Observational studyEuropean journal of clinical investigation2025
Phenotypic patterns of metabolic dysfunction-associated steatotic liver disease in type 2 diabetes: The impact of insulin.
Observational study in European journal of clinical investigation, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT02248311 ("Preventing Cardiovascular Ischemic Events and Arresting Their Consequences in Type 2 Diabetic Population), which is not on this map. Cited by 6 papers.
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The trial behind it
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"Preventing Cardiovascular Ischemic Events and Arresting Their Consequences in Type 2 Diabetic Population: a Multidisciplinary Clinical and Experimental Approach" (PRECISED)
Who cites it
6 citing papers in PubMed.
- Metabolic phenotype stratification identifies patients at high risk of poor glycemic control in type 2 diabetes mellitus: Insights into hepatic metabolic dysfunction.BMC endocrine disorders · 2026Article
- Iron-related intercellular communication in the liver: Main players and mechanisms.European journal of clinical investigation · 2026Review
- Disentangling metabolic impairment in the liver-heart axis: tissue-specific insulin sensitivity in type 2 diabetes.Frontiers in endocrinology · 2026Article
- First-trimester fatty liver index and hepatic steatosis index independently predict gestational diabetes risk: a prospective cohort study.Frontiers in nutrition · 2026Article
- Phenotypic patterns of metabolic dysfunction-associated steatotic liver disease in type 2 diabetes: The impact of insulin.European journal of clinical investigation · 2025Observational
- ALT/AST ratio as an early marker of metabolic multimorbidity in young adults: A community-based study.Journal of multimorbidity and comorbidityArticle
Corrections and comments
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Authors and funding
13 authors.
Funding
Abstract
backgroundMetabolic dysfunction-associated steatotic liver disease (MASLD) often leads to hepatic insulin resistance (IR), yet its link to liver-specific insulin-mediated glucose uptake (IGLU) in type 2 diabetes (T2D) remains unclear. We aimed to explore this MASLD-T2D relationship, addressing organ-specific IR for personalized management and risk prevention.
methodsThis cross-sectional study included 41 T2D participants enrolled in a clinical trial (NCT02248311) undergoing biochemical analyses, anthropometric measurements and [
findingsTwo MASLD-T2D phenotypes were identified according to their IGLU patterns, that is, with low (HepGluc[+], n = 21) and with high (HepGluc[-], n = 20) hepatic response to insulin. HepGluc[+] participants exhibited increased systemic IR (HOMA-IR, p = .012), inflammation (interleukin 6, p = .005); alanine and aspartate aminotransferase ALT, AST (p = .015 and p = .007); gamma-glutamyl transferase GGT (p = .019) and steatosis markers (liver volume, p = .006); NAFLD liver fat score, p = .0017; hepatic steatosis index, p = .02; fatty liver index, p = .008; liver stiffness measurements (LSM) (p = .049). No statistical differences in serum-based liver fibrosis scores were shown. To identify MASLD-T2D phenotypes in a friendly manner, the MASLD-T2D score based on support vector machines was developed using AST, ALT and GGT (AUC = .83), as well as with MASLD indices including LSM and NAFLD liver fat score (AUC = .90). IMPLICATIONS: Two new MASLD-T2D phenotypes have been identified, HepGluc[+] and HepGluc[-], according to IGLU patterns, with HepGluc[+] being more deleterious due to higher systemic IR, steatosis and inflammation. Phenotypes can be identified using a new function, the MASLD-T2D score.
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