ArticleDiabetology & metabolic syndrome2025
Insulin resistance aggravates myocardial fibrosis in non-diabetic hypertensive patients by altering the function of epicardial adipose tissue: a cardiac magnetic resonance study.
Article in Diabetology & metabolic syndrome, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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4 citing papers in PubMed.
- Immunometabolic Organ Crosstalk in Heart Failure with Preserved Ejection Fraction: The Role of Dietary Patterns in Obesity-Related Inflammation.Nutrients · 2026Review
- Oxidative Stress in Diabetic Cardiomyopathy: Molecular Mechanisms and Emerging Therapeutic Targets.Biomolecules · 2026Review
- Heart-guarding or heart-harming? The dual role of epicardial adipose tissue in cardiovascular health and disease.International journal of obesity (2005) · 2025Review
- The Role of Iron Homeostasis Imbalance in T2DM-Associated Cognitive Dysfunction: A Prospective Cohort Study Utilizing Quantitative Susceptibility Mapping.Human brain mapping · 2025Article
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11 authors.
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Abstract
backgroundThe effect of insulin resistance (IR) on epicardial adipose tissue (EAT) remains uncertain. This study aimed to investigate how early-stage IR influences EAT, contributing to myocardial fibrosis and left ventricular dysfunction in non-diabetic patients with hypertension.
methodsA total of 166 hypertensive patients who underwent cardiovascular magnetic resonance (CMR) treatment at two medical centers in China from June 2015 to August 2024 were included. Triglyceride-glucose index (TyG) was calculated, cardiac MRI parameters and EAT were measured. Patients were divided into two groups based on the median TyG. Binary logistic regression model, subgroup analysis and causal mediation analysis were used to evaluate the correlation between EAT, TyG and CMR parameters. Thirty healthy volunteers served as the control group.
resultsThe high TyG group exhibited greater EAT volume, higher Native T1, and increased ECV (All P < 0.001) compared to the low TyG group. Additionally, significant differences were observed in GRS (P = 0.025), GLS (P = 0.015), and GCS (P = 0.048). Binary logistic regression analysis indicated that TyG and indexed EAT volume were independently associated with high ECV value (TyG: OR 2.808, p = 0.002;indexed EAT volume: OR 1.038, p = 0.002), with results remaining stable after adjusting for confounding factors. Mediation analysis showed that even after adjusting for confounding factors, EAT continued to play a role in TyG-mediated ECV (indirect effect: 0.8844, [95% CI 0.4539-1.3666]).
conclusionsIR in non-diabetic individuals at an early stage may change the physiological function of EAT and lead to the onset of myocardial fibrosis. Addressing IR early on could potentially improve the physiological function of EAT.
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