Clin Mol Hepatol.
2025 Jan;31(1):74-89. 10.3350/cmh.2024.0631.
Long-term outcomes and risk modifiers of metabolic dysfunction-associated steatotic liver disease between lean and non-lean populations
- Affiliations
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- 1Department of Internal Medicine, Texas Tech University Health Sciences Center, Lubbock, TX, USA
- 2Immunology Unit, Department of Microbiology, Faculty of Medicine, Chiang Mai University, Chiang Mai, Thailand
- 3Faculty of Medicine Siriraj Hospital, Mahidol University, Bangkok, Thailand
- 4Division of Gastroenterology and Hepatology, Stanford University School of Medicine, Stanford, CA, USA
- 5Division of Gastroenterology and Hepatology, Department of Medicine, University of Arizona College of Medicine, Phoenix, AZ, USA
- 6Division of Gastroenterology and Hepatology, Department of Internal Medicine, Banner University Medical Center, Phoenix, AZ, USA
- 7BIO5 Institute, University of Arizona College of Medicine-Phoenix, Phoenix, AZ, USA
- KMID: 2563408
- DOI: http://doi.org/10.3350/cmh.2024.0631
Abstract
- One-third of adults across the globe exhibit metabolic dysfunction-associated steatotic liver disease (MASLD)―formerly known as nonalcoholic fatty liver disease (NAFLD). To date, MASLD is the fastest-growing etiology of chronic liver disease and hepatocellular carcinoma (HCC). Besides the population with obesity, MASLD can also be found in lean populations, accounting for 13% of the global population, especially Asians. Notably, individuals with lean MASLD face equal or higher overall mortality rates compared to their non-lean counterparts. Risk modifiers encompass advanced age, hepatic fibrosis, and type 2 diabetes mellitus (T2DM). Moreover, the population with lean MASLD is associated with an increased risk of HCC, while their non-lean counterparts are more prone to cardiovascular outcomes and T2DM. Existing evidence indicates a similar risk of liver-related events and extrahepatic cancer between the two groups. However, MASLD-related genetic variants, such as PNPLA3 and TM6SF2, did not significantly affect mortality between the two populations. Still, underreporting alcohol consumption and regional representation limits the study’s comprehensiveness. Longitudinal studies and mechanistic explorations are needed to understand differences in lean versus non-lean MASLD populations. This review highlights the need for awareness and tailored interventions in managing MASLD, considering lean individuals’ unique risks.
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