Lower Alanine Aminotransferase Research Articles

A nutritional intervention that promotes increased vegetable intake in Japanese with non-alcoholic fatty liver disease: a six-month trial.

The aim of this study was to investigate whether a nutritional intervention motivating increased vegetable consumption would be an effective treatment and diet therapy for patients with non-alcoholic fatty liver disease. We examined 15 patients with this disease (5 men and 10 women). During the 6-month intervention period, all participants received a small amount of vegetables twice a month as a nutritional education tool aimed at increasing vegetable consumption. They also received nutritional counseling and underwent ultrasound and blood biochemical examinations at baseline and 3 and 6 months after initiation of the intervention. Moreover, they were requested to submit dietary records for any 2 days. Green, white, and total vegetable intakes were significantly higher at 3 and 6 months than at baseline in 8 patients. These patients had significantly lower alanine amino­transferase and triglyceride concentrations than those whose vegetable intake did not increase. Additionally, green vegetable intake significantly negatively correlated with weight at 3 and 6 months (r = −0.617, p = 0.032 and r = −0.848, p = 0.008, respectively). These results suggest that our nutritional approach effectively increased vegetable consumption in at least some patients with non-alcoholic fatty liver disease, consequently improving their condition.

Study of the effect of laurel plant (Laurus Nobilis) on some biochemical markers in diabetic mellitus rats

The present study is aimed to introduce the effect of laurus nobilis extracts on blood glucose level, liver function, lipid profile, and body weight in diabetic rats. Three experiment was done for seventy- two albino male rats (150-200) grams were divided into twelve groups, in each study experiment rats were divided to four groups (6 rats for each) , first group treated with distilled water and served as control group, second group served as positive diabetic and treated with 100 mg/kg, BW single dose of alloxan. Third group treated with 250 mgkg of oil, flavonoids and tannins extracted from Laurus nobilis, while fourth group was served as diabetic and treated with 250 mgkg b. w of laurus nobilis extract, all groups were treated orally, the following results were evaluated, fasting blood glucose, triglyceride (TG), total cholesterol (TC), high density lipoprotein-cholesterol (HDL-c), low density lipoprotein-cholesterol (LDL-c), very low density lipoprotein-cholesterol (VLDL-c), alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP) and body weight .After 4 weeks of treating by250 mgkg BW bay leave extracts there was significant decrease in fasting blood glucose , TG, TC, LDL, VLDL, ALT, AST, ALP, and a significant increase in HDL and body weights.

Clinical Implications of HBV PreS/S Mutations and the Effects of PreS2 Deletion on Mitochondria, Liver Fibrosis, and Cancer Development.

PreS mutants of HBV have been reported to be associated with HCC. We conducted a longitudinal study of the role of HBV preS mutations in the development of HCC, particularly in patients with chronic hepatitis B (CHB) having low HBV DNA or alanine aminotransferase (ALT) levels, and investigated the effects of secretion-defective preS2 deletion mutant (preS2ΔMT) on hepatocyte damage in vitro and liver fibrosis in vivo. Association of preS mutations with HCC in 343 patients with CHB was evaluated by a retrospective case-control follow-up study. Effects of preS2ΔMT on HBsAg retention, endoplasmic reticulum (ER) stress, calcium accumulation, mitochondrial dysfunction, and liver fibrosis were examined. Multivariate analysis revealed a significant association of preS mutations with HCC (HR, 3.210; 95% CI, 1.072-9.613; P=0.037) including cases with low HBV DNA or ALT levels (HR, 2.790; 95% CI, 1.133-6.873; P=0.026). Antiviral therapy reduced HCC risk, including cases with preS mutations. PreS2ΔMT expression promoted HBsAg retention in the ER and unfolded protein response (UPR). Transmission electron microscopic examination, MitoTracker staining, real-time ATP assay, and calcium staining of preS2ΔMT-expressing cells revealed aberrant ER and mitochondrial ultrastructure, reduction of mitochondrial membrane potential and ATP production, and calcium overload. Serum HBV secretion levels were ~100-fold lower in preS2ΔMT-infected humanized Fah-/-/ Rag2-/-/Il2rg-/- triple knockout mice than in wild-type HBV-infected mice. PreS2ΔMT-infected mice displayed up-regulation of UPR and caspase-3 and enhanced liver fibrosis. PreS mutations were significantly associated with HCC development in patients with CHB, including those with low HBV DNA or ALT levels. Antiviral therapy reduced HCC occurrence in patients with CHB, including those with preS mutations. Intracellular accumulation of mutated HBsAg induced or promoted ER stress, calcium overload, mitochondrial dysfunction, impaired energy metabolism, liver fibrosis, and HCC.

Decreased Muscle-to-Fat Mass Ratio Is Associated with Low Muscular Fitness and High Alanine Aminotransferase in Children and Adolescent Boys in Organized Sports Clubs.

Decreased muscle-to-fat mass ratio (MFR) is associated with pediatric nonalcoholic fatty liver disease (NAFLD) and may reduce muscular fitness. Regular exercise in sports clubs has not led to reductions in obesity in children and adolescents; they may have decreased MFR. Decreased MFR could cause reduced muscular fitness, which may put them at risk for NAFLD development. We investigated whether MFR is related to muscular fitness and serum alanine aminotransferase (ALT), to determine whether MFR could be used to screen for NAFLD in children and adolescent boys belonging to sports clubs. Altogether, 113 participants (aged 7–17 years) who underwent body composition, laboratory, and muscular fitness measurements during a medical checkup were divided into tertiles according to their MFR. Lower extremity muscular fitness values were significantly decreased in the lowest MFR tertile (p < 0.001); conversely, serum ALT levels were significantly increased (p < 0.01). Decreased MFR significantly increased the risk of elevated ALT, which requires screening for NAFLD, after adjusting for age, obesity, muscular fitness parameters, and metabolic risk factors (odds ratio = 8.53, 95% confidence interval = 1.60–45.6, p = 0.012). Physical fitness and body composition assessments, focusing on MFR, can be useful in improving performance and screening for NAFLD in children and adolescents exercising in sports clubs.

Porous SiO2 -coated ultrasmall selenium particles nanospheres attenuate cerulein-induce acute pancreatitis in mice by downregulating oxidative stress.

To investigate the potential therapeutic role of porous SiO2 -coated ultrasmall selenium particles nanospheres (Se@SiO2 nanospheres) pretreatment in acute pancreatitis (AP) and to investigate the related mechanism. C57BL/6 mice were randomized to the normal control (CON) group, the AP (induced by cerulein injection) (CAE) group, and AP pretreated with Se@SiO2 nanocomposites at 1 and 2mg/kg (CAE + 1 or 2 mg/kg Se@SiO2 ) groups, respectively. Serum levels of amylase and lipase, inflammatory cytokines (interleukin [IL]-6, IL-1β and tumor necrosis factor [TNF]-α), alanine aminotransferase (ALT), aspartate aminotransferase (AST), blood urea nitrogen (BUN), and creatinine (Cr) were measured, and histopathology was performed to examine the tissue samples of the pancreas, lungs, kidneys and liver. Immunofluorescence assay of reactive oxygen species (ROS), myeloperoxidase (MPO) and terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling were conducted, and levels of MPO, malondialdehyde, superoxide dismutase and glutathione were evaluated. Finally, Western blot analysis was used to evaluate protein expressions of Nrf2, HO-1, NQO1, TLR4, MyD88 and p-p65 in pancreatic tissue. Se@SiO2 nanospheres alleviated pathological damage to the pancreas, and reduced pancreatic enzymes and inflammatory cytokines. Injury to other organs such as the liver, lungs and kidneys was also alleviated, as indicated by decreased ALT, AST, BUN, and Cr levels as well as improved histopathology. Moreover, Se@SiO2 nanospheres reduced oxidative stress, and ultimately inhibited TLR4/ MyD88/p-p65 pathway and increased the protein expressions of NQO1, Nrf2, and HO-1. Se@SiO2 nanospheres may alleviate AP by relieving oxidative stress and targeting the TLR4/Myd88/p-p65 and NQO1/Nrf2/HO-1 pathways.

Assessment of Some Biochemical Parameters in Vitreous Humor of Rabbits Exposed to Sodium Cyanide

Aim: The aim of this study was to assess some biochemical parameters in the vitreous humor of Rabbits exposed to sodium cyanide.&#x0D; Study Design: This study is an interventional study.&#x0D; Place and Duration of Study: This study was carried out at Animal House, Applied and Environmental Biology Department, Rivers State University, Port Harcourt, Rivers State, Nigeria, between April 2020 and November 2020.&#x0D; Methodology: A total of twelve (12) rabbits as indicated by Mead’s formula constituted the sample size. The study was divided into three groups including the control. 1 mg/kg sodium cyanide was administered to the rabbits orally in group one and vitreous humor was collected using standard procedure after thirty minutes. In group two the rabbits were put to death mechanically and 1 mg/kg sodium cyanide was administered to the rabbits after thirty minutes, vitreous humor was collected after thirty minutes using standard procedure. The rabbits in group three, control group, were put to death mechanically and nothing was given to the rabbits, then after thirty minutes vitreous humor was collected using standard procedure. Biochemical parameters investigated included vitreous glucose, total cholesterol, triglycerides, high density lipoprotein cholesterol, low density lipoprotein cholesterol, very low density lipoprotein cholesterol, total proteins (TP), albumin (ALB), total bilirubin, conjugated bilirubin, aspartate aminotransferase (AST) and alanine aminotransferase (ALT) activities. Data were expressed as mean ± SD. Statistical differences between groups were computed using Graph pad prism 7.0 version developed by Graph pad software, San Siago, Califonia, USA. Results were analyzed using analysis of variance (ANOVA) and significance between groups was taken at p&lt;.05.&#x0D; Results: Vitreous biochemical results showed significant (p&lt;.05) increase in levels of TC, LDL-C, AST, ALT, TB and CB in rabbits given 1 mg/kg sodium cyanide compared to control. Significant (p&lt;.05) decrease in levels of glucose, TP and ALB were also observed. This study also revealed that there was no significant (p&lt;.05) difference in biochemical results of rabbits given 1 mg/kg sodium cyanide thirty minutes after they were put to death mechanically compared to the control. It can be concluded that a lethal dose of sodium cyanide (1 mg/kg) may lead to alterations in vitreous biochemical parameters and this may enhance death differentiation due to sodium cyanide poisoning and other causes of death for example mechanical death. &#x0D; Conclusion: The findings of this study support a central role for vitreous humor biochemistry in many postmortem forensic and pathological evaluations and it could also be used for death differentiation in sodium cyanide poisoning.

Study on anti-hyperlipidemia effect of Linderae Radix via regulating reverse cholesterol transport

This article aims to investigate the ameliorative effect of Linderae Radix ethanol extract on hyperlipidemia rats induced by high-fat diet and to explore its possible mechanism from the perspective of reverse cholesterol transport(RCT). SD rats were divided into normal group, model group, atorvastatin group, Linderae Radix ethanol extract(LREE) of high, medium, low dose groups. Except for the normal group, the other groups were fed with a high-fat diet to establish hyperlipidemia rat models; the normal group and the model group were given pure water, while each administration group was given corresponding drugs by gavage once a day for five weeks. Serum total cholesterol(TC), triglyceride(TG), high density lipoprotein-cholesterol(HDL-c), low density lipoprotein-cholesterol(LDL-c), alanine aminotransferase(ALT), and aspartate aminotransferase(AST) levels were measured by automatic blood biochemistry analyzer; the contents of TC, TG, total bile acid(TBA) in liver and TC and TBA in feces of rats were detected by enzyme colorimetry. HE staining was used to observe the liver tissue lesions; immunohistochemistry was used to detect the expression of ATP-binding cassette G8(ABCG8) in small intestine; Western blot and immunohistochemistry were used to detect the expression of peroxisome proliferator-activated receptor gamma/aerfa(PPARγ/α), liver X receptor-α(LXRα), ATP-binding cassette A1(ABCA1) pathway protein and scavenger receptor class B type Ⅰ(SR-BⅠ) in liver. The results showed that LREE could effectively reduce serum and liver TC, TG levels, serum LDL-c levels and AST activity, and increase HDL-c levels, but did not significant improve ALT activity and liver index; HE staining results showed that LREE could reduce liver lipid deposition and inflammatory cell infiltration. In addition, LREE also increased the contents of fecal TC and TBA, and up-regulated the protein expressions of ABCG8 in small intestine and PPARγ/α, SR-BⅠ, LXRα, and ABCA1 in liver. LREE served as a positive role on hyperlipidemia model rats induced by high-fat diet, which might be related to the regulation of RCT, the promotion of the conversion of cholesterol to the liver and bile acids, and the intestinal excretion of cholesterol and bile acids. RCT regulation might be a potential mechanism of LREE against hyperlipidemia.

Bone Marrow Fat Measured by a Chemical Shift-Encoded Sequence (IDEAL-IQ) in Patients With and Without Metabolic Syndrome.

Metabolic syndrome increases the risk of chronic diseases such as cardiovascular disease and diabetes. Metabolic syndrome also has an impact on bone mineral density. However, the relationship between metabolic syndrome and bone marrow fat is unclear. To determine factors associated with bone marrow fat concentration in subjects with and without metabolic syndrome. Retrospective. One hundred and one women with metabolic syndrome (31.0 years ±5.1) and 96 female living liver transplant donors (32.0 years ±3.7). Our institutional review board approved the study. Each subject signed written informed consent. 3.0 T MRI system and a commercially available chemical shift-encoded 3D sequence (Iterative Decomposition of water and fat with Echo asymmetry and Least Square Estimation). Proton density fat fraction (PDFF) in liver, vertebral body, and paraspinal muscle (erector spinae) were measured from a single acquisition by a 15-year-experience orthopedic radiologist. The factors associated with PDFF were acquired. The analysis of covariance test, after adjustment for body mass index and age, was used to analyze the differences between metabolic syndrome and non-metabolic syndrome groups. A stepwise multiple regression analysis was used to determine which variables were independently associated with PDFF. Mean vertebral PDFF and alanine aminotransferase (ALT) were significantly lower in donors than subjects with metabolic syndrome (both P < 0.05). Serum vitamin D concentration, ferritin, and high-density lipoprotein (HDL) cholesterol were significantly higher in donors than subjects with metabolic syndrome (all P < 0.05). Multiple regression analysis revealed antidiabetic medicine, higher serum vitamin D concentration, lower waist circumference, lower ferritin, lower HDL, absence of metabolic syndrome, and lower ALT were significantly associated with lower vertebral PDFF (all P < 0.05). Multiple factors affect bone marrow fat concentration in subjects with metabolic syndrome. Serum vitamin D concentration and antidiabetic medicine are associated with low bone marrow fat, whereas waist circumference, serum ferritin, metabolic syndrome, imbalanced lipid metabolism, and abnormal liver function are associated with high bone marrow fat. 3 TECHNICAL EFFICACY STAGE: 1.

Extremely Low Serum Alanine Transaminase Level Is Associated with All-Cause Mortality in the Elderly after Intracranial Hemorrhage.

ObjectiveExtremely low alanine transaminase (ALT) levels are associated with all-cause mortality in frail elderly individuals; the clinical significance of ALT as a reliable biomarker is now being considered. Predicting mortality with routine tests at the time of diagnosis is important for managing patients after intracranial hemorrhage. We aimed to investigate whether an extremely low ALT level is associated with mortality in the elderly after intracranial hemorrhage. MethodsA retrospective review was performed on 455 patients with intracranial hemorrhage admitted to a university-affiliated tertiary care hospital from February 2014 to May 2019. Multivariate Cox regression analysis was performed for all ages and for each age group to determine whether an extremely low ALT level is an independent predictor of mortality only in the elderly. ResultsOverall, 294 patients were enrolled, and the mean age of the subjects was 59.1 years, with 99 (33.8%) aged ≥65 years. The variables associated with all-cause mortality in all subjects were age, C-reactive protein (CRP) levels, hemoglobin (Hb) levels (<11 g/dL), and initial Glasgow coma scale (GCS) scores. In young patients, CRP, low Hb levels, and initial GCS scores were significantly associated with all-cause mortality. However, in the elderly (≥65 years), the variables significantly associated with allcause mortality were extremely low levels of ALT (<10 U/L) (adjusted hazard ratio, 3.313; 95% confidence interval, 1.232–8.909; p=0.018) and initial GCS scores. ConclusionExtremely low ALT level (<10 U/L) at the time of diagnosis is a significant risk factor for all-cause mortality in the elderly after intracranial hemorrhage.

Impact of Dietary Supplementation with Moringa oleifera Leaves on Performance, Meat Characteristics, Oxidative Stability, and Fatty Acid Profile in Growing Rabbits.

Simple SummaryRabbit meat is mostly preferred by consumers owing to its high nutritive value and potential health benefits. However, rabbit meat is commonly more prone to lipid peroxidation during storage, with negative effects on quality traits of meat, due to its elevated level of unsaturation of fatty acids. Moringa oleifera leaves have gained great interest owing to their high nutritional value and low anti-nutritional factors. Moringa oleifera leaves could possibly avoid oxidation damage and exhibit antioxidant activities that can conquer free radicals and reactive oxygen species synthesis. Therefore, the objective of the current study was to evaluate the effects of feeding Moringa oleifera leaves on performance, carcass characteristics, antioxidant capacity, blood biochemical constituents, meat quality, and fatty acids profile of growing rabbits. Moringa oleifera leaves supplementation improved weight gain, feed conversion ratio, antioxidant status, and meat quality characteristics. Dietary Moringa oleifera leaves supplementation enhanced PUFA contents, n-3 fatty acid, crude protein, and color of meat, but lowered the relative content of ether extract of the meat. Our findings suggested that Moringa oleifera could be used at a level of 1.5 g/kg of the growing rabbits’ diets with beneficial impacts on performance and the nutritional value of the meat. Moringa oleifera leaves (MOL) have gained great interest as a non-traditional feed ingredient due to their unique nutritional value. Therefore, the objective of the current study was to evaluate the effects of graded dietary supplementation levels with MOL on performance, carcass characteristics, antioxidant capacity, blood biochemical constituents, meat quality, and fatty acids profile of growing rabbits. A total of 120 weaned New Zealand white rabbits (6 weeks old) were randomly allotted into 4 dietary groups with 5 replicates each (n = 6), which were fed for 42 days with a basal diet as control or 3 experimental diets supplemented with 5, 10, or 15 g/kg MOL. The results showed that, compared to the control group, the dietary inclusion of MOL at a level of 10 and 15 g/kg DM linearly increased (p < 0.01) final live weight (2403.3 and 2498.2 vs. 2166.6) and average daily weight gain (36.5 and 35.51 g/d vs. 28.72 g/d), and enhanced feed conversion ratio (2.49 and 2.50 vs. 3.14). The dietary supplementation with MOL linearly increased dressing out percentage, spleen index, intestinal length, and decreased abdominal fat index (p < 0.01). Greater serum levels of total protein and globulin, but lower alanine aminotransferase and aspartate aminotransferase were observed in the MOL-fed rabbits (p < 0.01). Serum levels of total triglycerides, cholesterol, and low-density lipoprotein (p < 0.05) were decreased linearly and quadratically in the MOL groups compared with the control. Glutathione peroxidase activity increased (p < 0.01), whereas malondialdehyde decreased (p < 0.01) linearly and quadratically in both serum and meat, in response to dietary MOL supplementation. Dietary MOL supplementation increased the meat crude protein content but lowered the relative content of ether extract in the meat (p < 0.05). The relative content of the meat n-3 PUFA was increased by about 33.71%, 29.46%, and 24.36% for the MOL0.5%, MOL1%, and MOL1.5% groups compared to control. In conclusion, MOL could be used at a level of 1.5g/kg of the growing rabbits’ diets with beneficial impacts on performance, antioxidant capacity, and the nutritional value of the meat.

Association between the severity of liver fibrosis and cardiovascular outcomes in patients with type 2 diabetes.

Cardiovascular disease (CVD) is the principal cause of death in patients with type 2 diabetes (T2D). In this study, we assessed whether liver fibrosis predicted the risk of CVD in patients with T2D. A total of 1481 patients who had commenced oral antidiabetic drugs to treat newly diagnosed T2D between 2006 and 2010 were recruited. The fibrosis-4 index (FIB-4), non-alcoholic fatty liver disease fibrosis score (NFS), and BARD score were used to assess fibrotic burden at the time of T2D diagnosis. During the follow-up period (median 88.1 [interquartile range 36.6-113.6] months), 242 (16.3%) patients developed CVD. CVD occurred frequently in older patients and was associated with hypertension; metabolic syndrome; obesity; smoking; administration of statin, which is an antihyperlipidemic drug; lower platelet counts; lower alanine aminotransferase, total cholesterol, and HbA1c levels; higher C-peptide and homeostatic model assessment of insulin resistance levels; and higher FIB-4, NFS, and BARD score (all P<0.05). FIB-4 (hazard ratio [HR]=1.163), NFS (HR=1.322), BARD score (HR=1.564), metabolic syndrome (HR=1.556), smoking (HR=2.829), and statin use (HR=0.603) independently predicted the risk of CVD (all P<0.05). The cumulative incidence of CVD was significantly different among groups stratified by liver fibrotic burden (all P<0.05, log-rank test). Competing risk analysis showed a significant association between the severity of liver fibrosis and CVD development (all P<0.001, Gray's test). The severity of liver fibrosis independently predicted CVD in patients with T2D. Thus, assessment of liver fibrosis might allow physicians to optimize the timing of appropriate cardiovascular interventions in such patients.

An early experience on the effect of solid organ transplant status on hospitalized COVID-19 patients.

We compared the outcome of COVID-19 in immunosuppressed solid organ transplant (SOT) patients to a transplant naïve population. In total, 10356 adult hospital admissions for COVID-19 from March 1, 2020 to April 27, 2020 were analyzed. Data were collected on demographics, baseline clinical conditions, medications, immunosuppression, and COVID-19 course. Primary outcome was combined death or mechanical ventilation. We assessed the association between primary outcome and prognostic variables using bivariate and multivariate regression models. We also compared the primary endpoint in SOT patients to an age, gender, and comorbidity-matched control group. Bivariate analysis found transplant status, age, gender, race/ethnicity, body mass index, diabetes, hypertension, cardiovascular disease, COPD, and GFR <60mL/min/1.73m2 to be significant predictors of combined death or mechanical ventilation. After multivariate logistic regression analysis, SOT status had a trend toward significance (odds ratio [OR] 1.29; 95% CI 0.99-1.69, p=.06). Compared to an age, gender, and comorbidity-matched control group, SOT patients had a higher combined risk of death or mechanical ventilation (OR 1.34; 95% CI 1.03-1.74, p=.027).

A Potential Role for SerpinA3N in Acetaminophen-Induced Hepatotoxicity

Acetaminophen (APAP) is a commonly used pain and fever reliever but is also the most frequent cause of drug-induced liver injury. The mechanism pertaining acetaminophen toxicity has been well documented, whereas mechanisms of hepatotoxicity are not well established. Serine (or cysteine) peptidase inhibitor, clade A, member 3N (SerpinA3N), a serine protease inhibitor, is synthesized in the liver but the role of SerpinA3N in relation to APAP-induced liver injury is not known. Wild-type and hepatocyte-specific SerpinA3N knockout (HKO) mice were injected intraperitoneally with a single dose of PBS or APAP (400 mg/kg) for 12 hours, and markers of liver injury, cell death, and inflammation were assessed. SerpinA3N expression was highly induced in mice with APAP overdose. SerpinA3N HKO mice had diminished liver injury and necrosis as shown by lower alanine aminotransferase and interleukin-6 levels, accompanied by suppressed inflammatory cytokines and reduced neutrophil infiltration. The reduced oxidative stress was associated with enhanced antioxidant enzyme capabilities. Taken together, hepatocyte SerpinA3N deficiency reduced APAP-induced liver injury by ameliorating inflammation and modulating the 5' AMP-activated protein kinase-unc-51-like autophagy activating kinase 1 signaling pathway. Our study provides novel insights into a potential role for SerpinA3N in APAP-induced liver injury. SIGNIFICANCE STATEMENT: Our studies indicate that serine (or cysteine) peptidase inhibitor, clade A, member 3N (SerpinA3N) may have a pathophysiological role in modulating acetaminophen (APAP)-induced liver injury. More specifically, mice with hepatic deletion of SerpinA3N suppressed inflammation and liver injury to reduce APAP-induced hepatotoxicity. Controlling the inflammatory response offers possible approaches for novel therapeutics; therefore, understanding the pathophysiological role of SerpinA3N in inducing liver injury may add to the development of more efficacious treatments.

Lactobacillus spp. reduces ethanol-induced liver oxidative stress and inflammation in a mouse model of alcoholic steatohepatitis.

Alcoholic steatohepatitis (ASH) is a complex multifactorial disease that can lead to liver fibrosis and cirrhosis if not treated promptly. Alcohol-induced oxidative stress and inflammation are the main factors that cause steatohepatitis and liver injury; however, probiotic bacteria in the gastrointestinal tract have been revealed to regulate immune responses and reduce oxidative stress, suggesting that functional probiotics could help to prevent ASH and liver injury. Despite numerous reports on the interactions between ASH and probiotics, the mechanisms underlying probiotic-mediated liver protection remain unknown. Therefore, the aim of the present study was to screen probiotics with high antioxidant capacity and investigate the ability of different probiotic combinations to reduce alcoholic liver disease (ALD) in a mouse model. It was identified that Lactobacillus plantarum (TSP05), Lactobacillus fermentum (TSF331) and Lactobacillus reuteri (TSR332) neutralized free radicals and displayed high antioxidant activity in vitro. In addition, these three functional probiotic strains protected mice from alcohol-induced liver injury in vivo. Mice treated with the probiotics demonstrated significantly lower alanine aminotransferase, aspartate aminotransferase and triglyceride levels, which were associated with the downregulation of the proinflammatory cytokines TNF-α and IL-6. Furthermore, probiotic treatment upregulated glutathione and glutathione peroxidase activity, which are bioindicators of oxidative stress in the liver. Collectively, the present results indicated that Lactobacillus strains TSP05, TSF331 and TSR332 reduced oxidative stress and inflammatory responses, thus preventing ASH development and liver injury.

Gallbladder condition in patients with rheumatic fever and acquired valve defects of rheumatic origin

Gallbladder (GB) and heart are linked by viscero-visceral reflexes, but little is known about the connections between GB and heart in patients with acute and chronic rheumatic heart disease.&#x0D; Purpose of the study. To assess the GB condition in patients with acute and chronic rheumatic disease and the difference in structural and functional sonographic parameters of heart in dependence of GB condition.&#x0D; Materials and methods. We examined 136 patients including 58 patients with active rheumatism (mean age 36,72 ± 3,00 years), 44 patients with chronic rheumatic heart disease (CRHD), who underwent surgical correction of the valvular defect (mean age 54,00 ± 3,69 years), and 34 patients with CHD, who were treated as inpatients withour surgery (mean age 61,48 ± 4,50 years).&#x0D; Results. Among 136 patients with acute and chronic forms of rheumatic heart disease, GB changes were significantly more common than intact GB (62,5 ± 4,1% vs. 37,5 ± 4,1%, p &lt; 0,05). The incidence of GB disorders was the highest in patients with CRHD, who underwent drug treatment (76,5 ± 7,3% vs. 58,7 ± 6,5% and 50,0 ± 7,5%, both p &lt; 0,05), which were characterized by older age. No significant differences in the incidence of various pathological conditions of GB were revealed between acute and chronic rheumatic heart disease groups. The most common pathological GB changes included signs of cholecystitis, biliary sludge and cholesterosis, cholelithiasis, the least common – GB removal due to cholelithiasis. Patients with biliary autonomic viscero-visceral cardioneuropathy differed from those with intact GB by the thickening of the interventricular septum and posterior wall of the left ventricle, which correlated with the increased duration of inpatient treatment, diastolic hypertension and lower alanine aminotransferase.&#x0D; Conclusions. In patients with acute and chronic forms of rheumatic heart disease, the GB condition is often changed. These changes affect heart condition, blood pressure and carbohydrate metabolism.

AP39 ameliorates high fat diet-induced liver injury in young rats via alleviation of oxidative stress and mitochondrial impairment

Non-alcoholic fatty liver disease (NAFLD) is a complication of childhood obesity and an oxidative stress-related multisystem disease. A mitochondria-targeting hydrogen sulfide (H2S) donor AP39 has antioxidant property, while the mechanism underlying the function of AP39 on pediatric NAFLD remains undefined. Here, 3-week-old SD rats were received a high-fat diet (HFD) feeding and injected with AP39 (0.05 or 0.1 mg/kg/day) via the tail vein for up to 7 weeks. AP39 reduced weight gain of HFD rats and improved HFD-caused liver injury, as evidenced by reduced liver index, improved liver pathological damage, decreased NAFLD activity score, as well as low alanine transaminase (ALT) and aspartate transaminase (AST) activities. AP39 also reduced serum total cholesterol (TC), triglyceride (TG), low-density lipoprotein-cholesterol (LDL-C) concentrations but increased high-density lipoprotein-cholesterol (HDL-C). Moreover, AP39 prevented reactive oxygen species (ROS) generation, reduced MDA content and increased glutathione (GSH) level and superoxide dismutase (SOD) activity. Furthermore, AP39 increased H2S level, protected mitochondrial DNA (mtDNA), reduced mitochondrial swelling, and restored mitochondrial membrane potential (MMP) alteration. Notably, AP39 diminished HIF-1α mRNA and protein level, possibly indicating the alleviation in mitochondrial damage. In short, AP39 protects against HFD-induced liver injury in young rats probably through attenuating lipid accumulation, oxidative stress and mitochondrial dysfunction.

Real-world Effectiveness and Safety of Direct-acting Antiviral Agents in Patients with Chronic Hepatitis C Genotype 2 Infection: Korean Multicenter Study.

BackgroundThe advancement of treatment with direct-acting antiviral (DAA) agents has improved the cure rate of hepatitis C virus (HCV) infection close to 100%. The aim of our study was to assess the real-world effectiveness and safety of DAA regimens for the treatment of patients with chronic HCV genotype 2.MethodsWe retrospectively analyzed the clinical data of patients treated with sofosbuvir plus ribavirin (SOF + RBV) or glecaprevir/pibrentasvir (G/P) for chronic HCV genotype 2 infection at seven university hospitals in the Korean southeast region.ResultsSOF + RBV therapy produced an 89% and 98.3% sustained virologic response 12 week (SVR12) after treatment completion in the full analysis set and per-protocol set, respectively, and the corresponding values for G/P therapy were 89.5% and 99.2%, respectively. The difference between the treatments was probably because 6.2% (59/953) of patients in the SOF + RBV group did not complete the treatment and 9.8% (14/143) in the G/P group did not test HCV RNA after treatment completion. Adverse events (A/Es) were reported in 59.7% (569/953) and 25.9% (37/143) of the SOF + RBV and G/P groups, respectively. In the SOF + RBV group, 12 (1.26%) patients discontinued treatment owing to A/Es, whereas no patients discontinued treatment because of A/Es in the G/P group.ConclusionIn both treatment groups, SVR was high when treatment was completed. However, there was a high dropout rate in the SOF + RBV group, and the dropout analysis showed that these were patients with liver cirrhosis (LC; 43/285, 15.1%), especially those with decompensated LC (12/32, 37.5%). Therefore, an early initiation of antiviral therapy is recommended for a successful outcome before liver function declines. Furthermore, patients with decompensated LC who are considered candidates for SOF + RBV treatment should be carefully monitored to ensure that their treatment is completed, especially those with low hemoglobin and high alanine transaminase.

Protective Effect of Yerba Mate on Rats Fed on High Cholesterol Diet- An Experimental Study

Introduction: Yerba mate tea, a concoction made from the leaf extracts of the tree Ilex paraguariensis, is a broadly consumed non alcoholic beverage in Latin America which is gaining rapid introduction into the world market. Aim: To explore the influence of Yerba Mate (Ilex paraguariensis) powder and beverage on induced hypercholesterolemic rats. Materials and Methods: The experiment was carried out for a duration of one year from February 2020 to January 2021 at University of Ha’il, Ha’il, Saudi Arabia, on 48 male Albino rats divided into six subgroups; Control (-) group: group fed a basal diet. Rats in the other five groups fed on basal diet containing 2% cholesterol+0.25% bile salts for two weeks to induce hypercholesterolemia. Then those rats were subdivided into: control(+)group:groupthatremainedhypercholesterolemic.Yerba Mate Powdered (YMP) 15% group: fed on hypercholesterolemic diet+YMP15%; YMP 10% Group: fed on hypercholesterolemic diet+YMP10%; Yerba Mate Beverage (YMB) 15% group: fed on a hypercholesterolemic diet+YMB 15%; and YMB 10% group: fed on a hypercholesterolemic diet+YMB 10%. Results: It was found that, with increasing the amount of Yerba Mate powder or beverage, the total cholesterol, triglycerides, Low Density Lipoprotein-Cholesterol (LDL-C), Aspartate Transaminase (ALT), Alanine Transaminase (ALT), urea nitrogen and glucose levels decreased significantly (p&lt;0.05) and the best result belonged to the group of rats that fed on Yerba Mate 15% powder. Conclusion: It can be concluded that, supplementation with high percentage of Yerba Mate powder (15%) exerts a positive impact on the lipid profile and other biochemical parameters in hypercholesterolemic rats.

Prevalence and risk factors for hepatitis c virus co-infection among human immunodeficiency virus-infected patients and effect of hepatitis c virus infection on acquired immunodeficiency syndrome cases at baseline.

Background:Hepatitis C virus (HCV) co-infection with human immunodeficiency virus (HIV) exists as both viruses have the common routes of transmission. HIV infection has adverse effect on the natural history of HCV infection; however, the effect of HCV infection on the natural history of HIV infection is unclear.Materials and Methods:This study was cross-sectional comprising of treatment-naïve adult HIV-infected patients attending clinics at Usmanu Danfodiyo University Teaching Hospital, Sokoto and Specialist Hospital Sokoto. The study participants were screened for HCV anti]body and assayed for transaminases and CD4+ T-lymphocytes count levels. The symptoms of acquired immunodeficiency syndrome (AIDS)-defining illnesses were asked among the study participants. The questionnaire was used for the collection of data, and SPSS software version 20 was used for the analysis of data. Student's t-tests, Pearson’s, Chi-square, and Fisher's exact tests were used for the statistical analysis, and P < 0.05 was considered statistically significant.Results:The prevalence of HIV/HCV co-infection was 20.6%. Self-intravenous drugs usage was not statistically significant (P = 0.210). HIV mono-infected patients had significantly lower alanine aminotransferase levels compared to HIV/HCV co-infected study participants (P = 0.048). AIDS status at the baseline was comparable between HIV mono-infected and HIV/HCV co-infected study participants. (P = 0.227; 0.200; 0.130).Conclusion:Moderately high prevalence of HIV/HCV co-infection was observed in the current study. HCV co-infection had no effect on AIDS status at baseline. There is a need for routine screening of HCV infection in HIV-infected individuals.

Recent updates on the management of autoimmune hepatitis.

Autoimmune hepatitis (AIH) is an immunoinflammatory chronic liver disease with dynamic and rather heterogeneous disease manifestations. A trend of increasing prevalence of AIH has been observed worldwide, along with a relative increase in the percentage of male patients. AIH is characterized and diagnosed based on serum biochemistry and liver histology: elevated aminotransferases and serum immunoglobulin G (IgG), the presence of serum anti-nuclear antibody or anti-smooth muscle antibody, and interface lympho-plasmacytic hepatitis. Clinical manifestations differ among disease subtypes with distinct time-frames, i.e., AIH with a chronic insidious onset, and acute-onset AIH (the diagnosis of which is often challenging due to the lack of typical serum findings). The absence of disease-specific biomarkers or histological findings may expand the disease phenotype into drug-induced AIH-like liver injury. Corticosteroids and azathioprine are recommended first-line treatments for AIH. The complete normalization of aminotransferases and serum IgG is an essential treatment response to ensure long-term overall survival. An incomplete response or intolerance to these drugs is considered an indication for second-line treatment, especially with mycophenolate mofetil. Life-long maintenance treatment is required for the majority of patients, but the few who achieve prolonged and stringent biochemical remission with lower alanine aminotransferase and IgG within the normal range may be able to discontinue the medications. In the future, the quality of life of AIH patients should be managed by personalized medicine, including the appropriate selection and dosing of first-line therapy and perhaps alternating with potential therapeutics, and the prediction of the success of treatment withdrawal.