Latin America’s unique epidemiological profile for SLD is shaped by an alarming rise in obesity and type 2 diabetes prevalence. These metabolic conditions act as cornerstones in MASLD pathogenesis, precipitating hepatic steatosis and fostering a milieu conducive to inflammation and fibrosis. Compounding this metabolic burden is a high prevalence of harmful alcohol use, which independently contributes to hepatic injury and worsens clinical outcomes in patients harboring steatotic livers. The concomitant presence of these risk factors defines the region’s mounting challenge in managing this multifaceted liver pathology.

Genetic predisposition also plays a pivotal role in the heightened vulnerability of Latin American populations to SLD. Particularly notable is the high frequency of deleterious variants in the PNPLA3 gene, which encodes the patatin-like phospholipase domain-containing protein 3 enzyme. This variant has been shown to significantly predispose individuals to fat accumulation in hepatocytes, disease progression, and the development of advanced liver pathology, including steatohepatitis and hepatocellular carcinoma. The genetic landscape thus interacts synergistically with metabolic and alcohol-related insults, accelerating the trajectory from benign steatosis to life-threatening liver disease.

Clinically, the consequences of this confluence are dire. Patients with SLD are at increased risk not only for the progression to nonalcoholic steatohepatitis (NASH) or alcoholic steatohepatitis but also for advanced fibrosis, cirrhosis, and hepatocellular carcinoma (HCC). These advanced manifestations herald significant morbidity and mortality, imposing a growing burden on healthcare systems ill-equipped to meet these challenges. In Latin America, the epidemiological shift towards higher rates of metabolic dysfunction and alcohol-related liver injury portends an impending rise in liver-related complications that will demand urgent public health attention.

Despite the evident clinical and epidemiological weight of SLD in Latin America, the region grapples with structural health-system deficiencies that undermine effective disease management. Fragmented healthcare delivery systems compromise continuity and quality of care, while limited availability of hepatology specialists constrains diagnosis accuracy and therapeutic interventions. Furthermore, the scarcity of advanced diagnostic tools such as transient elastography and histological expertise impairs early detection and staging of liver disease, leading to delayed treatment and poorer outcomes.

Therapeutic options remain comparatively limited, and access to emerging treatment modalities is often restricted by economic and infrastructural barriers. This constraint is exacerbated by low rates of participation in clinical trials, which hinders the development of evidence-based, region-specific management strategies. The lack of robust clinical research tailored to Latin American populations leaves clinicians reliant on data generated from predominantly European or North American cohorts, which may not fully capture the genetic and environmental nuances influencing disease progression locally.

The current state of research and surveillance in Latin America highlights significant knowledge gaps that must be addressed to curb the escalating burden of SLD. Comprehensive epidemiological studies are urgently needed to delineate the true prevalence and natural history of MASLD and ALD in diverse populations across the continent. Moreover, improved surveillance mechanisms would enable timely identification of at-risk individuals and facilitate monitoring of disease progression, thereby informing targeted interventions and resource allocation.

Prevention strategies focused on mitigating metabolic risk factors—such as obesity and diabetes—are paramount. Public health initiatives promoting healthy diets, physical activity, and metabolic health optimization could play a substantial role in reducing the incidence of MASLD. Simultaneously, harm reduction policies aimed at curbing harmful alcohol consumption are crucial to attenuate the impact of ALD and the overlapping metabolic-alcohol-related liver disease subtype that compounds clinical complexity.

Health system strengthening is critical to mounting an effective response to the SLD epidemic. Investments in hepatology training and capacity building can expand the specialist workforce necessary to manage complex liver disease cases. Enhancing access to diagnostic and therapeutic technologies, including non-invasive fibrosis assessment tools and novel pharmacological treatments, would enable earlier diagnosis and improved clinical management. Such improvements would also facilitate greater inclusion of Latin American populations in clinical trials, ensuring that advancements in liver disease treatment are both applicable and accessible to this high-risk region.

Policymakers must prioritize the implementation of comprehensive liver health policies that integrate prevention, early detection, and treatment within broader health system frameworks. Cross-sector collaboration involving public health authorities, academic institutions, and international organizations can galvanize efforts to reduce the morbidity and mortality associated with SLD. Such coordination is essential to bridge existing gaps in care and research and to foster sustainable, population-level health improvements.

It is imperative to recognize the multifactorial nature of SLD and its interwoven etiologies—metabolic derailments, alcohol misuse, and genetic susceptibility—that jointly magnify disease impact in Latin America. This complexity demands a multifaceted, evidence-based approach encompassing public health interventions, clinical management advances, and research innovations. Only through such concerted actions can the escalating tide of steatotic liver disease be stemmed, averting widespread liver failure and cancer that threaten the well-being of millions.

Emerging research has also begun to illuminate molecular pathways underpinning SLD, revealing potential therapeutic targets. For instance, the PNPLA3 I148M variant disrupts normal lipid remodeling processes in hepatocytes, leading to pathological triglyceride accumulation. Targeting pathways related to lipid metabolism and inflammation could yield novel treatments tailored to genetically predisposed populations. Furthermore, understanding the epigenetic and environmental modulators of gene expression may open avenues for personalized medicine approaches in SLD care.

Future directions in tackling the SLD crisis in Latin America must incorporate the development and validation of non-invasive biomarkers to supplant liver biopsy, currently the gold standard but limited by invasiveness and accessibility issues. Advanced imaging techniques and serum markers could revolutionize disease staging and monitoring, facilitating large-scale screening and surveillance initiatives. Integration of such tools into primary care settings offers the potential to democratize liver health assessment and prompt earlier clinical intervention.

The integration of digital health technologies, including telemedicine and electronic health records, represents another frontier for improving liver disease management in resource-constrained environments. These technologies can extend hepatology expertise beyond urban centers, enable remote monitoring of disease progression, and foster patient engagement in lifestyle modifications. Tailored digital platforms designed for Latin American populations could enhance adherence to preventive measures and treatment regimens, thereby improving overall outcomes.

Addressing socio-economic determinants of health is also integral to attenuating the SLD burden in Latin America. Poverty, educational disparities, and limited access to nutritious foods intersect with the metabolic and behavioral risk factors driving liver disease. Public policies that encompass social welfare, food security, and health literacy initiatives can create an enabling environment for sustained liver health improvements and lower disease incidence at a population level.

The synthesis of current knowledge underscores an urgent call to action to confront the burgeoning SLD epidemic in Latin America. Comprehensive strategies that integrate molecular research, clinical innovation, public health initiatives, and health system reforms are imperative. Through collaborative, region-specific efforts bolstered by global support, there lies a promising path to mitigate this formidable liver health challenge and improve quality of life for millions affected across Latin America.

Subject of Research: Steatotic liver disease epidemiology, clinical burden, and management in Latin America

Article Title: Steatotic liver disease in Latin America: current views and perspectives

Article References: Idalsoaga, F., Díaz, L.A., Barrera, F. et al. Steatotic liver disease in Latin America: current views and perspectives. Nat Rev Gastroenterol Hepatol (2026). https://doi.org/10.1038/s41575-026-01219-3

Image Credits: AI Generated

The study in question employed a robust cohort design encompassing over fifteen thousand individuals diagnosed with MASLD alongside a frequency-matched control group exceeding seventy-five thousand participants. The analytical framework rigorously evaluated seven metabolic risk factors in parallel, elucidating their independent contributions to MASLD risk. Notably, type 1 diabetes was intentionally excluded from multivariable models due to its distinct pathophysiology. This large-scale approach permitted stratified analyses by race, ethnicity, and age, thereby allowing for refined insights into heterogeneity among affected populations.

Obesity emerged as a dominant metabolic risk factor, with affected individuals exhibiting a striking 66.1% prevalence versus 41.3% in controls. This epidemiological signature underscores obesity’s pivotal role in hepatic lipid dysregulation and progression of steatotic pathology. Additional metabolic contributors—hypertension, type 2 diabetes, hyperlipidemia, obstructive sleep apnea, and hypothyroidism—also bore significant independent associations with MASLD, each amplifying disease risk and complicating clinical management. The prevalence of these conditions was substantially higher in MASLD subjects, revealing a complex interplay of systemic metabolic dysfunction converging on liver health.

Intriguingly, ethnicity-specific patterns emerged: obesity was the strongest metabolic risk factor in Asian, White, and Hispanic cohorts, especially pronounced in individuals under 50 years of age. Conversely, hypertension surfaced as the paramount risk factor among Black patients, suggesting distinct pathophysiological drivers influenced by genetic, environmental, or socio-economic determinants. Such findings emphasize the necessity for tailored diagnostic approaches and therapeutic regimens that consider demographic variability to optimize clinical outcomes.

Beyond metabolic parameters, MASLD portended a markedly elevated incidence of hepatic and cardiac adverse events, spanning cirrhosis, hepatocellular carcinoma, coronary artery disease, and myocardial infarction. The hepatic sequelae reflect ongoing fibrotic remodeling and oncogenic transformation likely fueled by sustained metabolic insults. Simultaneously, the cardiac comorbidities illustrate the systemic nature of metabolic syndrome, wherein liver pathology is but one facet of widespread vascular and organ system compromise. These overlapping disease burdens highlight MASLD as a nexus of multisystem risk necessitating interdisciplinary healthcare strategies.

Biochemical markers further corroborated clinical severity; MASLD cases frequently displayed elevated liver enzymes such as alanine aminotransferase (ALT), aspartate aminotransferase (AST), and alkaline phosphatase (ALP). These transaminase derangements provide accessible surrogates for hepatic inflammation and cholestasis, serving as critical diagnostic adjuncts in detecting disease activity and progression. The significant divergence in enzyme levels between MASLD and control groups reinforces their utility in ongoing disease surveillance.

Clinically, the overlapping clustering of obesity, hypertension, diabetes, and lipid disorders within MASLD patients reflects metabolic syndrome’s central role in driving hepatic steatosis and fibrosis. Pathophysiologically, excess adiposity generates free fatty acids and pro-inflammatory cytokines, impairing insulin sensitivity and fostering lipotoxicity. Hypertension and dyslipidemia exacerbate endothelial dysfunction and promote oxidative stress, further injuring hepatic parenchyma. The presence of obstructive sleep apnea and hypothyroidism complicates this milieu by contributing hypoxia and hormonal imbalances, respectively, which augment metabolic dysregulation.

The findings from the All of Us cohort underscore an urgent need to adopt precision medicine paradigms in MASLD management. Recognizing distinct metabolic risk profiles across ethnic groups and age strata calls for customized screening protocols and personalized intervention plans, integrating lifestyle modification, pharmacotherapy, and potentially emerging hepatoprotective agents. Early identification and mitigation of these metabolic insults could attenuate progression toward cirrhosis and hepatocellular carcinoma, improving both liver-specific and cardiovascular prognoses.

Furthermore, this large-scale study epitomizes the power of comprehensive electronic health record-linked databases to unravel complex disease phenotypes and risk factor interactions within real-world populations. Analytical models dissecting independent and combined effects of metabolic variables provide invaluable granularity, informing clinical decision-making and public health policy. Cross-disciplinary collaboration blending hepatology, endocrinology, cardiology, and sleep medicine will be essential to holistically address MASLD’s multifactorial nature.

Taken together, the compelling evidence delineated in this investigation reinforces MASLD as a multisystem, metabolically driven disease with variable risk determinants shaped by demographic characteristics. The marked elevation in biochemical and clinical manifestations highlights the necessity for comprehensive assessment and targeted therapeutic strategies capable of addressing the intertwined metabolic dysfunctions. Continuous research leveraging large biobanks will further illuminate the pathogenesis and inform the development of precision interventions, ultimately reducing the substantial burden MASLD imposes globally.

As MASLD continues to rise in prevalence consistent with expanding metabolic syndrome epidemics, advancing our mechanistic understanding and refining risk stratification remain paramount. The innovative insights provided by the All of Us Research Program exemplify progress toward this goal, offering a roadmap for future studies and clinical applications. Addressing metabolic complexity at the individual and population levels promises to transform MASLD from a silent epidemic into a manageable, well-characterized clinical entity.

In summary, the comprehensive scrutiny of metabolic risk factors and clinical outcomes in MASLD via expansive cohort analyses illuminates critical interrelationships between systemic metabolic derangements and liver pathology. The research supports the conceptualization of MASLD as an emblematic metabolic disorder requiring integrated approaches to diagnosis, risk assessment, and intervention—embracing heterogeneity across populations and age groups. Ultimately, precision medicine frameworks leveraging such data can revolutionize MASLD care, improving liver health and preventing severe sequelae linked to this pervasive condition.

Subject of Research: Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD) and associated metabolic risk factors.

Article Title: Metabolic Risk Factors and Clinical Presentations of Metabolic Dysfunction-associated Steatotic Liver Disease Using Data from the All of Us Research Program

News Publication Date: 27-Jan-2026

Web References: https://www.xiahepublishing.com/journal/jcth, http://dx.doi.org/10.14218/JCTH.2025.00393

Image Credits: Ke-Qin Hu

Keywords: Metabolic dysfunction, MASLD, hepatic steatosis, obesity, hypertension, type 2 diabetes, hyperlipidemia, obstructive sleep apnea, hypothyroidism, liver enzymes, cirrhosis, hepatocellular carcinoma, coronary artery disease

The research addresses MASLD, a spectrum of liver conditions characterized predominantly by aberrant fat accumulation in hepatocytes, progressing beyond the former nomenclature of non-alcoholic fatty liver disease (NAFLD). Notably, MASLD is intricately linked with metabolic dysregulation encompassing insulin resistance, visceral adiposity, and dyslipidemia. The shift in terminology reflects the expanding understanding of metabolic contributions, positioning MASLD as a distinctive entity tethered to systemic metabolic health rather than hepatic pathology alone.

Utilizing a robust cross-sectional design, the authors conducted a population-based survey targeting adolescents aged 12 to 18 years, deploying an integrative approach combining anthropometric measurements, biochemical assays, and non-invasive liver imaging techniques. The selection of Hainan Province—a subtropical island with unique socioeconomic and lifestyle variables—offers invaluable insights into how environmental and ethnic factors interplay with metabolic derangements. This methodological rigor enabled precise characterization of MASLD prevalence and elucidation of associated determinants.

Results delineate a worrisome prevalence rate of MASLD within this age bracket, markedly higher than previously reported in comparable demographic studies elsewhere in China and globally. The study highlights an estimated prevalence exceeding 25%, signaling a silent yet rapidly escalating public health burden. Furthermore, the data reveal a predilection for male adolescents, and a pronounced correlation with indices of obesity, central adiposity, and impaired glucose metabolism, substantiating the metabolic underpinnings of disease pathogenesis.

The pathophysiological mechanisms underpinning MASLD among adolescents appear multifactorial. Crucial contributors include heightened insulin resistance precipitating increased lipolysis and free fatty acid flux to hepatic tissue, mitochondrial dysfunction exacerbating oxidative stress, and inflammatory cascades mediating hepatocellular injury and fibrogenesis. The researchers emphasize that these complex biological pathways are intricately influenced by genetic predispositions, epigenetic modifications, and environmental exposures peculiar to the Hainan context.

Lifestyle variables bear heavily on MASLD risk profiles. Diets enriched with saturated fats and refined sugars, coupled with sedentary behaviors, amplify the metabolic disruption driving hepatic steatosis and inflammation. The study identifies excessive fructose consumption and decreasing physical activity levels in adolescents as pivotal modifiable risk factors. The authors advocate for culturally sensitive lifestyle interventions aimed at nutritional education and increased exercise to attenuate the early onset of MASLD and its downstream complications.

Intriguingly, the investigation explores the socioeconomic landscape shaping adolescent health behaviors and access to healthcare resources in Hainan. The data illustrate disparities in MASLD prevalence linked to socioeconomic status, with lower-income families exhibiting higher disease burdens. This finding underscores the interplay between social determinants of health and biological vulnerability, highlighting the necessity of multi-tiered public health strategies incorporating social equity considerations.

Genetic analyses incorporated in the study reveal polymorphisms in genes such as PNPLA3 and TM6SF2 known to modulate hepatic fat accumulation and inflammation susceptibility. The prevalence of these alleles in the adolescent cohort offers insights into inherited risk amplifiers, potentially informing personalized risk stratification and precision medicine approaches. These genetic factors do not act in isolation but synergize with environmental triggers, necessitating holistic investigative frameworks.

The study further delves into the longitudinal implications of adolescent MASLD, emphasizing the trajectory towards advanced liver disease manifestations including steatohepatitis, fibrosis, and cirrhosis. Early identification of MASLD in youth portends substantial future healthcare burdens due to progression in adulthood, compounded by concomitant cardiovascular and metabolic morbidities. This underscores the critical window for early intervention to alter disease course and improve long-term outcomes.

In its discussion, the research team advocates for integration of MASLD screening protocols within routine pediatric healthcare settings, especially in areas exhibiting high prevalence such as Hainan. The deployment of non-invasive biomarkers and transient elastography offers pragmatic avenues for early diagnosis, circumventing invasive liver biopsies which carry inherent risks and resource constraints. Scaling such diagnostic modalities can facilitate timely therapeutic measures and disease monitoring.

Public health implications of this study are profound. The evident epidemic proportions of MASLD in adolescents necessitate concerted efforts spanning governmental policy, healthcare system strengthening, and community engagement. Emphasis on school-based health programs, nutritional reforms, and physical activity promotion form cornerstone initiatives. Additionally, tackling socioeconomic inequities stands imperative to bridging disparities and enabling equitable health improvements.

The authors also call attention to the need for expanded research focused on understanding MASLD heterogeneity across various ethnicities and geographic niches within China. Hainan Province’s unique demographic composition offers a paradigm but also points to potential differences nationwide requiring tailored epidemiological mapping and intervention strategies. Collaboration across disciplines including hepatology, endocrinology, nutrition, and social sciences is pivotal.

The findings from this survey illuminate a critical public health concern with broad implications for pediatric and adolescent medicine worldwide. As metabolic disorders escalate in younger populations, MASLD emerges not merely as a hepatic ailment but a systemic metabolic dysregulation marker with intricate ties to lifestyle and genetics. This comprehensive investigation provides a clarion call to healthcare providers, policymakers, and researchers to prioritize prevention, early detection, and innovative management paradigms.

In conclusion, the multidisciplinary approach and meticulous analysis presented in Zhou et al.’s study offer a seminal contribution to the understanding of MASLD among adolescents in Hainan Province. By unraveling the multifaceted risk factor landscape and emphasizing early intervention, the research charts a path toward mitigating a burgeoning epidemic with significant societal and medical ramifications. Moving forward, translating these insights into actionable health policies and personalized care will be paramount in curbing the trajectory of adolescent MASLD.

Subject of Research: Metabolic dysfunction-associated steatotic liver disease (MASLD) prevalence and risk factors among adolescents in Hainan Province.

Article Title: Current status survey and risk factor analysis of metabolic dysfunction-associated steatotic liver disease among adolescents in Hainan Province.

Article References: Zhou, S., Zhang, D., Chen, R. et al. Current status survey and risk factor analysis of metabolic dysfunction-associated steatotic liver disease among adolescents in Hainan Province. Sci Rep (2026). https://doi.org/10.1038/s41598-026-45173-1

Image Credits: AI Generated

DOI: 10.1038/s41598-026-45173-1

Keywords: Metabolic dysfunction-associated steatotic liver disease, MASLD, adolescent health, liver steatosis, metabolic syndrome, epidemiology, Hainan Province, insulin resistance, liver fibrosis, pediatric hepatology, lifestyle factors, genetic polymorphisms.

Nonalcoholic steatohepatitis represents an advanced stage of nonalcoholic fatty liver disease and is characterized by liver fat accumulation along with inflammation and varying degrees of fibrosis. Conventional treatments have remained elusive as the etiology of NASH intertwines metabolic factors with gut-liver axis disturbances. The present study focuses on the impact of 2’-FL on a choline-deficient fat diet (CDFD)-induced NASH model in mice, elucidating critical mechanistic insights into how modulating the microbiome can translate into hepatic benefits.

The authors synthesized 2’-FL, a trisaccharide known for its immunomodulatory capabilities in infants, and administered it to mice subjected to a CDFD, a widely accepted method to induce NASH and simulate the pathological milieu seen in humans. Over a 12-week intervention period, 2’-FL supplementation mitigated the hallmark pathological features of NASH including steatosis, hepatocyte ballooning, and immune cell infiltration. Remarkably, these improvements correlated with pronounced shifts in the composition of the intestinal microbiota, establishing a profound link between microbial ecology and liver health.

Detailed metagenomic sequencing revealed that 2’-FL administration enriched beneficial bacterial taxa such as Bifidobacterium and Lactobacillus, known producers of short-chain fatty acids (SCFAs) and crucial modulators of gut barrier integrity. The study posits that these microbial shifts lead to the restoration of gut barrier function, thereby reducing the translocation of bacterial endotoxins such as lipopolysaccharides (LPS) into the portal circulation, which is a critical driver of hepatic inflammation in NASH.

Furthermore, the team’s investigation uncovered that 2’-FL downregulated pro-inflammatory cytokines including TNF-α and IL-6 in liver tissue, illustrating its systemic anti-inflammatory properties. Coupled with improved liver enzyme profiles, these data suggest that 2’-FL directly modulates immune pathways both locally in the gut and distally in the liver, highlighting the intertwined nature of the gut-liver axis in metabolic disease.

One of the standout findings of the research is the demonstration that 2’-FL’s benefits surpass simple dietary intervention, acting as a prebiotic that selectively nourishes beneficial microorganisms. This not only curbs pathogenic bacterial overgrowth but also enhances microbial diversity, which has been consistently associated with better metabolic outcomes. The authors argue that 2’-FL supplementation represents a novel microbiome-targeted therapeutic strategy for metabolic liver disease without the adverse effects commonly seen with pharmacological agents.

The methodology included a comprehensive array of analytical techniques ranging from histopathological scoring of liver sections to cutting-edge 16S rRNA gene sequencing, providing robust and multifaceted evidence for the role of 2’-FL in NASH management. Liver histology revealed marked reduction in fibrosis scores post-treatment, underscoring the potential of 2’-FL to reverse fibrotic progression which remains a critical unmet need in clinical hepatology.

Importantly, the safety profile of 2’-FL was thoroughly assessed, with no observable toxicity or adverse metabolic effects noted in the treated mice. This safety and tolerance aspect adds a translational advantage to 2’-FL, especially considering its natural presence in human breast milk, suggesting potential for future clinical trials in human subjects suffering from NASH.

The study also delves into the biochemical pathways through which 2’-FL exerts its effects. The authors highlight the upregulation of SCFA production and consequent activation of G-protein-coupled receptors (GPCRs) involved in maintaining intestinal homeostasis. This crosstalk between microbial metabolites and host receptors elucidates a critical mechanism by which 2’-FL orchestrates systemic metabolic benefits, bridging microbiome modulation with host physiology.

Looking forward, this research paves the way for new interventions in liver metabolic diseases by targeting the gut microbiota with defined oligosaccharides. While animal models have inherent limitations, the translational potential of these findings is immense, especially as gut microbiome modulation gains traction as a therapeutic frontier. Future clinical studies will illuminate the efficacy and dosing strategies necessary for incorporating 2’-FL into therapeutic regimens for patients with NASH.

The implications of these findings extend beyond liver disease. Given that the gut microbiome influences a spectrum of metabolic and inflammatory conditions, 2’-FL and similar oligosaccharides may emerge as versatile modulators in diseases ranging from diabetes to inflammatory bowel disease. The integrative approach combining dietary supplementation with microbial ecology represents a paradigm shift in personalized medicine.

This pioneering work underscores a fundamental concept in modern biomedical research: the gut microbiome is a modifiable determinant of systemic health. Harnessing natural molecules such as 2’-FL found in human milk not only unlocks therapeutic potential but also reaffirms the wisdom embedded in evolutionary biology. The study is a testament to the intersection of nutrition science, microbiology, and hepatology driving innovative treatment modalities.

In conclusion, the study by Zhang, Cheng, Chen, and colleagues is a seminal contribution to metabolic liver disease research. By illuminating how 2’-Fucosyllactose remodels gut microbiota, restores intestinal barrier function, attenuates hepatic inflammation, and reverses fibrosis in a NASH model, it opens novel avenues for treatment. This natural compound offers hope for an accessible, effective, and safe therapeutic option against a condition that currently lacks FDA-approved drugs.

The scientific community and clinicians alike will be watching closely as further investigations translate these promising findings from bench to bedside. The era of microbiome-centric therapeutics is emerging rapidly—and 2’-FL could well become a cornerstone molecule in the management of chronic liver diseases and beyond, heralding a new dawn in metabolic health interventions.

Subject of Research:
The impact of 2’-Fucosyllactose (2’-FL) on gut microbiota remodeling and its therapeutic effects on choline-deficient fat diet-induced nonalcoholic steatohepatitis (NASH).

Article Title:
2’-Fucosyllactose (2’-FL) alleviates choline-deficient fat diet-induced nonalcoholic steatohepatitis (NASH) by remodeling intestinal flora.

Article References:
Zhang, S., Cheng, X., Chen, L. et al. 2’-Fucosyllactose (2’-FL) alleviates choline-deficient fat diet-induced nonalcoholic steatohepatitis (NASH) by remodeling intestinal flora. Food Sci Biotechnol (2025). https://doi.org/10.1007/s10068-025-02034-3

Image Credits:
AI Generated

DOI:
https://doi.org/10.1007/s10068-025-02034-3