ArticleFrontiers in endocrinology2025
Metabolite perturbations in type 1 diabetes associated with metabolic dysfunction-associated steatotic liver disease.
Article in Frontiers in endocrinology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Hepatic steatosis risk in nonobese Chinese adults with type 1 diabetes.Journal of diabetes investigation · 2026Article
- The Emerging Potential of Diabetes Technology to Improve Metabolic Dysfunction-Associated Steatotic Liver Disease in Patients with Type 1 Diabetes: A Narrative Review.Biomedicines · 2026Review
- Substrate supply, compartmentation, and utilization in hepatic de novo lipogenesis.Trends in endocrinology and metabolism: TEM · 2026Review
- Multi-omics reveals microbiota, metabolite, and immunological heterogeneity of age-related endotypes in type 1 diabetes.Signal transduction and targeted therapy · 2026Article
- Black Sesame Pigment Ameliorates Non-Alcoholic Fatty Liver Disease via Modulation of the Gut-Liver Axis and HIF-1 Signaling Pathway.Antioxidants (Basel, Switzerland) · 2026Article
- Metabolomic Signatures of MASLD Identified by the Fatty Liver Index Reveal Gamma-Glutamyl Cycle Disruption and Lipid Remodeling.Metabolites · 2025Article
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17 authors.
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Abstract
Background: Metabolic dysfunction-associated steatotic liver disease (MASLD), formerly called non-alcoholic fatty liver disease (NAFLD) is the hepatic manifestation of the metabolic syndrome. Although MASLD has been widely studied in persons with Type 2 diabetes (T2D), far less in known about the pathogenesis and severity of MASLD in Type 1 diabetes (T1D). Objectives: Determine metabolic perturbations associated with MASLD in persons with T1D. Study Design: We conducted a cross-sectional study of 30 participants with T1D. Based on the results of a FibroScan, participants were stratified as cases (MASLD) or controls. Metabolomic analyses were performed on plasma obtained from all participants after an overnight (after midnight) fast. Results: 17 of 30 participants were classified as cases (MASLD) and 13 as controls. Cases had higher BMI (p=<0.001) and were taking higher daily insulin doses than controls (p=0.003). Metabolomic analyses revealed that those with MASLD had elevated levels of gluconeogenic substrates pyruvate (p=0.001) and lactate (p=0.043), gluconeogenic amino acids alanine (p<0.001) and glutamate (p=0.004), phenylalanine (p=0.003), and anthranilic acid (p=0.015). Lipidomics revealed, elevated ceramides (P=0.02), diacylglycerols (p=0.0009) and triacylglycerols (P=0.0004) in MASLD group. In those with MASLD, the acylcarnitines, isovalerylcarnitine (CAR.5.0) (P=0.002) and L-Palmitoylcarnitine (CAR.16.0) (P=0.048), were elevated. Pathway analyses using MetaboAnalyst 5.0 Software revealed that, pathways including phenylalanine and tyrosine metabolism, tryptophan metabolism, glucose-alanine cycle, glutamate metabolism, and glutathione metabolism were significantly enriched in those with MASLD. Conclusion: Participants with T1D and MASLD manifest features of insulin resistance and metabolite perturbations suggesting enhanced gluconeogenesis, dysfunctional fat synthesis, and perturbed TCA cycle activity.
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