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Updated: Sep 27, 2026

In Vitro Modeling of Fat Deposition in Metabolic Dysfunction-Associated Steatotic Liver Disease
Published on: July 19, 2024
The Emerging Potential of Diabetes Technology to Improve Metabolic Dysfunction-Associated Steatotic Liver Disease in
Anna Garmpi1, Vaia Lambadiari2, Chrysi Koliaki2
1First Propaedeutic Department of Internal Medicine and Diabetes Center, Laiko General Hospital, Medical School, National and Kapodistrian University of Athens, 17 Agiou Thoma Street, 11527 Athens, Greece.
Abstract:
Metabolic dysfunction-associated steatotic liver disease (MASLD) has emerged as an increasingly common comorbidity in individuals with type 1 diabetes (T1D), driven by the rising prevalence of obesity and insulin resistance in this population. Modern diabetes technologies have transformed T1D management and may favorably influence several pathophysiological pathways implicated in T1D-associated MASLD. We aimed to summarize and critically appraise current evidence regarding the emerging potential of diabetes technologies, such as continuous glucose monitoring (CGM), continuous subcutaneous insulin infusion (CSII) and automated insulin delivery (AID) systems, to influence MASLD-related outcomes in adults with T1D, and further discuss therapeutic implications and remaining evidence gaps. The existing evidence remains limited and is predominantly based on observational cross-sectional studies. The available data suggest that diabetes technologies may favorably influence the metabolic milieu associated with MASLD by increasing time in range, reducing glycemic variability and hypoglycemia, optimizing insulin delivery and improving the overall metabolic control. However, evidence for an association with hepatic outcomes remains limited, indirect and inconsistent. Emerging observational data have linked less favorable CGM-derived metrics, particularly lower time in range and greater glycemic variability, with hepatic steatosis and fibrosis, although some studies have identified insulin resistance as a stronger determinant than glycemic metrics alone. CSII therapy has been associated with favorable metabolic profiles, but confounding factors may limit causal interpretation. No study has demonstrated yet a direct beneficial effect of AID systems on hepatic steatosis or fibrosis in patients with T1D. In conclusion, diabetes technologies may favorably influence several pathophysiological pathways involved in T1D-associated MASLD. However, current evidence regarding potential hepatic benefits remains limited and indirect, precluding technology-specific recommendations for MASLD prevention or treatment in T1D. Adequately powered, prospective randomized studies with standardized imaging-based hepatic outcomes are needed to establish causality and define evidence-based clinical recommendations.
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