Identification of Myocardial Insulin Resistance by Using Liver Tests : A Simple Approach for Clinical Practice
Herance, José Raul (Hospital Universitari Vall d'Hebron. Institut de Recerca)
Martín-Saladich, Queralt (Universitat Pompeu Fabra. Departament de Tecnologies de la Informació i les Comunicacions)
Velásquez, Mayra Alejandra (Hospital Universitari Vall d'Hebron. Institut de Recerca)
Hernández, Cristina (Hospital Universitari Vall d'Hebron. Institut de Recerca)
Aparicio-Gómez, Carolina (Hospital Universitari Vall d'Hebron. Institut de Recerca)
Ramírez Serra, Clara (Hospital Universitari Vall d'Hebron. Institut de Recerca)
Ferrer Costa, Roser (Hospital Universitari Vall d'Hebron. Institut de Recerca)
Giralt-Arnaiz, Marina (Hospital Universitari Vall d'Hebron. Institut de Recerca)
González Ballester, Miguel Ángel 1973- (Universitat Pompeu Fabra. Departament de Tecnologies de la Informació i les Comunicacions)
Pericàs, Juan M. (Hospital Universitari Vall d'Hebron. Institut de Recerca)
Castell-Conesa, Joan (Hospital Universitari Vall d'Hebron. Institut de Recerca)
Aguadé-Bruix, Santiago (Hospital Universitari Vall d'Hebron. Institut de Recerca)
Simó Canonge, Rafael (Hospital Universitari Vall d'Hebron. Institut de Recerca)
Universitat Autònoma de Barcelona

Date:	2022
Abstract:	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.
Grants:	Ministerio de Economía y Competitividad PI16/02064 Instituto de Salud Carlos III PI20/01588 Agència de Gestió d'Ajuts Universitaris i de Recerca 2017/SGR-1303
Rights:	Aquest document està subjecte a una llicència d'ús Creative Commons. Es permet la reproducció total o parcial, la distribució, la comunicació pública de l'obra i la creació d'obres derivades, fins i tot amb finalitats comercials, sempre i quan es reconegui l'autoria de l'obra original.
Language:	Anglès
Document:	Article ; recerca ; Versió publicada
Subject:	Type 2 diabetes ; Myocardial insulin resistance ; Non-alcoholic fatty liver disease ; Cardiovascular risk
Published in:	International journal of molecular sciences, Vol. 23 (august 2022) , ISSN 1422-0067

DOI: 10.3390/ijms23158783
PMID: 35955920

12 p, 2.2 MB

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