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Type 2 diabetes mellitus (T2DM) is a chronic metabolic disorder characterized by insulin resistance, in which target tissues such as the liver, muscle, and adipose tissue respond poorly to insulin. It is also associated with inadequate compensatory insulin secretion, where pancreatic β-cells fail to produce sufficient insulin. Together, these abnormalities lead to persistent hyperglycemia.EtiologyT2DM develops through a complex interaction of genetic predisposition and environmental or...
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A Zebrafish Model of Diabetes Mellitus and Metabolic Memory
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Genetics of MASLD: a diabetes perspective.

Josh Bilson1, Hanieh Yaghootkar2,3

  • 1School of Human Development and Health, Faculty of Medicine, University of Southampton, Southampton, UK.

Diabetologia
|June 8, 2026
PubMed
Summary

Genetic factors explain why metabolic dysfunction-associated steatotic liver disease (MASLD) varies in people with type 2 diabetes. Understanding these genetic pathways can improve risk assessment and treatment for MASLD.

Keywords:
GeneticsLiver fatMASLDMetabolic dysfunction-associated steatotic liver diseaseReviewType 2 diabetes

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Area of Science:

  • Genetics and Metabolic Diseases
  • Hepatology
  • Diabetes Research

Background:

  • Metabolic dysfunction-associated steatotic liver disease (MASLD) is common in type 2 diabetes, but its clinical course is unpredictable.
  • Conventional risk factors do not fully explain the heterogeneity of MASLD in diabetic patients.
  • Human genetic studies reveal distinct biological pathways underlying hepatic steatosis and its complications.

Purpose of the Study:

  • To review the genetic architecture of hepatic steatosis and MASLD in the context of type 2 diabetes.
  • To explore how genetic variations influence disease mechanisms, clinical outcomes, and treatment responses.
  • To discuss the translational implications of MASLD genetics for patient management and therapeutic development.

Main Methods:

  • Review of family studies, genome-wide association studies (GWAS), imaging genetics, and Mendelian randomization.
  • Analysis of genetic loci affecting liver fat, disease severity, and progression.
  • Examination of gene-diabetes and gene-environment interactions.

Main Results:

  • Multiple genetic loci influence liver fat accumulation and MASLD progression through diverse mechanisms.
  • Genetic variations contribute to heterogeneous clinical presentations and outcomes in diabetic patients with MASLD.
  • Similar degrees of liver fat can reflect different underlying biological processes with varying clinical implications.

Conclusions:

  • Genetic evidence supports a mechanism-based framework for understanding MASLD heterogeneity in diabetes.
  • Genetics offers a foundation for more precise risk stratification and personalized management strategies.
  • Future research needs ancestry-diverse studies, improved phenotyping, and integration of genetic data into clinical trials.