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Diabetes Management and Research / Liver Disease Diagnosis and Treatment / Diabetes and Associated Disorders · Review
Biomedicines · September 3, 2026
Raises a question worth testing. It does not answer one.
This narrative review examines whether modern diabetes technologies (CGM, CSII, AID systems) may influence metabolic dysfunction-associated steatotic liver disease in type 1 diabetes. The authors conclude that while these technologies favourably influence glycemic control and metabolic metrics, current evidence for direct beneficial effects on hepatic steatosis or fibrosis remains limited, indirect, and inconsistent, and no randomized trials have yet demonstrated liver benefit.
Narrative review. Adults with type 1 diabetes, particularly those with comorbid obesity, insulin resistance, and metabolic dysfunction-associated steatotic liver disease.
Diabetes technologies may increase time in range, reduce glycemic variability and hypoglycemia, and optimize insulin delivery Less favourable CGM-derived metrics, particularly lower time in range and greater glycemic variability, have been linked with hepatic steatosis and fibrosis in observational studies Some studies identified insulin resistance as a stronger determinant of hepatic outcomes than glycemic metrics alone
Safety was not reported in the material analysed. Check the source before drawing any conclusion about harm.
Clinicians should not currently recommend diabetes technology specifically for MASLD prevention or treatment in type 1 diabetes, as the evidence base remains too limited and indirect. Prospective randomized studies with standardized imaging-based hepatic outcomes are needed before technology-specific clinical recommendations can be made.
A narrative review synthesizing observational evidence that raises mechanistic questions about diabetes technology and liver disease, but reports no direct clinical outcomes and explicitly acknowledges evidence remains limited, indirect, and inconsistent.
As stated by the source record.
Clinicians should not currently recommend diabetes technology specifically for MASLD prevention or treatment in type 1 diabetes, as the evidence base remains too limited and indirect. Prospective randomized studies with standardized imaging-based hepatic outcomes are needed before technology-specific clinical recommendations can be made.
Graded across the dimensions that decide whether you should act, each from what the source actually supports. There is no single score, and where a dimension was not assessed it says so.
What is missing. This record has no reported figures. That is a gap in the analysis, not a judgement about the study.
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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