Hyperammonemia as a potential contributor to fatigue in metabolic dysfunction-associated steatotic liver disease: A mechanistic review

doi:10.4254/wjh.124519

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World Journal of Hepatology

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1948-5182

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Baishideng Publishing Group Inc, 7041 Koll Center Parkway, Suite 160, Pleasanton, CA 94566, USA

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Copyright: ©Author(s) 2026. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution-NonCommercial (CC BY-NC 4.0) license. No commercial re-use. See permissions. Published by Baishideng Publishing Group Inc.

World J Hepatol. Oct 27, 2026; 18(10): 124519
Published online Oct 27, 2026. doi: 10.4254/wjh.124519

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Figure 1 Ammonia metabolism in the liver. Detoxification of ammonia in the liver occurs via two spatially separated pathways: The highly efficient urea cycle, or ureagenesis, in periportal hepatocytes converts ammonia to urea, whereas residual ammonia is utilized by glutamine synthetase in perivenous hepatocytes by binding ammonia with glutamate to form glutamine. OTC: Ornithine transcarbamylase; CPS1: Carbamoyl phosphate synthetase 1; ASS1: Argininosuccinate synthetase 1; ASL: Argininosuccinate lyase; ARG: Arginase; GS: Glutamine synthetase; GLS: Glutaminase.

Citation: Sheptulina AF, Golubeva JA, Valeeva DL, Kiselev AR, Drapkina OM. Hyperammonemia as a potential contributor to fatigue in metabolic dysfunction-associated steatotic liver disease: A mechanistic review. World J Hepatol 2026; 18(10): 124519
URL: https://www.wjgnet.com/1948-5182/full/v18/i10/124519.htm
DOI: https://dx.doi.org/10.4254/wjh.124519

Sheptulina AF, Golubeva JA, Valeeva DL, Kiselev AR, Drapkina OM. Hyperammonemia as a potential contributor to fatigue in metabolic dysfunction-associated steatotic liver disease: A mechanistic review. World J Hepatol 2026; 18(10): 124519 [DOI: 10.4254/wjh.124519]

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