Morgante C, Camma C, Petta S, Guarnotta V, Arnaldi G. Relation between cortisol and metabolic dysfunction-associated steatotic liver disease: A dog chasing its tail. World J Gastroenterol 2026; 32(16): 116142 [DOI: 10.3748/wjg.v32.i16.116142]
Corresponding Author of This Article
Giorgio Arnaldi, Full Professor, Department of Health Promotion, Mother and Child Care, Internal Medicine and Medical Specialties, Section of Endocrinology, University of Palermo, Piazza delle Cliniche 2, Palermo 90127, Sicilia, Italy. giorgio.arnaldi@unipa.it
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Gastroenterology & Hepatology
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Minireviews
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Apr 28, 2026 (publication date) through Apr 17, 2026
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World Journal of Gastroenterology
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1007-9327
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Morgante C, Camma C, Petta S, Guarnotta V, Arnaldi G. Relation between cortisol and metabolic dysfunction-associated steatotic liver disease: A dog chasing its tail. World J Gastroenterol 2026; 32(16): 116142 [DOI: 10.3748/wjg.v32.i16.116142]
World J Gastroenterol. Apr 28, 2026; 32(16): 116142 Published online Apr 28, 2026. doi: 10.3748/wjg.v32.i16.116142
Relation between cortisol and metabolic dysfunction-associated steatotic liver disease: A dog chasing its tail
Cesare Morgante, Calogero Camma, Salvatore Petta, Valentina Guarnotta, Giorgio Arnaldi
Cesare Morgante, Department of Medicine, Catholic University of the Sacred Heart, Rome 00168, Lazio, Italy
Cesare Morgante, Valentina Guarnotta, Giorgio Arnaldi, Department of Health Promotion, Mother and Child Care, Internal Medicine and Medical Specialties, Section of Endocrinology, University of Palermo, Palermo 90127, Sicilia, Italy
Calogero Camma, Salvatore Petta, Section of Gastroenterology and Hepatology, Department of PROMISE, University of Palermo, Palermo 90127, Sicilia, Italy
Author contributions: Morgante C, Camma C, and Arnaldi G conceptualized the work; Morgante C, Petta S, Camma C, and Arnaldi G searched the literature; Morgante C wrote the first draft; Camma C, Petta S, Guarnotta V, and Arnaldi G supervised and revised the work. All authors approved the final version to publish.
Conflict-of-interest statement: All the authors report no relevant conflicts of interest for this article.
Corresponding author: Giorgio Arnaldi, Full Professor, Department of Health Promotion, Mother and Child Care, Internal Medicine and Medical Specialties, Section of Endocrinology, University of Palermo, Piazza delle Cliniche 2, Palermo 90127, Sicilia, Italy. giorgio.arnaldi@unipa.it
Received: November 4, 2025 Revised: December 21, 2025 Accepted: March 3, 2026 Published online: April 28, 2026 Processing time: 164 Days and 18.5 Hours
Abstract
Patients with hypercortisolism and metabolic dysfunction-associated steatotic liver disease (MASLD) share several common comorbidities. Notably, individuals with Cushing’s syndrome appear to have a higher prevalence of MASLD, suggesting a potential pathogenic role of cortisol in the development of this liver condition. The liver is a key target of cortisol action, and it promotes both gluconeogenesis and lipogenesis. Simultaneously, the liver is a major site for cortisol metabolism and clearance. This dual role supports the notion that the liver should be considered an integral component of the hypothalamic-pituitary-adrenal axis. In this minireview, we examine current evidence linking MASLD with hypercortisolism, discuss the principal molecular and metabolic pathways through which cortisol affects liver function, and explore the potential of using cortisol metabolites as novel biomarkers of liver status in this context.
Core Tip: Hypercortisolism and metabolic dysfunction-associated steatotic liver disease share multiple comorbidities, with a higher prevalence in Cushing’s syndrome, indicating that cortisol contributes to liver pathogenesis. As a key target and major metabolic site of cortisol, the liver is integral to the hypothalamic-pituitary-adrenal axis. This minireview summarizes their association, underlying molecular pathways, and cortisol metabolites as potential liver biomarkers.
