Chronic hepatitis D (CHD) causes severe chronic hepatitis. Knowledge is limited about factors correlating with ALT in treatment-naïve patients with CHD. This study analysed the pattern and determinants of ALT elevation in a large cohort of patients with CHD, including young adults, compared to propensity score-matched (PSM) patients with chronic hepatitis B (CHB). We identified 2382 treatment-naïve HBsAg+ adults with CHD (HDV RNA positive) and 1553 with CHB attending a liver center in Mongolia during 2015-2023. The correlation between ALT levels, virological, biochemical, and fibrosis parameters was assessed using Spearman coefficient (rho). Logistic regression analysis was used to identify determinants of elevated ALT in 1371 PSM pairs with CHD and CHB matched on age, sex, metabolic factors, and date of initial test. In CHD, 78.5% of patients had ALT elevation, with the highest prevalence in the 18-20 years group (n = 219, 84.5%). This age group displayed 8.2-adjusted odds ratio (aOR) for elevated ALT, 2.7-aOR for elevated GGT, and 4.5-aOR of cirrhosis than matched CHB group (all p < 0.05). In CHD, ALT correlated weakly with HDV RNA (rho = 0.23) and liver stiffness (rho = 0.37), moderately with GGT (rho = 0.48), while showed no correlation with HBV DNA or HBsAg. Independent factors for elevated ALT were age < 30 years, elevated GGT and HDV RNA levels. In this large cohort of Asian patients, an earlier and more severe inflammatory process could be demonstrated in CHD compared to CHB regardless of liver cirrhosis. Longitudinal studies are warranted to risk-stratify and prioritise patients for therapies.

Background: Chronic kidney disease (CKD) is a progressive disorder defined by a persistent reduction in glomerular filtration rate below 60 mL/min/1.73 m² for at least three months. Oxidative stress(OS) play key roles in CKD progression and may be aggravated by repeated hemodialysis sessions. Sulfiredoxin-1 (Srx-1) is a recently identified antioxidant protein involved in reversing oxidative damage and regulating redox signaling; however, its clinical relevance in CKD remains unclear. Methods: A total of 140 participants were enrolled, including 100 CKD patients on hemodialysis and 40 healthy controls. Serum levels of Srx-1, kidney injury molecule-1 (KIM-1), and interleukin-18 (IL-18) were measured using enzyme-linked immunosorbent assay. Alanine aminotransferase (ALT), aspartate aminotransferase (AST), and alkaline phosphatase (ALP) were determined using standard BIOLABO (France) biochemical kits. Results: Compared with healthy controls, CKD patients showed significantly elevated levels of Srx-1, IL-18, KIM-1, and ALP, along with significantly reduced ALT and AST levels. ALT levels increased significantly after hemodialysis compared with pre-dialysis values. Patients receiving twelve dialysis sessions per month exhibited higher Srx-1, IL-18, and KIM-1 levels than those undergoing eight sessions monthly, while ALP levels were lower. No significant differences were observed regarding age, disease duration, or underlying causes between the groups. Conclusion: The findings demonstrate a close relationship between OS inflammation, and dialysis frequency in CKD. Elevated Srx-1 levels with increased dialysis frequency may represent a compensatory antioxidant response to cumulative OS. Nevertheless, Srx-1 may not be a reliable standalone biomarker, emphasizing the need for further large-scale studies to clarify its clinical significance.

Deficiency in beclin1 alleviates doxorubicin-induced liver injury through inhibiting ferroptosis and autophagy.

Could taurine supplementation improve graft functions after liver transplantation? A randomized clinical trial among liver transplant recipients.

Oligosaccharides ameliorate insulin resistance and hepatic metabolism by promoting the leptin/POMC axis to accelerate short stature growth and development.

Efficacy of Jadwar (Delphinium denudatum Wall. ex Hook.f. & Thomson) in subclinical hypothyroid patients: A single-blind, randomized placebo controlled trial.

Solanum americanum, or American black nightshade, is a common weed in Pakistan with a rich history of medicinal applications. Traditionally, its leaves and fruits have been employed to treat various conditions, including skin problems, inflammation, and menstrual irregularities. The plant's therapeutic potential is attributed to its diverse phytochemical composition, encompassing alkaloids, glycosides, and flavonoids. Its traditional use highlights the reliance on folk knowledge for treating liver disease. This study aimed to investigate the pharmacognostic features and evaluate the hepatoprotective activity of the crude fruit extract of S. americanum against ethanol-induced liver toxicity in rats. An aqueous ethanolic extract of S. americanum fruit was administered to rats with ethanol-induced liver toxicity. Silymarin was used as a reference drug for comparison. Hepatoprotective activity was assessed through biochemical analysis of aspartate transaminase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP), total bilirubin, and total protein levels. Histopathological examination of liver tissues was also conducted. The ethanol-treated group exhibited intense hepatocellular injuries and necrosis in liver tissues. Treatment with the aqueous ethanolic extract of S. americanum and silymarin resulted in near-normal lobular architecture, with only slight centrilobular degeneration of hepatocytes and minimal necrotic changes. The S. americanum extract demonstrated hepatoprotective activity, as evidenced by the partial normalization of liver biomarkers. However, its effect was less pronounced than that of silymarin. The aqueous ethanolic fruit extract of S. americanum possesses hepatoprotective properties against ethanol-induced liver toxicity in rats. S. americanum mitigates ethanol-induced liver toxicity in rats, partially normalizing liver biomarkers, likely through its antioxidant and nutritional properties, supporting its traditional use in liver disease management.

Dual actions of apelin-13 in TNBS-induced colitis: Colonic protection via the gut-liver axis but intrinsic hepatotoxic potential following systemic administration.

Sector-specific ambient air pollution and biomarkers of liver injury. Findings of a cross-sectional population-based survey.

Risk-associated and clinically informative biomarkers for cardiovascular risk stratification in metabolic dysfunction-Associated steatotic liver disease.

High temperature is a known abiotic stressor in broiler chickens, causing oxidative damage and altering gene expression. The present study was conducted to study the role of in ovo feeding of taurine against heat-induced damage in the broiler chickens. It was hypothesized that pre-hatch supplementation with taurine induces epigenetic changes such as DNA methylation and demethylation, which could help develop resistance to heat stress (HS) at later stages of life. For this, at 17.5 days of incubation, 360 fertile eggs from 37-week-old Arbor Acre breeder hens were divided into four groups: injected with distilled water (0TAU) × 2, and others injected with taurine at 1 %, 3 %, or 5 % concentrations (1TAU, 3TAU, 5TAU). For the in ovo feeding, a 23-gauge needle was used to deposit 0.6mL of solution into the amniotic sac. During rearing days 29 to 34, broiler chickens were exposed to a cyclic heat stress (HS, 31 ± 1 °C, 8 hours) or kept at a thermoneutral temperature (TN) zone (21 ± 1 °C). Hence, the treatment groups were: (i) 0TAU-TN, (ii) 0TAU-HS, (iii) 1TAU-HS, (iv) 3TAU-HS, and (v) 5TAU-HS. While the organ indices, average daily feed intake (ADFI) and feed conversion ratio (FCR) did not differ significantly, in ovo taurine linearly increased average daily gain (ADG) during the heat stress (HS) period (p = 0.032). The 2,2-diphenyl-1-picrylhydrazyl radical scavenging activity% (DPPH-RSA%) in plasma showed a linear increase (p = 0.001) with taurine doses. Among the studied plasma metabolites, only alanine transaminase (ALT) was significantly affected, being lower in 1TAU-HS and 3TAU-HS compared to 5TAU-HS (p = 0.022). Individual gene expressions showed no significant variation across treatments. However, a planned contrast revealed upregulation of DNA methylation genes in the 5TAU-HS group compared to the 0TAU-TN group (p = 0.030). Strong positive correlations were observed among DNA methylation, demethylation, and NADPH oxidase (NOX) -related genes, suggesting coordinated regulation. Negative correlations between MDA and antioxidant enzymes indicated oxidative stress-related damage under HS. Hence, taurine linearly improved ADG under HS. While it did not significantly influence individual gene expression, 5TAU upregulated the overall DNA-methylation-related genes, suggesting a possible long-term adaptive response under HS.

Mechanistic exploration of methylglyoxal-induced hepatotoxicity involving oxidative stress, apoptosis, and gluconeogenic modulation.

Gallic acid attenuates LPS-induced hepatic injury via SIRT-1-dependent immunomodulation and anti-apoptotic mechanisms in rats.

This study evaluated the effects of treated walnut green husk (WGH) on growth performance, cecal microflora, jejunal morphology, nutrient digestibility, blood biochemistry, and meat quality in broiler chickens. A total of 180 day-old Ross 308 broilers were assigned to three dietary treatments for a 42-day trial, with six replicates (10 birds per cage). The dietary treatments consisted of a basal diet (control), the basal diet supplemented with 2.1 g/kg fermented WGH (FWGH), and the basal diet containing 2.0 g/kg WGH plus 0.1 g/kg multi-enzyme (EWGH). Both FWGH and EWGH improved broiler growth performance during the grower, finisher, and overall periods, as indicated by enhanced feed conversion ratio and European production efficiency index, with FWGH producing marginally greater improvements. Both treatments reduced cecal total aerobic bacteria, while FWGH additionally increased Lactobacillus spp. and decreased Clostridium perfringens. Jejunal villus height increased in both WGH-treated groups, whereas villus surface area improved in FWGH group. Both FWGH- and EWGH-supplemented diets increased ileal digestibility of dry matter, while FWGH also improved organic matter digestibility. Both FWGH and EWGH had a modulatory effect on blood parameters by increasing lymphocyte (L) percentage and decreasing WBC count, percentage of heterophil (H), H:L ratio, total cholesterol, low-density lipoprotein (LDL), and alkaline phosphatase (ALP) levels. In addition, FWGH increased high-density lipoprotein (HDL) level and reduced alanine transaminase (ALT) activity. Both FWGH and EWGH improved meat quality by reducing breast muscle press loss and malondialdehyde content in thigh muscle, while EWGH further decreased malondialdehyde and increased pH in breast muscle, and enhanced water-holding capacity and pH in thigh muscle compared with the control. Overall, the dietary inclusion of treated-WGH improved growth performance, intestinal health, nutrient digestibility, blood lipid profile, and meat quality in broiler chickens, with FWGH showing slightly superior effects.

Enhancement in the nutritional profile and hepatoprotective activity of pine pollen via Aspergillus niger fermentation.

Cholestatic liver diseases (CLDs) are characterized by impaired bile acid (BA) homeostasis, chronic inflammation, and progressive fibrosis, for which effective pharmacological options remain limited. Ursodeoxycholic acid (UDCA) offers modest benefits and obeticholic acid (OCA) is constrained by tolerability issues, underscoring the need for novel therapeutics. This study evaluated the hepatoprotective effects and underlying mechanisms of Bruceine D (BD), a natural quassinoid compound, in murine models of cholestasis. Two complementary models were employed: Multidrug resistance protein 2 knockout (Mdr2-/-) mice and α-naphthylisothiocyanate (ANIT)-induced cholestasis. Serum biochemistry, histopathology, bile acid profiling, and ultrastructural analyses were performed to assess hepatocellular injury and fibrosis. Mechanistic studies included gene and protein expression analyses, functional FXR luciferase reporter assays with pharmacological antagonism, and in vitro hepatocyte assays to interrogate BA metabolism, inflammatory responses, and FXR-dependent signaling. BD significantly reduced alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), and total bilirubin (TBIL) in both models, whereas direct bilirubin (DBIL) remained unaffected. Histological analyses demonstrated marked attenuation of hepatocellular injury, bile duct proliferation, fibrosis, and macrophage infiltration. Notably, BD selectively suppressed classical BA synthesis enzymes (CYP7A1, CYP8B1, CYP27A1), while sparing CYP7B1 and major BA transporters. Quantitative BA profiling revealed a shift from hydrophobic, hepatotoxic species (CDCA, DCA, CA) toward hydrophilic and conjugated bile acids (TUDCA, TDCA, β-TMCA), accompanied by restoration of canalicular ultrastructure. BD attenuated inflammatory cytokines and chemokines and reduced fibrogenic responses. Mechanistically, BD functionally restored FXR signaling and reactivated the FXR-SHP-FGF15/19 feedback axis suppressed under cholestatic conditions. Short-term toxicological evaluation revealed no significant adverse effects in major organs. BD ameliorates cholestatic liver injury by selectively inhibiting classical BA synthesis, quantitatively remodeling the BA pool toward a less hepatotoxic profile, and suppressing inflammation and fibrosis through functional restoration of FXR-dependent feedback signaling. Its synthesis-centered mechanism and favorable short-term safety profile support BD as a promising therapeutic candidate for cholestatic liver diseases.

Mechanisms underlying differential utilization of carbohydrates from diverse structures and sources in Nile tilapia (Oreochromis niloticus): Insights from glycolipid metabolism, protein deposition and liver health.

Artocarpin alleviates fenofibrate-induced hepatic dysfunction via regulating NLRP3/caspase-1, oxidative stress and bile acids synthesis: A biochemical, histological, and computational investigation.

Integrative metabolomics and lipidomics reveal Jian-Pi-Yi-Shen formula improves adenine-induced CKD rats by regulating intrarenal glycolipid metabolism.

Children with autoimmune liver disease (AILD) face unique challenges that may impair their health-related quality of life (HRQoL). This multicenter, prospective, longitudinal study evaluated HRQoL over time and identified associated clinical factors. A total of 162 participants from five centers completed at least one HRQoL assessment. Medical and laboratory data were abstracted within 3 months of each assessment. Fatigue and pruritus were reported at one center. Generalised linear mixed-effects modelling was used to examine longitudinal associations between HRQoL and clinical variables. Participants reported the lowest HRQoL scores in school and emotional domains, while the physical and social domains were less affected. Compared to healthy children, participants with AILD reported lower overall HRQoL. Longitudinal analysis revealed that caregivers of participants with overlap syndrome reported higher emotional, social, psychosocial, and total scores. Across all AILD subtypes, children with AILD-complications reported higher school scores. Prednisone use was associated with improved emotional scores, while azathioprine use was associated with lower social scores. Elevated alanine aminotransferase levels were associated with lower HRQoL scores, particularly in caregiver reports. Disease duration and presence of inflammatory bowel disease were not associated with HRQoL. In a single center subset, fatigue and pruritus were associated with lower HRQoL, and fatigue correlated with elevated liver enzymes and reduced rates of biochemical remission. These findings highlight overall AILD-related patterns in HRQoL rather than disease-specific effects and underscore the multidimensional impact of AILD. Studies with disease-specific cohorts and validated symptom instruments are needed to clarify subtype-specific mechanisms, particularly those related to fatigue. NCT03178630, NCT05750498.