Related Experiment Video
Updated: Sep 1, 2025

Assessing Insulin Clearance in Mice via In Situ Liver Perfusion
Published on: December 13, 2024
Identification of Myocardial Insulin Resistance by Using Liver Tests: A Simple Approach for Clinical Practice
José Raúl Herance1,2, Queralt Martín-Saladich1,3, Mayra Alejandra Velásquez4
1Medical Molecular Imaging Research Group, Vall d'Hebron Research Institute (VHIR), Nuclear Medicine, Radiology and Cardiology Departments, Vall d'Hebron University Hospital, Autonomous University Barcelona, 08035 Barcelona, Spain.
Background:
We report that myocardial insulin resistance (mIR) occurs in around 60% of patients with type 2 diabetes (T2D) and was associated with higher cardiovascular risk in comparison with patients with insulin-sensitive myocardium (mIS). These two phenotypes (mIR vs. mIS) can only be assessed using time-consuming and expensive methods. The aim of the present study is to search a simple and reliable surrogate to identify both phenotypes.
Methods:
Forty-seven patients with T2D underwent myocardial [18F]FDG PET/CT at baseline and after a hyperinsulinemic-euglycemic clamp (HEC) to determine mIR were prospectively recruited. Biochemical assessments were performed before and after the HEC. Baseline hepatic steatosis index and index of hepatic fibrosis (FIB-4) were calculated. Furthermore, liver stiffness measurement was performed using transient elastography.
Results:
The best model to predict the presence of mIR was the combination of transaminases, protein levels, FIB-4 score and HOMA (AUC = 0.95; sensibility: 0.81; specificity: 0.95). We observed significantly higher levels of fibrosis in patients with mIR than in those with mIS (p = 0.034). In addition, we found that patients with mIR presented a reduced glucose uptake by the liver in comparison with patients with mIS.
Conclusions:
The combination of HOMA, protein, transaminases and FIB-4 is a simple and reliable tool for identifying mIR in patients with T2D. This information will be useful to improve the stratification of cardiovascular risk in T2D.

