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Featured MASLD/MASH Educators

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Elizabeth Alqueza

PA-C

Elizabeth Alqueza, PA-C is a board certified Physician Associate at Beth Israel Deaconess Medical Center (BIDMC) in Boston, Massachusetts. She graduated from the University of Florida in 2004 with a Master of Physician Assistant Studies degree and subsequently completed the AASLD NP/PA Clinical Hepatology Fellowship. Elizabeth has worked in a variety of inpatient and outpatient settings with a strong commitment to patient care. Currently working at BIDMC Liver Center, Elizabeth has 5 years of dedicated experience in Hepatology. Her practice focuses primarily on steatotic liver disease, including Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD) and Metabolic Dysfunction-Associated Steatohepatitis (MASH). Elizabeth is an active member of Gastroenterology and Hepatology Advanced Practice Providers.

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Michelle Barnett

PA-C, MPAS, DFAAPA

Michelle Barnett is a highly experienced physician assistant specializing in patient-focused and evidence-based hepatology at Peak Gastroenterology Associates in Colorado Springs, Colorado. The most rewarding part of her position includes educating patients and collaborating with other GI advanced practice providers to enhance care for the growing MASLD/MASH population. She is now a subinvestigtor for hepatology clinical trials with Peak in Colorado Springs. With over 30 years in the GI and liver communities, she has held leadership roles, including serving as President of the Colorado Academy of Physician Assistants (CAPA) and receiving CAPA's Physician Assistant of the Year award. She is a national speaker and has given lectures for the AAPA, GHAPP and AANP. A graduate of Wichita State University and the University of Nebraska, Michelle has been recognized with the DFAAPA distinction and honors such as the Crohn’s and Colitis Foundation's IBD internship and the International Foundation for Gastrointestinal Disorders Ally Award. Passionate about holistic care, she incorporates lifestyle strategies like nutrition, yoga, and meditation into her practice. Outside of work, Michelle enjoys hiking, travel, musical theater, and supporting her favorite Colorado sports teams.

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Sherona Bau

NP

Sherona Bau graduated from University of California, Los Angeles in 2008, with Master of Science in Nursing dual program specialized in Acute Care Nurse Practitioner and Clinical Nurse Specialist. In 2010, she has joined UCLA Pfleger Liver Institute and Asian Liver Cancer Center working as an outpatient Nurse Practitioner specializing in liver diseases including viral hepatitis, hepatobiliary diseases, alcohol related liver diseases, Metabolic Dysfunction-Associated Steatotic Liver Disease/Steatohepatitis, autoimmune liver diseases, and hepatocellular carcinoma. Since 2016, she has been a guest lecturer at UCLA School of Nursing for Master Entry Clinical Nurse (MECN) and MSN Adult/Gero Acute Care program. She is also a preceptor for Adult/Gero Acute Care Program. She participated in Hepatitis C Screening in the Community Churches to promote awareness of hepatitis C and the importance of treatment of hepatitis C. She also participates in Patient Symposium at UCLA to give a lecture to update care of the liver transplant patients. She is also a faculty of Gastroenterology Hepatology Advanced Practice Provider (GHAPP) since 2018 and a speaker for both GHAPP National meeting and Regional GHAPP in Los Angeles. Since 2013, she has published total 14 research papers and case report including the most recent three are Recommendations for the Management of MASH by Advanced Practice Providers in the US, Clinicians and Patients Confront Practical Issues in Wilson Disease, and Overview of chronic Hepatitis B management.

MASLD/MASH Learning Center

Latest News & Blogs

Paired snRNA-seq and scRNA-seq analysis of MASLD patients to identify early-stage markers for disease progression

October 2025

CONCLUSIONS: Significant molecular and immune alterations occur in disease progression of MASLD to MASH, reflecting both localized hepatic changes and systemic immune dysregulation. The identified transcriptomic signatures provide a promising tool for fibrosis prediction and monitoring, underscoring the need to target early disease mechanisms for improved diagnosis and therapeutic strategies.

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Retatrutide Improves Steatohepatitis in an Accelerated Mouse Model of Diet-Induced Steatohepatitis with a Fructose Binge

October 2025

Fructose consumption contributes to metabolic dysfunction-associated steatohepatitis (MASH). Retatrutide is a novel triple receptor agonist that improves obesity and hepatic steatosis in humans. The aims of this study were to develop a shortened and clinically relevant dietary mouse model of diet-induced steatohepatitis, and to evaluate the effects of a retatrutide intervention in this model. C57BL/6N mice were subjected to a single fructose binge (10 mg/g body weight), or a new 31-day mouse...

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Clinical Predictors of Progression From Metabolic Dysfunction-Associated Steatotic Liver Disease to Cirrhosis: A Narrative Review

October 2025

Metabolic dysfunction-associated steatotic liver disease (MASLD) continues to affect many people around the globe and may increase the likelihood of liver-related morbidity and mortality. Early identification of individuals at risk for progression to liver cirrhosis is crucial to the mitigation of the disease effects. This review aims to summarize the current evidence on clinical factors predicting MASLD progression to cirrhosis. A comprehensive literature search was conducted in PubMed,...

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Involvement of ferroptosis in metabolic dysfunction-associated steatohepatitis-related liver diseases

October 2025

Metabolic dysfunction-associated steatotic liver disease (MASLD), as a metabolic liver disease, is emerging as the most prevalent chronic liver disease worldwide. Metabolic dysfunction-associated steatohepatitis (MASH) is the severe form of MASLD, which progresses from simple steatosis to an inflammatory state, even fibrosis and hepatocellular carcinoma. Accumulating evidence has proved that cell death is a hallmark of MASH, while the specific pathogenesis remains unclear. Several cell deaths,...

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Exploring multiorgan mitochondrial dysfunction in the switch toward progressive MASLD in AMLN mice

October 2025

Hepatic mitochondrial maladaptation features the transition from metabolic dysfunction-associated steatotic liver disease (MASLD) to Steatohepatitis (MASH) up to fibrosis/cirrhosis. However, it is still unexplored whether mitochondrial alterations also affect adipose tissue, muscle and heart during disease progression. C57Bl/6 mice were fed an AMLN diet to recapitulate the human MASLD spectrum. In the liver, TEM depicted a progressive morphologic dysfunction of mitochondria, which appeared...

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Effect of Non-Statin Lipid-Lowering Therapy on Hepatic Outcomes in Metabolic Dysfunction-Associated Steatotic Liver Disease and Steatohepatitis: A Systematic Review

October 2025

Metabolic dysfunction-associated steatotic liver disease (MASLD) and metabolic dysfunction-associated steatohepatitis (MASH) are significant health concerns affecting a large segment of the population and are known to be associated with adverse cardiovascular outcomes. As a result, various lipid-lowering medications are commonly employed in clinical practice to address the elevated cardiovascular risk in these patients. This systematic review summarizes the current evidence on emerging...

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Reevaluating the causal link between liver fat and hyperglycaemia

October 2025

CONCLUSION: The absence of a causal relationship between hepatic steatosis and glycaemic traits suggests that hyperglycaemia in metabolic dysfunction-associated steatotic liver disease may involve additional mechanisms beyond liver fat accumulation.

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Healthcare costs and treatment patterns associated with glucagon-like peptide 1 receptor agonist use among patients with metabolic dysfunction-associated steatohepatitis

October 2025

Aim: While only recently approved for the treatment of metabolic dysfunction-associated steatohepatitis (MASH), many patients with MASH have taken glucagon-like peptide-1 receptor agonists (GLP-1 RAs) for the treatment of comorbid Type 2 diabetes (T2D) or obesity. This real-world study evaluated treatment patterns, weight loss, healthcare resource utilization, and costs among patients with MASH who initiated GLP-1 RAs. Materials & methods: In a linked electronic health records (Veradigm Network...

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Sterile inflammation in MASH: emerging role of extracellular RNA and therapeutic strategies

October 2025

Metabolic dysfunction-associated steatotic liver disease (MASLD) and its advanced form, metabolic dysfunction-associated steatohepatitis (MASH), are major global health issues involving metabolic dysfunction, hepatic lipotoxicity, and chronic inflammation. A key driver of MASH pathogenesis is sterile inflammation, a non-infectious immune response triggered by molecules that are released from injured or dying liver cells. These molecules termed as damage-associated molecular patterns (DAMPs),...

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Hepatic steatosis and pyroptosis are induced by the hepatitis B virus X protein via B56α-METTL3 interaction-mediated m6A modification of the NLRP3 mRNA

October 2025

Metabolic dysfunction-associated steatohepatitis (MASH) is one of the fastest-growing chronic liver diseases and is characterized by excessive steatosis, inflammation, and progressive liver injury. The hepatitis B virus (HBV) X protein (HBx) is a major viral factor that contributes to the onset and progression of MASH. Emerging evidence highlights the role of epigenetic modifications, particularly N6-methyladenosine (m6A), as prevalent modifications of mRNAs that play crucial roles in MASH...

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TLR4 promotes liver fibrosis in metabolic dysfunction-associated steatohepatitis by a mechanism independent of hepatocytes and inflammatory cells

October 2025

In metabolic dysfunction-associated steatotic liver disease (MASLD), liver fibrosis is the most important prognostic factor, and fibrosis can lead to hepatic cirrhosis and cancer. In the liver toll-like receptor 4 (TLR4) signaling promotes fibrosis. To investigate the role of TLR4 in the development of MASLD, we used a mouse model of MASLD, and we deleted the Tlr4 gene either in the whole body or selectively in inflammatory cells or hepatocytes. Mice with a whole-body deletion of Tlr4 developed...

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Reliable monitoring of patients with MASLD using imaging: a systematic literature review and meta-analysis on measurement repeatability

October 2025

As treatments for patients with metabolic dysfunction-associated steatotic liver disease (MASLD) emerge, patient eligibility assessment and monitoring is increasingly important. To assess the reliability of non-invasive imaging technologies in MASLD, we systematically reviewed the literature for studies on technical repeatability. PubMed Central and MEDLINE were searched (2015-2025) for studies in MASLD that examined the repeatability of: magnetic resonance (MR)-derived iron-corrected T1 (cT1),...

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beta-sitosterol attenuates hepatic lipid accumulation and fibrosis via NLRP3 signaling in MASH mice

October 2025

Β-sitosterol (SIT), a natural phytosterol, has not been fully explored for its therapeutic potential in metabolic dysfunction-associated steatohepatitis (MASH). In this study, MASH was induced in mice via a high-fat, high-cholesterol (HFHC) diet, and lipid accumulation in HepG2 cells was triggered with oleic acid (OA), while the role of the NLRP3 inflammasome was explored in NLRP3-knockout (NLRP3^(-/-)) mice treated with or without SIT. SIT treatment significantly alleviated HFHC-induced hepatic...

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Ursodeoxycholic acid acts as an ileal FXR agonist in male mice with hepatic deficiency of FXR

October 2025

CONCLUSION: The data strongly suggest that UDCA seems to act as an FXR agonist, especially in the ileum, which contrasts with previous reports that UDCA acts as a gut FXR antagonist. In addition, UDCA seems to be exerting liver protective effects predominantly in the male mice.

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Three-Dimensional Dynamic Cell Models for Metabolic Dysfunction-Associated Steatotic Liver Disease Progression

October 2025

Objective: Metabolic dysfunction-associated steatotic liver disease (MASLD) is a complex, progressive disorder involving multiple cell types, ranging from simple steatosis to metabolic dysfunction-associated steatohepatitis (MASH), characterized by pro-inflammatory macrophage activation, and can eventually advance to fibrosis, initiated by hepatic stellate cells (HSCs). In vitro multi-cell coculture models are vital tools for elucidating the mechanisms underlying MASLD. Impact Statement:...

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Angelica sinensis and Scutellaria baicalensis synergistically alleviates metabolic dysfunction-associated steatohepatitis via promoting adipose tissue-to-liver tissue communication

October 2025

CONCLUSION: As-SbG synergistic therapy activates Nrg4 expression in adipose tissue, which specifically binds to ErbB receptors in liver tissue, thereby modulating downstream signal transduction pathways involved in fat metabolism, anti-inflammatory responses, and anti-apoptotic processes. This inter-communication between adipose and liver tissues helps restore hepatic lipid homeostasis, attenuates inflammation, and reduces hepatocyte injury, fibrosis, and apoptosis, ultimately ameliorating MASH...

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Discovery of novel FABP1 inhibitors for the treatment of metabolic dysfunction-associated steatohepatitis and hepatic fibrosis

October 2025

The fatty acid-binding protein 1 (FABP1) has drawn increasing attention as a promising target for the treatment of metabolic dysfunction-associated steatohepatitis (MASH). However, efforts to validate pharmacological effects of FABP1 are restricted by the lack of relevant inhibitors. Herein, we identified the lead compound 1 with potent inhibition on FABP1 through screening from our in-house library. Further comprehensive structure-activity relationship (SAR) study based on compound 1 resulted...

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Sodium nitrate protects against metabolic syndrome by sialin-mediated macrophage rebalance

October 2025

Metabolic syndrome, characterized by metabolic dysfunction-associated steatotic liver disease (MASLD) and type 2 diabetes mellitus (T2DM), poses a significant threat to patients' health worldwide; however, efficient treatment is currently unavailable. Here, we show that oral administration of sodium nitrate (NaNO(3)) greatly attenuates the development and advancement of MASLD-like and T2DM-like phenotypes in mice induced by choline-deficient high-fat, western, or methionine/choline-deficient...

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ER stress upregulates S100A11 in steatohepatitis models via epigenetic modifications within the lipotoxicity influenced enhancer

September 2025

Metabolic dysfunction-associated steatohepatitis (MASH) is a progressive liver disease characterized by complex interactions between lipotoxicity, ER stress responses, and immune-mediated inflammation. We identified enrichment of the proinflammatory alarmin S100 calcium-binding protein A11 (S100A11) on extracellular vesicles stimulated by palmitate-induced lipotoxic ER stress with concomitant upregulation of hepatocellular S100A11 abundance in an IRE1A-XBP1s dependent manner. We next...

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Shared mechanistic pathways of glucagon signalling: Unlocking its potential for treating obesity, metabolic dysfunction-associated steatotic liver disease, and other cardio-kidney-metabolic conditions

September 2025

Glucagon is a pancreatic peptide hormone whose receptor (GCGR) is expressed in the liver, kidney, and, to a lesser extent, various other tissues. Glucagon is well known as the counterpart to insulin in glucose homeostasis. However, recent evidence has revealed other potential roles of glucagon, which include the regulation of amino acid metabolism via a liver-pancreatic alpha cell axis, stimulation of lipolysis and mitochondrial fat oxidation in the liver (and possibly in other tissues),...

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