Serum Aspartate Aminotransferase Research Articles

Clinical utility of fibrosis-4 index in predicting increased right atrial pressure

Abstract Introduction Fibrosis-4 (FIB-4) index, derived from serum aspartate transaminase, alanine aminotransferase, platelet count and age, is an easily measurable marker reflecting hepatic fibrosis. Recently, FIB-4 index has been reported to be associated with cardiac events in heart failure (HF) patients. We examined whether FIB-4 index was useful in predicting elevated right atrial pressure (RAP) in comparison with directly measured RAP. Methods We studied consecutive 293 HF patients who underwent right heart catheter (RHC) examinations at our institution between Sep 2021 and May 2023. The exclusion criteria were as follows: viral or metabolic chronic hepatic diseases, thrombocytopenia. The subjects received RHC examination and blood test on the same day, and echocardiography within 3 days from the RHC examination. On top of FIB-4 index, diameter of inferior vena cava (IVC) and its respiratory changes were measured as a conventional method to estimate RAP. Results A total of 252 patients (mean 64.7 years of age, 52.8% men) were eligible for this study. FIB-4 index was significantly correlated with mean RAP (r = 0.39, p < 0.001). ROC curve analysis revealed that 1.80 was the optimal cutoff value of FIB-4 index to predict increased RAP > 10mmHg (AUC 0.74, p < 0.001, sensitivity 76.1%, specificity 74.0%). As shown in Figure, the diagnostic accuracy increased when FIB-4 index was combined with IVC diameter (AUC 0.77), which was significantly higher than the combination (AUC 0.71) of IVC diameter alone (AUC 0.71, p < 0.001, cutoff 17mm, sensitivity 67.6%, specificity 71.8%) and IVC respiratory changes alone (AUC 0.61, p = 0.005, cutoff 53%, sensitivity 77.5%, specificity 44.2%). Conclusions FIB-4 index was clinically useful in predicting increased RAP, especially when it was combined with IVC diameter.

Growth performances of Clarias gariepinus juveniles fed with Jatropha curcas seed meal

Jatropha curcas is an oil producing seed with high nutritional qualities for consumption. However, due to inherent anti-nutritional factors, appropriate processing is necessary to improve its nutrients utilization. This study was aimed at processing J. curcas using solvent-extraction method and evaluating its inclusion effects in the diet for Clarias gariepinus on its growth status. J. curcas meal was extracted using 80 % methanol to remove phorbol esters and other anti-nutrients. Thereafter, five iso-nitrogenous diets (40 % crude protein) were formulated containing J. curcas meal replacements of soybeans meal at 0 % (TRT0), 25 % (TRT25), 50 % (TRT50), 75 % (TRT75) and 100 % (TRT100) and fed to C. gariepinus for 70 days. Results showed that TRT25 fish had the highest mean weight gain and specific growth. The serum alkaline phosphate, alanine aminotransferase, and aspartate aminotransferase levels began to rise significantly (p ≤ 0.05) at 50 % replacement. Likewise, the assessment of gut ecology and morphology indicated that TRT25 had significantly (p ≤ 0.05) the highest gut bacteria colony forming unit (2.60 ×104±0.02cfu/g) and most favorable area of absorption (0.16±0.01 cm2). The histopathological observation of the fish intestine, liver and gills indicated no visible deformity in TRT0 and TRT25 fish. However, various degrees of degenerations were observed in the fish fed with 50 % and higher inclusion of J. curcas. This study showed that methanol-extracted J. curcas meal can be effectively utilized for C. gariepinus at 25 % of replacement.

Iodine Bioavailability and Biochemical Effects of Brassica oleracea var. sabellica L. Biofortified with 8-Hydroxy-7-iodo-5-quinolinesulfonic Acid in Wistar Rats

Background: Iodine is one of the essential trace elements for human life. The main objective of the biofortification of plants with iodine is to obtain food with a higher content of this element compared to conventional food. Biofortification of plants with iodine can increase the intake of this trace element by different populations. In addition, it may reduce the risk of iodine deficiency diseases. Objectives: The aim of the study was to investigate the effect of kale biofortified with 8-hydroxy-7-iodo-5-quinolinesulfonic acid (8-OH-7-I-5QSA) on iodine bioavailability and biochemical effects in Wistar rats. Methods: Kale biofortified with (8-OH-7-I-5QSA) was tested for iodine levels in urine, feces, and selected tissues using the ICP-MS/MS technique. The feeding experiment was designed to investigate potential changes in selected thyroid-regulated biochemical parameters in blood serum of Wistar rats. Results: The dietary intake of Wistar rats fed kale biofortified with (8-OH-7-I-5QSA) from both the “Oldenbor F1” and “Redbor F1” cultivars for 8 weeks resulted in significantly (p ≤ 0.05) higher iodine concentrations in the urine and kidneys of rats, which proves iodine bioavailability. Rats’ diets with “Oldenbor F1” and “Redbor F1” kale non- and -biofortified with 8-OH-7-I-5QSA had a significantly (p ≤ 0.05) lower or a tendency for lower concentration of TSH, triglyceride, total and direct bilirubin, TBARs, uric acid, aspartate aminotransferase (AST) and alanine aminotransferase (ALT) concentrations in serum. Dietary intake of “Oldenbor F1” and “Redbor F1” kale biofortified with 8-OH-7-I-5QSA significantly (p ≤ 0.05) increased the total antioxidant status (TAS). Conclusions: Our study confirms that kale biofortified with iodine in organic form iodoquinoline 8-OH-7-I-5QSA is bioavailable and well absorbed by the Wistar rat and has a positive effect on selected biochemical parameters. The results obtained in this study may be highly predictive for further studies in humans.

Biochemical perturbations associated with Salmonella gallinarum infection in laying hens:Is oxidative stress implicated?

The aim of this study was to investigate some biochemical and tissue changes associated with Salmonella gallinarum infection in laying hens (LHs), and the complicities of oxidative stress (OS). Fifty LHs were assigned to two groups of 25 LHs infected with S. gallinarum (109 cfu*mL-1 of S. gallinarum) and 25 uninfected controls. Biochemical assays and histopathology were carried out following standard procedures. There was a significant loss of body weight, drop in egg production, as well as 28% mortality in the infected group. Serum alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase and superoxide dismutase (SOD) activities, as well as serum total protein, globulin, total cholesterol, total bilirubin, uric acid, creatinine and malondialdehyde (MDA) levels were significantly higher, whereas serum albumin levels were significantly lower in infected LHs. There were inflammatory, degenerative and necrotic changes observed in the affected organs. Considering the significant elevation in MDA levels coupled with elevated SOD activity in the infected LHs, OS may play a significant role in the pathology of fowl typhoid and may suggest a possible treatment of infected layers with antioxidants.

Elevated Serum Syndecan-1 Levels are Associated with Obesity-Related Complications in Children

Background: Syndecan-1 plays a crucial role in cell differentiation, growth, adhesion, wound healing, and inflammatory processes. It has been linked to obesity, particularly overweight and chronic low-grade inflammation. Objectives: This study aimed to compare serum syndecan-1 levels between obese children and a healthy control group and to investigate the relationship between serum syndecan-1 levels and renal and cardiovascular complications associated with obesity in children. Methods: We assessed 30 obese and 30 healthy children aged 8 - 16 years. Blood samples were collected from both groups to measure serum aspartate aminotransferase (AST), syndecan-1, fasting blood glucose (FBG), alanine aminotransferase (ALT), creatinine, and urea concentrations. In the obese group, high-density lipoprotein cholesterol (HDL-C), insulin, triglyceride (TG), and low-density lipoprotein cholesterol (LDL-C) levels were also measured, along with homeostasis model assessment of insulin resistance (HOMA-IR). Results: The mean serum syndecan-1 levels in the obese and control groups were 15.65 ± 10.01 ng/mL and 6.99 ± 3.79 ng/mL, respectively, with a significantly higher level observed in the obese group (P < 0.005). Significant differences were also found in BMI, BMI SDS, creatinine, AST, and ALT levels between the two groups (P < 0.05), with all parameters being higher in the obese group. A significant positive linear association was identified between syndecan-1 levels and creatinine, TG, and BMI SDS (r = 0.711, r = 0.630, r = 0.682, P < 0.01). Additionally, a strong negative correlation was found between syndecan-1 and HDL-C levels (r = -0.609, P < 0.001). No significant linear relationship was detected between syndecan-1 levels and LDL-C, ALT, AST, glucose, urea, insulin levels, or HOMA-IR measurements (P > 0.05). Linear regression analysis revealed that serum creatinine levels and BMI SDS were significantly linked to changes in syndecan-1 levels. Conclusions: Syndecan-1 is elevated in obese children due to inflammation and may serve as an early biomarker for endothelial damage. It can be useful in detecting obesity-related renal damage and cardiovascular risk in children.

Pueraria lobata extract ameliorates D-GalN/LPS-induced liver injury through targeting TLR4/NF-κB signalling pathway and regulating gut microbiota

AbstractKudzu root (Pueraria lobata), known for its dual role as a medicinal herb and food ingredient, has proven anti-inflammatory and antioxidant properties. This study explored the effects of P. lobata extract (PLE) on D-galactose/lipopolysaccharide (D-GalN/LPS)-induced liver inflammation and oxidative stress in mice, along with its impact on gut microbiota. The in vivo studies indicated that PLE significantly reduced hepatic levels of pro-inflammatory cytokines (tumour necrosis factor-α, interleukin-1β, and interleukin-6) and increased the anti-inflammatory cytokine interleukin-10. It also lowered serum aspartate aminotransferase and alanine aminotransferase activities, indicating reduced liver damage, and mitigated oxidative stress by decreasing malondialdehyde levels while restoring superoxide dismutase activity. Western blot analysis revealed that PLE inhibited the phosphorylation of NF-κB pathway proteins (p65 and IκB) and suppressed TLR4 expression, highlighting its role in this inflammatory pathway. Additionally, PLE ameliorated D-GalN/LPS-induced gut microbiota dysbiosis, reducing Proteobacteria abundance and promoting beneficial genera such as Lactobacillus, Bifidobacterium, and Akkermansia. These findings suggest that PLE protects against liver inflammation and oxidative stress, while improving gut microbiota composition, offering potential therapeutic strategies for liver-related diseases.

Trimetazidine protects against acute indomethacin-induced gastric mucosal, hepatic, and renal injury in rats

Background: Peptic ulcers are increasingly reported as a challenging disease in clinical settings. Several medications are employed in the management of peptic ulcers. Thus far, there is no medication devoid of any adverse effects that may achieve a 100% curative rate or provide a total remedy for the ailment. Aim: We aimed to examine the healing effects of trimetazidine against indomethacin-induced gastric ulcers in albino rats. Methodology: A total of 25 rats were used, divided into five groups (each group contained five rats): a negative control group that was only treated with distilled water, a positive control group that was only treated with a single dose of indomethacin (30 mg/kg) orally, a group that received indomethacin (30 mg/kg) and low doses of trimetazidine (17.5 mg/kg) orally, a group that received indomethacin (30 mg/kg) and medium doses of trimetazidine (35 mg/kg) orally, and a group that received indomethacin (30 mg/kg) and high doses of trimetazidine (52.5 mg/kg) orally. The induction of gastric ulcers occurred on the first day of the experiment through the administered indomethacin and, subsequently, the rats were treated orally with either trimetazidine or distilled water, three times daily, for 7 days. Serum urea, creatinine, alanine aminotransferase (ALT), aspartate aminotransferase (AST), and albumin levels were measured. Stomachs were excised from the rats’ bodies and opened along the greater curvature; they were then rinsed with saline, extended on a white corkboard, and examined macroscopically. The stomach tissues were also processed in order to generate microscopic slides for microscopical examination. Results: Indomethacin administration caused multiple ulcerations in the gastric mucosa, significant elevations in serum urea, creatinine, AST, and ALT levels, and a significant reduction of the serum albumin levels. The treatment with trimetazidine significantly healed the indomethacin-induced gastric ulcers. Conclusion: The present study indicates that the nonsteroidal anti-inflammatory drug (NSAID) indomethacin can induce substantial gastric ulcers, which may be linked to a direct toxic effect on the histological architecture of the gastric linings in addition to the reduction of blood flow to gastric mucosa; this effect can be treated by administration of trimetazidine. Ultimately, this study suggests that administering the optimal dosage of trimetazidine can be advantageous in treating stomach ulcers caused by NSAIDs. Moreover, the study suggests that the indomethacin-induced liver and renal dysfunction can also be alleviated by the use of trimetazidine.

Dietary ferulic acid supplementation enhances antioxidant capacity and alleviates hepatocyte pyroptosis in diquat challenged piglets

BackgroundOxidative stress significantly impacts growth performance and liver function in piglets. Ferulic acid (FA) works as an antioxidant, however, the role and mechanism of FA in the regulation of diquat-induced oxidative stress in piglets are less known. This study was designed to investigate the effects of FA on growth performance and antioxidant capacity in piglets with diquat challenge.MethodsThirty-two healthy DLY (Duroc × Landrace × Yorkshire) piglets (13.24 ± 0.19 kg) were randomly divided into one of two diets including 0 or 4 g/kg FA for 14 d. On d 15, all pigs were intraperitoneally injected diquat or sterile saline.ResultsDietary supplementation with ferulic acid (FA) significantly improved the average daily gain (ADG) and decreased feed-gain ratio (F/G) of piglets. Here, dietary FA supplementation reduced serum aspartate aminotransferase (AST), alanine aminotransferase (ALT) activities in diquat challenged piglets. Furthermore, diquat infusion increased reactive oxygen radicals (ROS) level in liver, decreased the activities of total superoxide dismutase (T-SOD) and glutathione peroxidase (GSH-Px), total antioxidant capacity (T-AOC) and increased malondialdehyde (MDA) content in the liver and serum. Supplementation with FA significantly increased T-AOC and T-SOD activities and decreased MDA and ROS levels. FA down-regulated gene and protein expression of Keap1, and up-regulated protein expression of Nrf2 and HO-1 in the liver of piglets with diquat challenge. Importantly, diquat challenge increased the ratio of late apoptosis, increased serum levels of IL-1β, IL-18 and lactate dehydrogenase (LDH), and up-regulated pyroptosis-related genes in the liver. FA supplementation reduced the ratio of late apoptosis and down-regulated mRNA expression of Caspase-1. Accordingly, FA addition reduced concentration of IL-1β, IL-18, and LDH under diquat challenge.ConclusionsDiquat-induced oxidative stress reduced growth performance and impaired liver function in piglets. Dietary FA supplementation enhanced the antioxidant capacity and reduced the degree of hepatocyte pyroptosis, thereby alleviating the oxidative damage in the liver and mitigating the impact of diquat on growth performance of piglets.

The impact of hydrogen sulfide on mesenchymal stem cells in rats suffering from liver fibrosis via suppression of TGF-β signaling

Worldwide, liver fibrosis (LF) causes complications and has an elevated death rate. The prevalence of mesenchymal stem cell therapy (MSC) is a result of the lack of liver donors. In recent years, the study of stem cell therapy has advanced into a promising and cutting-edge field of study. The purpose of this study is to assess the possible value of in vitro preconditioning of bone marrow-derived mesenchymal stem cells (BMSCs) with sodium hydrogen sulfide (NaHS), which aims to encourage rats to benefit from stem cell therapy with carbon tetrachloride-induced liver fibrosis. Materials and Methods: Fifty male albino rats (6 weeks old & 120–150 g) were divided equally into 5 groups (10 rats each); the 1st group served as a negative control, the 2nd group was a positive control, in which rats received 2 mL/kg CCl4 (1:1 corn oil) twice a week for five weeks, and the remaining three groups received, in addition to CCL4, a NaHS solution (10 μmol/kg) every 2 days for 6 weeks, one dose of BMSCs (3 × 106 cells per rat) intravenously, and a single dose of BMSCs (3 × 106 cells per rat) in culture with 200 μmol/L NaHS for 24 h. Quantitative gene expression of transforming growth factor-beta (TGF-β), Smad, collagen, α-SMA, MAPK, β-catenin, GSK-3B, and CBS was carried out using real-time polymerase chain reaction; whereas the serum levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), and albumin were estimated using colorimetric analysis. Also, the relative expression of MAPK, β-catenin, and GSK-3B by Western blot was done. Histopathological analysis was used to gauge the progression of LF. Results: The liver fibrosis group exhibited significantly increased serum ALT and AST levels, along with decreased serum albumin levels, compared to controls. Additionally, compared to controls, there was a rise in the gene expression of TGF-β, Smad, collagen, α-SMA, MAPK, β-catenin, and GSK-3B, while the gene expression of CBS is decreased. The biochemical parameters indicated above were greatly improved by BMSCs pretreated with H2S, and the liver sections produced from this group demonstrated a notable improvement in histopathology. Conclusion: The study investigated and demonstrated how NaHS affected the efficacy of BMSC therapy in rats with CCl4-induced liver fibrosis.

A-098 Reducing Hemolyzed Specimen Rejection for Aspartate Aminotransferase (AST): A Quality Improvement Initiative to Further Optimize Concentration-Specific H-index Thresholds

Abstract Background Serum aspartate aminotransferase (AST) is a commonly ordered test useful for diagnosing and monitoring hepatocellular damage. The hemolysis (H) index interference threshold for the Roche Cobas AST reagent is H=20, which is the lowest of all tests on Roche chemistry platforms (Cobas c701, c502, and e801). Previous optimization studies supported the implementation of an AST concentration-specific tiered hemolysis interference threshold schema: AST<100 U/L (H=50), AST=100-200 U/L (H=100), AST=201-300 U/L (H=200) and AST>301 U/L (H=500). This schema significantly reduced redraws; however, a significant number of rejected samples were noted to have AST results within the reference interval (RI). The aim of this study was to establish an H-index threshold for samples with AST results within the RI. Methods Twelve pools of residual serum samples were created with AST concentrations ranging from 17-66 U/L. Each pool was split into 2 aliquots, receiving either 10% of a lab-produced hemolysate solution generating H-indices from 62-508 or 10% of a 0.9% saline control. Aliquots were mixed in equal portions to create a series of 5 samples with increasing hemolysis according to CLSI guideline EP-07 and analyzed in EP Evaluator. Median(interquartile range (IQR)) H-index thresholds were calculated for error limits beginning at +5 U/L and increasing incrementally (+1 U/L) to +10 U/L. Clinical cases with an H-index slightly above the hemolysis interference threshold (50≤H≤70) and results within the RIs (Male:8-48U/L; Female:8-43U/L) were reviewed by the Chemistry Resident/Fellow on-call (n=68) over a period of 8 months. Results were released with a comment if risk of clinical misinterpretation due to a falsely elevated result was low. Previous, non-hemolyzed AST results were compared within 45 days, if available, by paired-Wilcoxon test (Graphpad Prism). Results The median(range) of initial AST results in the serum pools was 20(17-66) U/L. The calculated H-index thresholds (median(IQR)) using error limits of +5, +6, +7, +8, +9, +10 U/L were 49(43-53), 56(52-63), 66(61-78), 78(72-81), 91(84-91) and 101 (96-107), respectively. All slightly hemolyzed AST results (50≤H≤70) within the RI were released with a comment upon chart review. Previously reported AST values (n=23) were compared to current (hemolyzed) concentrations and found to be statistically significantly increased relative to previous results from the same patient (median(range) difference: 3.7(-3.6-11)U/L, p=0.009). However, the median difference was <5U/L or 10%, the laboratory’s criteria used to define a clinically significant difference. Conclusions A median H-index limit of up to 100 can be applied to samples when AST is within the RI. The risk of misinterpretation for results with mild-moderate hemolysis was low in the cases reviewed. Sample rejection rates and reporting delays can be diminished by implementing this practice. Interpretation can be further enhanced by appending the following comment to hemolyzed samples: “Specimen was received with hemolysis slightly above the accepted threshold. This degree of hemolysis is associated with a false increase of approximately 5-10 U/L. Interpret in conjunction with other laboratory and clinical findings.”

Gut microbiota of miR-30a-5p-deleted mice aggravate high-fat diet-induced hepatic steatosis by regulating arachidonic acid metabolic pathway.

Patients with non-alcoholic fatty liver disease (NAFLD) often exhibit hepatic steatosis and dyslipidemia. Studies have shown that intestinal microorganisms are closely related to the occurrence of NAFLD and atherosclerosis. Our previous study has underscored the protective role of microRNA-30a-5p (miR-30a-5p) against atherosclerosis. In the present study, we aimed to elucidate the effect and underlying mechanism of the intestinal microorganisms of miR-30a-5p knockout (KO) mice on NAFLD. Our findings demonstrated that KO exacerbated high-fat diet (HFD)-induced hepatic steatosis and disrupted liver function, as evidenced by elevated levels of total cholesterol, low-density lipoprotein, alanine aminotransferase, aspartate transaminase, and total bile acids in serum. Fecal microbiota from HFD-fed KO mice induced hepatic steatosis, dyslipidemia, and higher levels of enzymes indicative of liver damage in wild-type mice. Remarkably, KO mice significantly intensified the above effects. 16s rDNA sequencing and metabolomics of the intestinal microbiota in the HFD-treated KO and WT mice showed that the loss of miR-30a-5p resulted in intestinal microbiota imbalance and was highly related to the arachidonic acid metabolic pathway. Targeted metabolomic in the liver tissues unveiled upregulation of COX-related (PGF2a, 8-iso-PGF2a and PGF2) and LOX-related (LTB4, LTD4, 12S-HETE and 15S-HETE) factors in HFD-treated KO mice. Immunohistochemistry and transcriptional analyses showed that miR-30a-5p affected arachidonic acid metabolism through the LOX/COX pathways. Besides, COX/LOX pathways and hepatic steatosis were reversed after reintroducing miR-30a-5p in HFD-treated KO mice. This study reveals the pivotal mechanism by which miR-30a-5p and intestinal microbes regulate hepatic steatosis and abnormal lipid metabolism, offering promising avenues for NAFLD and atherosclerosis therapeutics. MiR-30a-5p deletion aggravated hepatic steatosis and lipid disorder induced by an HFD in mice. Gut microbiota participated in the regulation of hepatic steatosis in the context of miR-30a-5p. Gut microbiota metabolism-related arachidonic acid metabolic pathway contributed to miR-30a-5p-regulated hepatic steatosis and lipid disorder. Reintroducing miR-30a-5p reversed hepatic steatosis and arachidonic acid metabolism disorder caused by HFD and miR-30a-5p deletion.

Exploring the Mechanism of Action of Sericin in Ameliorating non-Alcoholic Fatty Liver Disease in Mice Based on the Nrf2- GPX4/ NF-κB p65 Pathway

Objective: To explore the ameliorative effect and mechanism of action of sericin on liver injury in Non-Alcoholic Fatty Liver Disease (NAFLD) model mice. Methods: Mice were fed a high-fat diet for 8 weeks to establish NAFLD model mice. The NAFLD mice were then randomly divided into 6 groups and given 0, 250, 500, and 1000 mg/kg body weight of sericin, 1000 mg/kg sericin + ML385 (a protein inhibitor of Nrf2), and Zhibitai Capsules (a positive drug), by gavage, respectively. The levels of TC, TG, low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), alanine aminotransferase (ALT), and aspartate aminotransferase (AST) in mouse serum and the levels of MDA, GSH, SOD, TNF-α, and IL-6 in liver tissues were measured. Pathological changes in liver tissues were evaluated using hematoxylin-eosin (HE) and Oil Red O staining. Protein expression of Nrf2, Keap1, HO-1, GPX4, and NF-κB p65 in liver tissues was detected by Western blotting, and the expression level of GPX4 in the liver was examined by immunohistochemistry. Results: Sericin and Zhibitai Capsules improved hepatic steatosis and lipid accumulation in NAFLD model mice. TC, TG, LDL-C, MDA, and TNF-α, IL-6 levels were down-regulated, and HDL-C and SOD levels were up-regulated. There was no significant difference in the expression of AST and ALT in all the groups. In addition, Sericin and Zhibitai Capsules upregulated the expression levels of Nrf2, keap1, HO-1, and GPX4 proteins and inhibited the expression of NF-κB p65 in the liver of NAFLD model mice. There was no significant difference in serum lipids and liver indices between the 1000 mg/kg sericin + ML385 group and the sericin dose groups. Conclusion: Sericin has an ameliorative effect on liver injury in NAFLD model mice by alleviating oxidative stress and inflammatory responses in liver injury. It remains to be explored whether this effect is regulated through the Nrf2- GPX4/ NF-κB p65 signaling pathway.

Immunological, Antioxidant, Growth Responses, and Disease Resistance of Rainbow Trout, Oncorhynchus mykiss, with Feeding Diets Supplemented with Lactobacillus salivarius and Lutein

Abstract The aim of the present study was to assess the effects of dietary supplementation with Lactobacillus salivarius (LS) ATCC 11741 and lutein (LU) on immunological, antioxidant, and growth responses, and resistance against Yersinia ruckeri infection in rainbow trout (Oncorhynchus mykiss). There were seven experimental diets containing un-supplemented diet (CTL), L. salivarius at 1 × 106 (LS6) and 1 × 108 (LS8) CFU/g, lutein at 50 (LU50) and 150 (LU150) mg/kg, L. salivarius at 1 × 106 CFU/g plus lutein at 50 g/kg (LS6+LU50), and L. salivarius at 1 × 108 CFU/g plus lutein at 150 g/kg (LS8+LU150). These diets were provided to the fish (N= 735; 14.0±0.38 g). After 60 days of feeding, all experimental treatments exhibited significantly higher growth performance, compared to the CTL treatment. The intestinal protease activity and the intestinal lactic acid bacteria population in the probiotic-treated fish were significantly higher than in the CTL fish. The intestinal lipase activity was only higher in the LS6+LU50 treatment, compared to the CTL treatment. Compared to the CTL treatment, the intestinal total bacterial count, and serum superoxide dismutase significantly increased in the LS6+LU50 and LS8+LU150 treatments. The serum catalase significantly increased in LU150, LS6+LU50, and LS8+LU150 treatments, and serum glutathione peroxidase significantly increased in the lutein-treated fish. All experimental treatments, particularly LS6+LU50 and LS8+LU150, had significantly lower serum malondialdehyde levels, compared to the CTL treatment. The levels of serum alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase, and lactate dehydrogenase in LU50, LS6+LU50, and LS8+LU150 treatments were significantly lower than the CTL. All experimental treatments showed significantly higher serum lysozyme (LYZ), complement, blood respiratory burst activity (RB), and skin mucus alkaline phosphatase (ALP), compared to the CTL treatment. The highest serum LYZ, C4, total immunoglobulin (Ig), blood RB activity, and skin mucus peroxidase, ALP, and Ig were observed in the LS6+LU50 and LS8+LU150 treatments. All the experimental treatments, especially LS6+LU50, exhibited significantly lower mortality after the bacterial challenge compared to the CTL. In conclusion, dietary supplementation with 1 × 106 CFU/g L. salivarius and 50 mg/kg lutein can maximally improve growth performance, digestive enzymes, antioxidant parameters, immune responses, intestinal lactic acid bacteria, and resistance against yersiniosis in rainbow trout.

Effects of including different levels of equal mix of soybean and flaxseed oils in Japanese quail diets on the growth, carcass quality, and blood biomarkers

Corn, the primary ingredient in modern poultry feeds, contains high levels of ω-6 fatty acids but lacks sufficient ω-3 fatty acids, creating an imbalance. Maintaining a balance between ω-6 and ω-3 fatty acids in poultry diets is crucial due to their competition. This study aimed to evaluate the effects of incorporating different concentrations of an equal mix of soybean oil (SO) and flaxseed oil (FO) into quail diets on growth performance, carcass quality, and blood biochemistry. One-week-old Japanese quail birds (n=200) were randomly assigned to four dietary groups, each comprising five replicates with 10 chicks per replicate. Four isonitrogenous/isocaloric basal diets were formulated. Group 1 (control) received a basal diet without SO or FO, while Groups 2-4 received basal diets supplemented with an equal mix of SO+FO at levels of 1.0%, 1.5%, and 2.0%, respectively. The inclusion of oil mixes significantly increased body weight (BW) at five weeks and daily weight gain (DWG) during weeks 3-5 and 1-5. The feed conversion ratio (FCR) improved with the addition of oil mixes throughout the trial period. Supplementing quail diets with oil mixes resulted in reduced serum total cholesterol (TC) and LDL cholesterol, elevated serum HDL cholesterol, and no significant effect on triglycerides (TG) and VLDL cholesterol levels. Quails fed oil-supplemented diets showed lower serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), and creatinine levels, while urea and uric acid were significantly affected. Birds fed diets with oil mixes also had increased serum concentrations of immunoglobulin G (IgY), immunoglobulin M (IgM), and superoxide dismutase (SOD). However, serum immunoglobulin A (IgA), malondialdehyde (MDA), and total antioxidant capacity (TAC) levels did not significantly change across experimental groups. Overall, adding up to 2% of the SO and FO mix in growing quail feeds improved growth performance, blood lipid profile, liver and kidney function markers, immune response, and antioxidant defense. The highest level of oil mix (2%) yielded the most beneficial effects.

AcFibroMASH Index for the Diagnosis of Fibrotic MASH and Prediction of Liver-related Events: An International Multicenter Study

Background & AimsMetabolic dysfunction-associated steatohepatitis (MASH) and fibrotic MASH are significant health challenges. This multi-national study aimed to validate the acMASH index (including serum creatinine and aspartate aminotransferase concentrations) for MASH diagnosis and develop a new index (acFibroMASH) for non-invasively identifying fibrotic MASH and exploring its predictive value for liver-related events (LREs). MethodsWe analyzed data from 3,004 individuals with biopsy-proven metabolic dysfunction-associated fatty liver disease (MAFLD) across 29 Chinese and nine international cohorts to validate the acMASH index and develop the acFibroMASH index. Additionally, we utilized the independent external data from a multi-national cohort of 9,034 patients with MAFLD to examine associations between the acFibroMASH index and the risk of LREs. ResultsIn the pooled global cohort, the acMASH index identified MASH with an AUROC of 0.802 (95%CI 0.786-0.818). The acFibroMASH index (including the acMASH index plus liver stiffness measurement) accurately identified fibrotic MASH with an AUROC of 0.808 in the derivation cohort and 0.800 in the validation cohort. Notably, the AUROC for the acFibroMASH index was 0.835 (95% CI 0.786-0.882), superior to that of the FAST score at 0.750 (95% CI 0.693-0.800, P<0.01) in predicting the 5-year risk of LREs. Patients with acFibroMASH >0.39 had a higher risk of LREs than those with acFibroMASH <0.15 (adjusted-hazard ratio: 11.23 95%CI 3.98-31.66). ConclusionsThis multi-ethnic study validates the acMASH index as a reliable, non-invasive test for identifying MASH. The newly proposed acFibroMASH index is a reliable test for identifying fibrotic MASH and predicting the risk of LREs.

A New Strain of Saccharomyces cerevisiae in Diets of Lactating Holstein Cows Improved Feed Efficiency and Lactation Performance

Abstract This study compared the effects of feeding a new strain of Saccharomyces cerevisiae HSA2020 with a commercial strain on in vitro rumen fermentation and production performance of dairy cows. Permeate was used as a substrate for the laboratory production of the new strain of S. cerevisiae after the hydrolysis by β-galactosidase (5000 µ/mL at 37°C). Two experiments were conducted: in Experiment 1, the effects of three levels (1, 2 and 3 g/kg dry matter) of S. cerevisiae on in vitro ruminal fermentation kinetics were evaluated. In Experiment 2, for 60 days, sixty multiparous Holstein cows (639±24.8 kg BW, 3±1 parity, 7±1 days in milk, with a previous milk production of 23±2.0 kg/d) during the previous lactation, were randomly assigned to 3 treatments in a completely randomized design. Cows were fed without any additives (control treatment) or supplemented with 2 g/kg feed daily of laboratory produced (PY) or commercial (CY) S. cerevisiae. In Experiment 1, inclusion of PY and CY increased (P&lt;0.05) gas production, propionate, and nutrient disappearance, while decreased (P&lt;0.05) methane production and protozoal count. Moreover, in Experiment 2, PY followed by CY increased (P&lt;0.01) nutrient digestibility, and serum concentrations of total protein, albumin, and glucose (P&lt;0.05). Higher daily milk yield, and milk energy output were observed with PY and CY without affecting concentrations of milk components or milk fatty acid profile. Compared to control, increased feed efficiency was observed with PY and CY. Compared to PY, CY increased serum concentrations of urea-N and decreased triglycerides, while PY decreased serum aspartate transaminase and increased concentration of conjugated linoleic acids in milk. In early lactating cow diets, both strains of S. cerevisiae improved production performance at 2 g/kg, and minimal differences between strains were found.

Protective effect of Zhizi Huangqi Shanzha formula on aflatoxin poisoning in mice and its effect on intestinal flora.

To evaluate the protective effect of Zhizi Huangqi Shanzha formula (, ZHSF) on aflatoxin-induced liver injury. The protective effect of ZHSF on the aflatoxin-induced liver injury was evaluated by histological observation, blood cell analysis, evaluation of liver function and immunity, and gut microbiota analysis. ZHSF can significantly up-regulate the percentage of lymphocytes and eosinophils in the blood of Aflatoxin B1-intoxicated mice, down-regulate the levels of serum aspartate aminotransferase, alanine aminotransferase, and malondialdehyde, and recover the liver tissue structure. Aflatoxin poisoning induces a variation of the intestinal flora of mice, and ZHSF may recover the variation of intestinal flora induced by Aflatoxin B1. Cluster analysis showed that the intestinal flora of mice in the intervention group was more similar to that of the control group. Correlation analysis showed that Lachnospiraceae, Desulfovibrio, and Lactobacillus may be the key flora for the pharmacological effects of ZHSF. ZHSF may protect against aflatoxin-induced liver damage, improve immunity, and inhibit oxidative stress by regulating the composition and relative abundance of intestinal flora, which makes it a promising liver-protective candidate drug.

Oxidative stress causes liver injury via the damage of redox system and the apoptosis induced by mitochondria of broiler

The aim of this study was conducted to explore the effects of oxidative stress on the redox system, mitochondrial function, and apoptosis in liver of broilers. 144 one-day-old male Ross-308 broilers from the same batch had been prepared in advance and were divided into 3 treatments: normal control group (without intraperitoneal injection), normal saline group (intraperitoneal injection of normal saline), and hydrogen peroxide (H2O2) group (intraperitoneal injection of H2O2) with 6 replicates of 8 chickens each. The experimental period was 42 days. The injection volumes were 1.0 mL/kg of Ross-308 broiler body weight. On the 42nd day of the experimental period, two Ross-308 broilers were randomly selected from each cage, a total of 36 broilers were stunned by electric shock and slaughtered to collect liver samples. The results showed that compared with the non-injection group and the injection of saline group, H2O2 exposure elevated the relative weight of liver and the activities of aspartate aminotransferase (AST) and alanine aminotransferase (ALT) in serum of Ross-308 broilers (p < 0.05). Meanwhile, compared with the non-injection group and the injection of saline group, the H2O2 exposure increased the levels of reactive oxygen species (ROS), MDA, lipid peroxide (LPO) and protein carbonyl, decreased the activities of total superoxide dismutase (T-SOD), catalase (CAT), total antioxidant capacity (T-AOC) and glutathione peroxidase (GSH-Px) (p < 0.05). Compared with the non-injection group and the injection of saline group, the H2O2 exposure caused microvesicular steatosis and mitochondrial vacuolisation in the liver tissues of broilers. Additionally, after H2O2 exposure, the levels of nuclear factor erythroid 2–related factor 2 (Nrf2) positive cells were reduced and the relative percentage of hepatocyte apoptosis were increased in the liver tissues of broilers (p < 0.05). The conclusion of this study is that the oxidative stress induced by intraperitoneal injection of H2O2 could induce excessive production of ROS in broiler liver, which damage the antioxidant status and mitochondrial function of liver cells, leading to cell apoptosis. HIGHLIGHTS Oxidative stress can cause severe damage to the liver of broilers. Oxidative stress can mainly damage liver antioxidant function Oxidative stress can induce cell apoptosis by damaging mitochondria in the liver of broilers

Modulation of liver metabolism and gut microbiota by Alhagi-honey alleviated heat stress-induced liver damage

Alhagi-honey (AH) is a well-established traditional ethnic medicine with advantageous effects against diarrhea and headaches. We aimed to explore the preventive effect of AH on liver damage induced by heat stress (HS) and its underlying mechanism. HS models were established by thermostat, and mice were treated at 39 ℃ for 10 h, lasting for 7 days. Hematoxylin–eosin (H&E) staining and Periodic Acid-Schiff (PAS) staining were used for histological observation, and transmission electron microscopy (TEM) was used for ultrastructure examination of hepatocytes. Gut microbiota (GM) composition and liver metabolites were respectively analyzed by 16S rRNA sequencing and non-targeted metabolome sequencing. AH pretreatment alleviated liver damage caused by heat stress in mice. The main manifestation was that AH alleviated serum aspartate transferase (AST) and aspartate transaminase (ALT). It was found that AH improved symptoms of hepatocyte damage. In addition, the relative abundance of f_Rikenellaceae, g_Incertae_Sedis and s_Staphylococcus_Orisratti, g_Lachnoclostridium, g_GCA-900066575, and s_Alistipes_inops were modified by AH and these bacterial genera showed association with 6 metabolites (2- (3,4-dihydroxyphenyl) acetamide, 3-hydroxy-3-methylpentanedioic acid, PC (17:0/17:1), Y-L-Glutamy-L-glutamic acid, L-Isoleucine, 5-Methyluridine, 8,8-dimethyl-2-phenyl-4H,8H-pyrano [2, 3-h] chromen-4-one). The Pearson analysis also showed a strong correlation between these microbes and 2 risk indicators (AST and ALT) of liver damage. AH alleviated HS-induced liver damage by regulating liver metabolism and maintaining normal GM. It demonstrated that AH held potential as a prophylactic drug for the prevention of HS-induced liver damage.

Effects of fermented oyster extract supplementation on free fatty acid and liver enzymes in older women with obesity

[Purpose] This study aimed to investigate the effects of a 12-week intake of fermented oyster extract on free fatty acids and liver enzymes in older women with obesity and to provide basic data for improving liver function in older individuals with obesity.[Methods] A randomized, double-blind, placebo-controlled clinical trial aimed to confirm the effects of fermented oyster extract intake on free fatty acid (FFA) levels and liver function in older women with obesity. The study included 40 older women with obesity with a body mass index ≥ 25 kg/m2. Participants were divided into a fermented oyster intake group (n = 20) and control group (n = 20). Serum FFA, aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP), and gamma-glutamyl transferase (GGT) levels were measured at weeks 0 and 12.[Results] Our results showed an interaction effect between the two groups in terms of serum FFA levels (&lt;i&gt;p&lt;/i&gt;&lt;0.05), with a post-intervention decrease in the FSO group (&lt;i&gt;p&lt;/i&gt;&lt;0.05). AST, ALT, and GGT levels also showed an interaction effect between the two groups (&lt;i&gt;p&lt;/i&gt;&lt;0.05), with a significant postintervention decrease in the FSO group (&lt;i&gt;p&lt;/i&gt;&lt;0.05).[Conclusion] The intake of fermented oyster extract significantly reduced FFA, ALT, AST, and GGT levels. These results suggested that the consumption of fermented oyster extract may improve liver function. However, the findings of this study were limited to elderly women with obesity, and the relatively short intake period and small sample size may limit the generalization of the results