An Update to the Epidemiology, Diagnostic Challenges, and Molecular Bases of Nonalcoholic Fatty Liver Disease: 2nd Edition

A special issue of Medicina (ISSN 1648-9144). This special issue belongs to the section "Gastroenterology & Hepatology".

Deadline for manuscript submissions: closed (30 April 2026) | Viewed by 971

Special Issue Editor


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Guest Editor
Head of the Immunometabolism Lab, Research Division, General Hospital of Mexico, 06720 Mexico City, Mexico
Interests: inflammatory immune; obesity; type 2 diabetes; non-alcoholic fatty liver disease
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Nonalcoholic fatty liver disease (NAFLD) is the most common cause of chronic hepatic illness today. NAFLD results from the abnormal accumulation of lipids in the liver, causing a disease spectrum ranging from simple steatosis to nonalcoholic steatohepatitis (NASH), cirrhosis, and hepatocellular carcinoma (HCC). The prevalence of NAFLD has increased worldwide in recent decades; however, we still do not know how emerging threats such as the coronavirus disease 2019 (COVID-19) pandemic and lockdown could have impacted the epidemiology of NAFLD. Furthermore, our conception of the molecular basis behind NAFLD has evolved from a single relationship with obesity to a complex network where de novo lipogenesis, fatty acid beta-oxidation, insulin resistance, and systemic inflammation interact to worsen NAFLD, even in non-obese patients. Finally, there is still a deep urgency to design a better disease risk score where circulating biomarkers combined with modern imaging techniques can help to diagnose NAFLD promptly to prevent the onset of NASH, cirrhosis, and HCC.

For these reasons, Medicina is launching a Special Issue which will publish original research and review articles, and clinical trials covering the most recent aspects of NAFLD’s epidemiology, diagnostic challenges, and molecular bases. The Special Issue is focused on, but not limited to:

  • Impact of COVID-19 on NAFLD incidence in different age groups of patients;
  • Unbalance between de novo lipogenesis and fatty acid beta-oxidation in NAFLD development;
  • Contribution of insulin resistance, glucose intolerance, and metabolic syndrome to NAFLD and NASH in non-obese or obese patients;
  • Characterization of immune cell profiles and cytokine networks mediating NASH, cirrhosis, and HCC;
  • Therapeutic targets to prevent NAFLD progression;
  • Design of noninvasive or minimally invasive NAFLD scores and diagnostic tools.

Dr. Galileo Escobedo
Guest Editor

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Keywords

  • fatty liver disease
  • steatohepatitis
  • fibrosis
  • COVID-19 lockdown
  • insulin resistance
  • metabolic syndrome
  • T cell
  • macrophage
  • computed tomography
  • magnetic resonance imaging

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Related Special Issue

Published Papers (2 papers)

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Research

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14 pages, 3479 KB  
Article
The Degree of Liver Steatosis Is Associated with Abnormally High Serum Levels of Markers of Blood–Brain Barrier Dysfunction and Systemic Inflammation in Patients with Morbid Obesity
by Gabriela Hurtado-Alvarado, Karol Iliana Ávila-Soto, Marlene Monserrat Juárez, Lucía Angélica Méndez-García, Verónica Cevallos-López, Juan Antonio Peralta-Calcaneo, Marcela Esquivel-Velázquez, Antonio González-Chávez, Julio César Zavala-Castillo, Ana Alfaro-Cruz, Jaime Héctor Gómez-Zamudio and Galileo Escobedo
Medicina 2026, 62(5), 821; https://doi.org/10.3390/medicina62050821 - 25 Apr 2026
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Abstract
Background and Objectives: The pathogenesis of liver steatosis is associated with obesity and systemic inflammation, particularly in subjects with body mass index (BMI) above 40 kg/m2 and altered serum levels of tumor necrosis factor alpha (TNF-α) and interleukin-10 (IL-10). Recent evidence [...] Read more.
Background and Objectives: The pathogenesis of liver steatosis is associated with obesity and systemic inflammation, particularly in subjects with body mass index (BMI) above 40 kg/m2 and altered serum levels of tumor necrosis factor alpha (TNF-α) and interleukin-10 (IL-10). Recent evidence suggests that disruption of the blood–brain barrier (BBB) may be associated with the development of steatosis, although limited data are available in humans. Thus, we assessed serum levels of neuron-specific enolase (NSE), transglutaminase 2 (TGM2), and glial fibrillary acidic protein (GFAP) as indirect markers of BBB dysfunction and examined their associations with steatosis severity, TNF-α and IL-10 in patients with morbid obesity. Materials and Methods: We biopsied the liver during bariatric surgery to assess steatosis by histology and serum markers by ELISA. Results: Most study subjects were women aged 38.7 ± 9.9 years with an average BMI of 42.3 ± 7.9 kg/m2 and a steatosis prevalence of 78.9%. After grading steatosis as none (n = 8), mild (n = 17), moderate (n = 8), or severe (n = 5), we found no differences in sex, age, BMI, comorbidities, or laboratory variables, including liver enzymes. One-way ANOVA showed that serum IL-10 was 4-fold less in severe steatosis than in mild steatosis (p = 0.038), whereas TNF-α levels increased twice in severe steatosis compared to no steatosis (p = 0.029). NSE and GFAP serum levels, but not TGM2, increased proportionally to steatosis stage, showing differences between severe steatosis and no steatosis (p = 0.012 and p = 0.0002, respectively). Pearson correlation coefficients showed that NSE and GFAP were significantly associated with TNF-α (r = 0.600 and r = 0.402, respectively), but not with IL-10. Conclusions: Steatosis severity is significantly associated with markers of BBB disruption and systemic inflammation in patients with morbid obesity, suggesting a link between the BBB and liver steatosis. Full article
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Review

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11 pages, 482 KB  
Review
From NAFLD to MASLD and MetALD: Conceptual Shifts in Metabolic Liver Disease and Their Implications for Mexico
by Alejandro Gutiérrez-Castillo, Ricardo Gutiérrez-Monterrubio, Paul Francisco Domínguez-Cardoso, Andrés Thomson Bejarano-Cayo, Ana Karen Mendoza-Ibáñez, Alondra Rosales-Padron, Sofia Mercedes Narvaez-Chavez, Mario García-Alanís, Luis Fernando Rubio-Acosta, Nahum Mendez-Sánchez, Victor Manuel Paez-Zayas and Ignacio García-Juárez
Medicina 2026, 62(5), 926; https://doi.org/10.3390/medicina62050926 (registering DOI) - 9 May 2026
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Abstract
Metabolic dysfunction-associated steatotic liver disease (MASLD), formerly known as non-alcoholic fatty liver disease (NAFLD), is now recognized as the leading cause of chronic liver disease worldwide. The updated terminology reflects a conceptual shift by emphasizing metabolic dysfunction rather than excluding alcohol consumption. This [...] Read more.
Metabolic dysfunction-associated steatotic liver disease (MASLD), formerly known as non-alcoholic fatty liver disease (NAFLD), is now recognized as the leading cause of chronic liver disease worldwide. The updated terminology reflects a conceptual shift by emphasizing metabolic dysfunction rather than excluding alcohol consumption. This redefinition introduced MetALD, a subtype characterized by the coexistence of cardiometabolic risk factors and moderate alcohol intake. In the world, misclassification of MetALD as MASLD is frequent, often due to underreporting of alcohol consumption, which may distort epidemiological estimates. In Mexico, where both obesity and alcohol use are highly prevalent, this reclassification carries important implications for diagnosis, prognosis, and public health policy. This review summarizes the current evidence on MASLD and MetALD, highlighting their prevalence, diagnostic challenges, and implications for liver transplantation and cancer surveillance. We advocate for integrating these diseases into national non-communicable disease policies and adopting a multidisciplinary, preventive approach tailored to the Mexican context. Full article
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