ArticleCureus2024
The Bidirectional Relationship Between Type 2 Diabetes and Metabolic Dysfunction-Associated Steatotic Liver Disease: A Retrospective Cohort Study.
Article in Cureus, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed.
- Key Hepatokines Linking MASLD and Type 2 Diabetes: From Pathophysiological Mechanisms to Therapeutic Modulation.International journal of molecular sciences · 2026Review
- Hepatogenous diabetes in the era of precision medicine: diagnosis, management, and future directions.Clinical and experimental medicine · 2026Review
- Metabolic dysfunction-associated steatotic liver disease as a systemic disorder: extrahepatic manifestations and the need for data-driven phenotyping.Frontiers in endocrinology · 2026Review
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Introduction Type 2 diabetes (T2D) and metabolic dysfunction-associated steatotic liver disease (MASLD) have shared pathophysiology. We aim to explore associations between these diseases and the impact of T2D therapies on MASLD-related outcomes in a real-world population. Methods A retrospective cohort study included 153 patients with biopsy-proven MASLD. Health records were reviewed for biochemical or radiological changes over follow-up and compared by T2D status. The rate of incident T2D was determined, and in those with T2D, the changes over follow-up were compared by prescribed treatment. The statistical significance of changes over follow-up was evaluated by Student's t-test, and logistic regression was undertaken to determine the impact of variables on T2D development. Results One hundred and fifty-three patients were included with a mean follow-up of 48.0±22.0 months. Patients with T2D (n=73) were older than patients without T2D (n=80; 56.3 vs 51.9 years, p<0.05). Patients with T2D had a greater stage of hepatic fibrosis (2.6 vs 1.7, p<0.001). Nine (12.3%) patients with T2D and four (5.0%) without T2D died during follow-up (p=0.10). Patients without T2D had greater glycosylated haemoglobin (HbA1c) over follow-up (3.0 mmol/mol, p<0.01), and 21 (26.3%) developed T2D. Patients with T2D treated with sodium-glucose transporter-2 inhibitors (SGLT-2i) and/or glucagon-like peptide-1 receptor analogues (GLP-1RA) had a reduction in FibroScan®-controlled attenuation parameter (-33.7dB/m, p<0.001) but not liver stiffness measure. There were no significant FibroScan® changes in those receiving other treatments. Conclusions Patients with T2D had greater hepatic fibrosis, and one in four patients with MASLD developed T2D over four years. Treatment with SGLT-2i and/or GLP-1RA in patients with T2D is associated with improved measures of steatosis but not fibrosis.
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