Articles tagged with Steatohepatitis
This study investigates the role of YTHDF1 in nonalcoholic fatty liver disease (NAFLD) and its epitranscriptomic control of NUPR1. The researchers found that YTHDF1 promotes hepatic steatosis by enhancing NUPR1 mRNA stability, leading to elevated NUPR1 protein levels and exacerbating NAFLD progression.
A $10 million grant from the National Institute of Environmental Health Sciences will support research on PFAS health effects and translate discoveries into real-world solutions. The study aims to identify links between PFAS exposure and metabolic conditions, such as obesity and type 2 diabetes.
A cross-sectional study found intestinal Candida albicans abundance correlates with subclinical coronary atherosclerosis in metabolic dysfunction-associated steatotic liver disease. Cirrhosis patients showed higher Candida albicans levels and more severe atherosclerosis.
Metabolic dysfunction-associated steatotic liver disease (MASLD) affects approximately 32% of the US adult population. Obesity was identified as the strongest independent MRF among Asians, Whites, and Hispanics, particularly in individuals younger than 50 years, whereas hypertension was the strongest independent MRF in Blacks.
A Salk Institute study identifies Fibroblast Growth Factor 1 (FGF1) as the molecular signal that tells the liver when to release fat into the bloodstream, following a precise rhythm timed to the body's internal clock.
A study identified exosomal microRNA-122-3p as a key driver of MASLD pathogenesis. Elevated miR-122-3p levels induced triglyceride accumulation and reactive oxygen species production in liver cells.
Researchers have found that semaglutide, an active ingredient in popular weight loss drugs, acts directly on a subset of liver cells to improve organ function and reduce inflammation, scarring, and enzyme levels. This finding challenges traditional assumptions about how GLP-1 medicines work in the liver.
Researchers compare viral and MASLD cirrhosis pathogenic mechanisms, identifying shared pathways and diagnostic differences. The study aims to establish a framework for prevention, diagnosis, treatment, and monitoring of MASLD cirrhosis.
A hormone called FGF21 reverses obesity in mice by signaling to the hindbrain, a region targeted by GLP-1 drugs. This finding provides insight into the naturally occurring hormone's benefits for weight loss and MASH treatment.
Elevated uric acid promotes liver damage and disease severity through inflammation, oxidative stress, and metabolic disturbances. Lifestyle interventions, medications, and potential biomarkers are being explored to improve diagnostic efficacy and treatment.
A new study has identified an altered expression of specific genes in individuals with obesity, metabolic dysfunction-associated steatotic liver disease (MASLD), and liver fibrosis. The research team found that inhibiting the gene expression can reduce liver fibrosis, offering a potential new treatment option.
This study reveals a bidirectional causal link between MASLD and sarcopenia, mediated by liver-muscle communication. Altered pathways in both liver and muscle tissues contribute to the development of these conditions.
This review synthesizes current applications of AI and smart devices in MASLD care, discussing their benefits and limitations. AI models leverage EHR, laboratory data, and multi-omics information to predict risk and severity, while also enhancing medical imaging interpretation and liver histopathology assessment.
A study found that the TF-rs1049296 C>T variant is associated with a higher risk of significant liver fibrosis in patients with MASLD, particularly in those with RES iron deposition. The variant was also linked to increased risk of SF in mixed hepatocellular/RES iron deposition patterns.
Researchers investigated the therapeutic potential and molecular mechanisms of oxytocin in metabolic dysfunction-associated steatotic liver disease (MASLD). Oxytocin attenuates lipid accumulation and accelerates lipid metabolism by regulating the AMPK/SREBP1c/FAS axis.
Nutrient-stimulated hormone-based therapies (NuSHs) show promise in managing MASH and preventing HCC progression. NuSHs improve metabolic parameters, reduce liver fat and fibrosis, and modulate immune-metabolic pathways that drive hepatocarcinogenesis.
Research on leptin reveals its multifaceted roles in MAFLD, including regulation of energy balance and metabolism. Leptin therapy shows promise in rare cases of leptin deficiency but is largely ineffective in obesity-associated hyperleptinemia.
This review highlights SIRT1 as a key regulator in MASLD, orchestrating metabolic homeostasis, immune modulation, and inter-organ communication. SIRT1's therapeutic potential is supported by natural product activators and synthetic small-molecule compounds.
This study reveals limited national strategies, weak guideline implementation, and underutilized multidisciplinary collaboration in MASLD care across the MENA region. The insights gathered from regional experts highlight systemic challenges and actionable opportunities for improvement.
Arctigenin, a monomer of Fructus Arctii, exhibits anti-inflammatory activity and prevents MASH progression through modulating the NLRP3/GSDMD-N axis in macrophages. ATG administration also reduces hepatic macrophage infiltration, serum enzyme levels, and lipid peroxidation while enhancing antioxidant enzyme activity.
This study found a significant association between urinary arsenic levels and the prevalence of metabolic dysfunction-associated steatotic liver disease. Higher arsenic exposure was linked to an increased risk of MASLD, particularly in females and individuals with higher incomes.
Researchers identified a significant association between perfluoroheptanoic acid (PFHpA) exposure and metabolic dysfunction-associated steatotic liver disease (MASLD) in adolescents. The study used advanced models to reveal PFHpA's role in disrupting biological pathways, leading to liver damage and inflammation.
Researchers developed innovative 3D dynamic cell co-culture models to simulate MASLD progression stages, addressing traditional 2D culture limitations. Pro-inflammatory macrophages were identified as drivers of hepatocyte lipid metabolism disruption.
Researchers have developed a new mRNA vaccine technology using albumin-recruiting lipid nanoparticles to deliver vaccines precisely to lymph nodes, avoiding liver toxicity. The approach outperformed traditional delivery systems in laboratory tests, producing strong antitumor T-cell responses and high levels of neutralizing antibodies.
People with MASLD emphasize affordability, accessibility and considerations for comorbidities in exercise care. Exercise-focused research should include standardized non-invasive outcomes and culturally responsive models to advance awareness and management of MASLD.
A study discovered six causal molecular biomarkers (CNPY4, ENTPD6, HLA-A) and eight clinical biomarkers for metabolic dysfunction-associated steatotic liver disease (MASLD). Serum total protein levels partially mediated the effect of HLA-A on MASLD.
This study found a significant association between arsenic exposure and MASLD in humans, with higher urinary arsenic levels increasing the risk ofMASLD. The analysis also showed that arsenic exposure persisted across key subgroups, suggesting its contribution to hepatic steatosis even at moderate exposure levels.
A substantial proportion of asymptomatic individuals in Greater Vancouver have undetected MASLD and significant fibrosis. Age, male sex, ethnicity, cardiac disease, diabetes, hypertension, and obesity were significantly associated with fibrosis.
A study from University of Louisville researchers found that perfluorooctane sulfonate (PFOS) can worsen liver damage when combined with alcohol consumption. The study showed that PFOS exposure can increase fat accumulation and markers of liver damage, disrupt the liver's ability to manage fats, and activate pathways that promote liver...
This review explores the roles of orphan nuclear receptors (ONRs) in metabolic dysfunction-associated steatotic liver disease (MASLD) pathogenesis. ONRs modulate key pathways involved in lipid metabolism, inflammation, and fibrosis, offering novel therapeutic avenues.
Researchers discovered that short-term physical activity decreases liver disease severity by breaking down branched-chain amino acids in skeletal muscle. This process enhances redox balance and inhibits lipid accumulation in hepatocytes.
Michael Karin, renowned for his work on chronic inflammation and cancer, will lead the Center for Metabolic and Liver Diseases at Sanford Burnham Prebys. He aims to develop new treatments for metabolic and liver diseases, which affect millions of patients worldwide.
Chronic liver diseases like MASLD and MASH affect 33% and 5% of adults worldwide, respectively. Experts propose doubling MASH diagnosis rate by 2027 to improve outcomes and reduce healthcare burdens. A paradigm shift towards preventive hepatology is key to addressing this growing public health threat.
Clinical trials for MASH cirrhosis have shown promising results, particularly with FGF21 analogues like efruxifermin and pegozafermin. The review emphasizes the need for effective interventions targeting advanced disease stages and highlights the importance of surrogate endpoints in accelerating approvals.
Researchers at the University of Oklahoma discovered that FGF21 can reverse fatty liver disease in mice by sending signals to both the brain and liver. The study provides valuable insight into the mechanism of action of FGF21, a target for a new class of highly anticipated drugs.
This study found that intestinal depletion of TM6SF2 exacerbates high-fat diet-induced MASLD by altering the gut microbiota and liver lipid content. The absence of TM6SF2 also led to increased serum biomarkers associated with MASLD progression.
A VCU-led study suggests that semaglutide, a medication approved for weight loss and blood sugar control, may also reverse liver damage in patients with non-cirrhotic non-alcoholic steatohepatitis (MASH). Researchers found that nearly 90% of participants remained on the medication after 72 weeks without significant side effects.
New research published in the New England Journal of Medicine shows that semaglutide effectively treats liver disease in two-thirds of patients with MASH. The substance has been found to halt and even reverse the disease, reducing steatohepatitis and improving liver fibrosis.
A study published in Hepatology reveals that children with metabolic dysfunction-associated steatotic liver disease (MASLD) are at a significantly increased risk of premature death and serious long-term health complications. The mortality rate was found to be nearly 40 times higher than the national average.
Researchers successfully treated atherosclerosis and fatty liver disease using DT-109 in nonhuman primates, which has potential as a dual therapy for two common conditions. The compound reduced the formation of atherosclerotic plaques and stopped critical processes that lead to vascular calcification.
Researchers investigated the therapeutic mechanisms of ursolic acid on metabolic dysfunction-associated steatotic liver disease. Ursolic acid was found to reduce inflammation by modulating estrogen conversion via HSD17B14, a crucial enzyme regulating estrogen balance.
A new study published in Liver International found that a mother's high-fat diet during pregnancy can lead to liver stress and changes in the fetus's bile acid levels. This may be a key factor in the development of metabolic dysfunction-associated steatotic liver disease (MASLD) later in life.
The study highlights the role of the Nwd1 gene in liver disease and its potential as a therapeutic target. Mice with Nwd1 gene deletion exhibited liver pathologies mirroring MASH, including excessive lipid accumulation and increased ER stress.
The study highlights the significant protective role of Asah1 in preventing NAFLD progression by regulating hepatic lipid homeostasis and cellular maintenance processes. The findings suggest that targeting Asah1 expression or activity may inform new therapeutic strategies for improving patient outcomes.
A new drug candidate has been developed to target and eliminate senescent cells in the liver, reducing fat buildup and preventing liver damage. The study demonstrates a safer and more effective approach to treating metabolic dysfunction-associated steatotic liver disease (MASLD) and potentially inhibiting liver cancer development.
Research identifies six clusters of metabolic dysfunction-associated steatotic liver disease (MASLD) with varying pathophysiology and clinical outcomes. These clusters may enable personalized risk prognosis and treatment through lifestyle modification programs and targeted therapies.
Long non-coding RNAs (lncRNAs) play a critical role in metabolic and fibrotic pathways, influencing lipid metabolism, inflammation, apoptosis, and fibrogenesis. Targeting pathogenic lncRNAs or enhancing protective ones may provide a dual approach for MASLD treatment.
SLC transporters contribute to the development of hepatic steatosis by regulating lipid metabolism, particularly with SLC2A2, GLUT4, and GLUT5. These proteins influence processes like de novo lipogenesis and insulin resistance in hepatocytes.
Researchers reveal senescence's impact on liver health, from repair and regeneration to chronic disease progression. Emerging therapies, such as senolytic treatments, aim to selectively eliminate senescent cells while preserving healthy tissue.
This study investigates SOX9's role in MASH pathogenesis and explores its underlying mechanisms. SOX9 overexpression alleviates hepatic lipid accumulation by activating the AMPK pathway.
Overexpressing hepatic SLC7A11 leads to glutamate and serine deficiency, promoting MASLD progression through ferroptosis. Serine supplementation rescues the disease phenotype.
Researchers discovered a novel combination of plasma-based biomarkers that can predict liver fibrosis in Latino adolescents with obesity. The study found that dihydroxyacetone phosphate (DHAP) and alanine transaminase (ALT) were significantly associated with fibrosis, suggesting a potential low-cost, noninvasive screening tool.
Researchers have identified three major pathomechanisms of MASLD: hepatic genetic component, metabolic de novo lipogenesis, and adipose tissue dysfunction. These subtypes have distinct risk factors for cardiovascular disease and type 2 diabetes. Novel pharmacological approaches may facilitate targeted therapies for each subtype.
GLP-1RAs improve liver histology, reduce liver fat, and enhance metabolic parameters in MASLD patients. However, challenges remain in assessing long-term liver benefits and clarifying the effects on liver fibrosis.
A new study has identified two distinct subtypes of metabolic dysfunction-associated steatotic liver disease (MASH) with similar histological features but different clinical outcomes. The research empowers clinicians to adopt subtype-specific treatments leveraging simple clinical markers, offering a clear path to improve patient outcomes.
A new study proves a suspected link between poor sleep and MASLD, a liver disorder that affects 30% of adults. Patients with MASLD experience significant sleep fragmentation, waking up 55% more often at night.
A new study reveals that an AI algorithm can accurately detect early-stage metabolic-associated steatotic liver disease (MASLD) in patients who meet the criteria, leaving 83% undiagnosed. This highlights the need for improved screening and diagnosis methods to prevent progression to advanced liver disease.
The 17-beta-hydroxysteroid dehydrogenase 13 gene plays a significant role in regulating liver lipid metabolism, with loss-of-function variants linked to reduced risk of chronic liver disease progression. HSD17B13 modulation may provide therapeutic benefits for individuals with metabolic liver disease.
A U.S.-based single-center retrospective cohort study found that advanced liver fibrosis is a primary risk factor for incident liver decompensation and liver-related events in patients with biopsy-proven metabolic dysfunction-associated steatotic liver disease. The study, published in the Journal of Clinical and Translational Hepatolog...