioembolic and large-artery atherosclerotic LVO strokes. There was an association between higher abundances of Acinetobacter and Enterobacteriaceae in the thrombi and a higher risk of perioperative adverse events and an association between a higher abundance of Acinetobacter in the thrombi and a higher risk of 90-day mortality.

Dietary fibers with different viscosity regulate lipid metabolism via ampk pathway: roles of gut microbiota and short-chain fatty acid.

Dietary fiber (DF) improves gastrointestinal health and has important associations with the alleviation of intestinal diseases and metabolic syndrome. However, due to DFs complex characteristics, such as solubility, viscosity, and fermentability, the mechanism in these was not consistent. As an herbivore, the goose has a prominent digestive ability to DF. Therefore, we choose low, medium, and high viscosity DFs (respectively resistant starch-3 []RS], inulin [INU], and ß-glucan [GLU]) as Magang goose diet treatment for 4 wk, to investigate the effect and potential mechanism of different viscosities DFs on the growth and development process of goose. In summary, three degrees of viscous DFs could decrease the mechanismic lipid level of geese by promoting acid-producing bacteria and short-chain fatty acid (SCFA) production, therefore, activating AMPK pathway-related genes through the gut-liver axis. High viscous DF has a greater lipid-lowering effect on geese, while medium viscous DF has preferable intestinal mucosal protection.

Exogenous Linoleic Acid Intervention Alters Hepatic Glucose Metabolism in an Avian Embryo Model.

In the present study, developmental changes of gluconeogenesis and glycolysis in an avian model were measured, and then the intervention effects of in ovo feeding (IOF) linoleic acid (LA) on hepatic glucose metabolism were evaluated. In Experiment 1, thirty fertilized eggs were sampled on embryonic days (E) of 16, 19, 22, 25, 28, 31, and thirty newly-hatched ducklings at hatch (E34 and E35). In Experiment 2, a total of 120 fertilized eggs (60 eggs for each group) were injected into the yolk sac with PBS as the control group and LA as the IOF LA group on E25. Twelve eggs were selected for sample collection on E28 and E31. Serum contents of glucose, pyruvate, and lactate increased ( p < 0.05) linearly or quadratically from E16 to hatch, as well as hepatic glycogen and pyruvate contents. Hepatic mRNA expression related to energy homeostasis, gluconeogenesis, and glycolysis increased ( p < 0.05) in embryogenesis, and the plateau period was presented on E25-E31. IOF LA decreased ( p < 0.05) serum contents of glucose, triacylglycerol, cholesterol, and hepatic oleic acid, unsaturated fatty acids on E28, as well as the gene expression relative to gluconeogenesis. IOF LA increased ( p < 0.05) pyruvate content in serum and liver, and hepatic gene expression relative to glycolysis on E31. In summary, hepatic gluconeogenesis and glycolysis were enhanced to meet the increasing energy demands of embryonic development during E25 - hatch. Exogenous LA intervention on E25 could inhibit hepatic gluconeogenesis and enhance glycolysis during the later developmental period, disrupting glucose embryonic homeostasis and energy status.

Combined Analysis of the Effects of Exposure to Blue Light in Ducks Reveals a Reduction in Cholesterol Accumulation Through Changes in Methionine Metabolism and the Intestinal Microbiota.

Monochromatic light is widely used in industry, medical treatment, and animal husbandry. Green-blue light has been found to stimulate the proliferation of satellite cells and the results of studies on the effects of blue light on poultry vary widely. It would be worthwhile to study the effect of blue light on poultry growth and how exposure to blue light affects metabolism and the intestinal microbiota. In this study, we irradiated Cherry Valley ducks with 460 nm wavelength light (blue light) for 3 weeks to explore the effects of blue light in comparison to those of white light (combined wavelength light) on animal growth and development. Our results showed that, under exposure to blue light, the body weight and average daily feed intake of ducks were decreased, but the leg muscle and relative length of the intestine were increased. Exposure to blue light chiefly enhanced the anti-inflammatory and antioxidant capacities of the animal and decreased lipid levels in serum and liver. Metabolomic analysis revealed that blue light heightened cysteine and methionine metabolism, and increased serum taurine and primary bile acid levels, as well as up-regulating the metabolites L-carnitine and glutamine. Treatment with blue light significantly increased the beta diversity of intestinal microbiota and the relative abundances of bile acid hydrolase-producing bacteria, especially Alistipes. These changes promote the synthesis of secondary bile acids to further enhance lipid metabolism in the host, thereby reducing cholesterol accumulation in ducks. These results should help us better understand the effects of exposure to blue light on metabolite levels and the intestinal microbiota, and suggest that it may be possible to use colored light to control the development of livestock and poultry.

Effect of Maternal Marginal Zinc Deficiency on Development, Redox Status, and Gene Expression Related to Oxidation and Apoptosis in an Avian Embryo Model.

Maternal severe zinc (Zn) deficiency resulted in growth retardation and high mortality during embryonic development in human. Therefore, this study is aimed at evaluating the effect of maternal marginal Zn deficiency on the development and redox status to avoid severe Zn deficiency using an avian model. A total of 324 laying duck breeders at 214 days old were randomly allotted into 3 dietary Zn levels with 6 replicates of 18 ducks per replicate. The birds were fed experimental diets including 3 dietary supplemental Zn levels of 0 mg/kg (maternal Zn-deficient group, 29.2 mg Zn/kg diet), 60 mg/kg (maternal Zn-adequate group), and 120 mg/kg (maternal Zn-high group) for 6 weeks. Dietary Zn levels had on effect on egg production and fertility (P > 0.05), whereas dietary Zn deficiency decreased breeder plasma Zn concentration and erythrocytic alkaline phosphatase activity at week 6 and inhibited erythrocytic 5'-nucleotidase (5'-NT) activity at weeks 2, 4, and 6 (P < 0.05), indicating that marginal Zn-deficient status occurred after Zn depletion. Maternal marginal Zn deficiency increased embryonic mortality and contents of superoxide anion radical, MDA, and PPC and reduced MT content and CuZnSOD activity in duck embryonic livers on E29. The MDA content was positively correlated with embryonic mortality. Maternal marginal Zn deficiency increased BCL2-associated X protein and Caspase-9 mRNA expressions as well as decreased B-cell lymphoma-2 and MT1 mRNA and signal AKT1 and ERK1 protein expressions (P < 0.05). Breeder plasma Zn concentration and erythrocytic 5'-NT activities at week 6 were positively correlated with GSH-Px activity and GPx, MT1, and BCL2 mRNA expressions in embryonic livers on E29. In conclusion, erythrocytic 5'-NT activity could be more rapid and reliable to monitor marginal Zn-deficient status. Marginal Zn deficiency impaired hatchability and antioxidant defense system and then induced oxidative damage and apoptosis in the embryonic liver, contributing to the greater loss of duck embryonic death.

Persistent Purine Metabolic Abnormality Induces the Aggravation of Visceral Inflammation and Intestinal Microbiota Dysbiosis in Magang Goose.

Gout is a disease involving abnormal purine metabolism that is widespread in mammals and birds. Goose is especially susceptible for gout in early stage. However, a few studies investigated the ontogenetic pattern of goslings with purine metabolic abnormality. Our studies were conducted to investigate whether persistent purine metabolic abnormality would lead to aggravation of visceral inflammation and intestinal microbiota dysbiosis in goose. A total of 132 1-day-old Magang geese were randomly divided into six replicates and fed a high-calcium and protein meal-based diet from 1 to 28 days. The experiment lasted for 28 days. Liver and kidney damages were observed in 14- and 28-day-old Magang geese, and liver inflammation increased with increasing age. In 28-day-old Magang geese, serum CAT and liver GSH-Px activity were significantly reduced. Furthermore, jejunum intestinal barrier was impaired and the abundance of Bacteroides was significantly reduced at the genus level. Collectively, the high-calcium and high-protein (HCP) meal-based diet caused liver and kidney damage in 28-day-old Magang geese, leading to hyperuricemia and gout symptoms, and the intestinal barrier is impaired and the intestinal flora is disrupted.

Ochratoxin A: its impact on poultry gut health and microbiota, an overview.

Ochratoxin A (OTA) is a widespread mycotoxin, that has strong thermal stability, and is difficult to remove from feed. OTA is nephrotoxic, hepatotoxic, teratogenic, immunotoxic, and enterotoxic to several species of animals. The gut is the first defense barrier against various types of mycotoxins present in feed that enter the body, and it is closely connected to other tissues through enterohepatic circulation. Compared with mammals, poultry is more sensitive to OTA and has a lower absorption rate. Therefore, the gut is an important target tissue for OTA in poultry. This review comprehensively discusses the role of OTA in gut health and the gut microbiota of poultry, focusing on the effect of OTA on digestive and absorptive processes, intestinal barrier integrity, intestinal histomorphology, gut immunity, and gut microbiota. According to the studies described to date, OTA can affect gut dysbiosis, including increasing gut permeability, immunity, and bacterial translocation, and can eventually lead to gut and other organ injury. Although there are many studies investigating the effects of OTA on the gut health of poultry, further studies are needed to better characterize the underlying mechanisms of action and develop preventative or therapeutic interventions for mycotoxicosis in poultry.