Association of Epicardial Adipose Tissue with Novel Inflammation and Heart Failure Biomarkers in Type 2 Diabetes Patients: Effect of Metabolic Control

Background: Type 2 diabetes (T2D patients) have a 74% increased risk of heart failure (HF), but traditional HF biomarkers lack sensitivity in early disease detection. Increased epicardial adipose tissue volume (EATv) is associated with cardiovascular risk in T2D, and novel biomarkers such as growth...

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Published in	Journal of clinical medicine Vol. 14; no. 13; p. 4687
Main Authors	Gil-Millan, Pedro, Rives, José, Viladés, David, García-Osuna, Álvaro, Genua, Idoia, Miñambres, Inka, Grau-Agramunt, Margarita, Gich, Ignasi, Camacho, Mercedes, Benitez, Sonia, Julve, Josep, Sánchez-Quesada, José Luis, Pérez, Antonio
Format	Journal Article
Language	English
Published	Switzerland MDPI AG 02.07.2025 MDPI
Subjects	Adipose tissues Biological markers Biomarkers Body fat Body mass index Complications and side effects Correlation analysis Creatinine Diabetes Ejection fraction Health aspects Heart failure Inflammation Insulin resistance Lipids Metabolism Optimization Oxidative stress Pericardium Risk factors Software Type 2 diabetes Spain United States > US heart failure (HF) GDF15 metabolic control (MC) Galectin-3 cardiovascular risk inflammatory biomarkers sST2 type 2 diabetes (T2D) epicardial adipose tissue (EAT)
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ISSN	2077-0383 2077-0383
DOI	10.3390/jcm14134687

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Abstract	Background: Type 2 diabetes (T2D patients) have a 74% increased risk of heart failure (HF), but traditional HF biomarkers lack sensitivity in early disease detection. Increased epicardial adipose tissue volume (EATv) is associated with cardiovascular risk in T2D, and novel biomarkers such as growth differentiation factor 15 (GDF15), Galectin-3, and soluble suppression of tumorigenicity 2 (sST2) are inflammation biomarkers linked to HF. Methods: We investigated associations between EATv, inflammation biomarkers, and the effect of metabolic control in 14 healthy controls (HCs) and 36 newly diagnosed T2D patients both before (poor glycemic control, PGC) and after 12 months of glycemic optimization (good glycemic control, GGC). EATv indexed to body surface area (iEATv) was quantified by multidetector computed tomography, and biomarker levels were measured by immunoassays. Results: PGC patients had higher iEATv (59.53 ± 21.67 vs. 36.84 ± 16.57 cm3/m2, p = 0.0017) and elevated GDF15, Galectin-3, and sST2 levels (all p < 0.05) than HC subjects. The glycemic optimization reduced iEATv (p = 0.0232) and sST2 (p = 0.048), while GDF15 and Galectin-3 remained unchanged. Multivariable analysis confirmed independent associations between iEATv, GDF15 (β = 0.27, p = 0.027) and sST2 (β = 0.29, p = 0.02). Conclusions: These results support the link between systemic inflammation, EAT expansion, and cardiac dysfunction, and they point to the role of epicardial fat in early HF risk of T2D patients.
AbstractList	Background: Type 2 diabetes (T2D patients) have a 74% increased risk of heart failure (HF), but traditional HF biomarkers lack sensitivity in early disease detection. Increased epicardial adipose tissue volume (EATv) is associated with cardiovascular risk in T2D, and novel biomarkers such as growth differentiation factor 15 (GDF15), Galectin-3, and soluble suppression of tumorigenicity 2 (sST2) are inflammation biomarkers linked to HF. Methods: We investigated associations between EATv, inflammation biomarkers, and the effect of metabolic control in 14 healthy controls (HCs) and 36 newly diagnosed T2D patients both before (poor glycemic control, PGC) and after 12 months of glycemic optimization (good glycemic control, GGC). EATv indexed to body surface area (iEATv) was quantified by multidetector computed tomography, and biomarker levels were measured by immunoassays. Results: PGC patients had higher iEATv (59.53 ± 21.67 vs. 36.84 ± 16.57 cm3/m2, p = 0.0017) and elevated GDF15, Galectin-3, and sST2 levels (all p < 0.05) than HC subjects. The glycemic optimization reduced iEATv (p = 0.0232) and sST2 (p = 0.048), while GDF15 and Galectin-3 remained unchanged. Multivariable analysis confirmed independent associations between iEATv, GDF15 (β = 0.27, p = 0.027) and sST2 (β = 0.29, p = 0.02). Conclusions: These results support the link between systemic inflammation, EAT expansion, and cardiac dysfunction, and they point to the role of epicardial fat in early HF risk of T2D patients. Background : Type 2 diabetes (T2D patients) have a 74% increased risk of heart failure (HF), but traditional HF biomarkers lack sensitivity in early disease detection. Increased epicardial adipose tissue volume (EATv) is associated with cardiovascular risk in T2D, and novel biomarkers such as growth differentiation factor 15 (GDF15), Galectin-3, and soluble suppression of tumorigenicity 2 (sST2) are inflammation biomarkers linked to HF. Methods : We investigated associations between EATv, inflammation biomarkers, and the effect of metabolic control in 14 healthy controls (HCs) and 36 newly diagnosed T2D patients both before (poor glycemic control, PGC) and after 12 months of glycemic optimization (good glycemic control, GGC). EATv indexed to body surface area (iEATv) was quantified by multidetector computed tomography, and biomarker levels were measured by immunoassays. Results : PGC patients had higher iEATv (59.53 ± 21.67 vs. 36.84 ± 16.57 cm[sup.3] /m[sup.2] , p = 0.0017) and elevated GDF15, Galectin-3, and sST2 levels (all p < 0.05) than HC subjects. The glycemic optimization reduced iEATv (p = 0.0232) and sST2 (p = 0.048), while GDF15 and Galectin-3 remained unchanged. Multivariable analysis confirmed independent associations between iEATv, GDF15 (β = 0.27, p = 0.027) and sST2 (β = 0.29, p = 0.02). Conclusions : These results support the link between systemic inflammation, EAT expansion, and cardiac dysfunction, and they point to the role of epicardial fat in early HF risk of T2D patients. Background : Type 2 diabetes (T2D patients) have a 74% increased risk of heart failure (HF), but traditional HF biomarkers lack sensitivity in early disease detection. Increased epicardial adipose tissue volume (EATv) is associated with cardiovascular risk in T2D, and novel biomarkers such as growth differentiation factor 15 (GDF15), Galectin-3, and soluble suppression of tumorigenicity 2 (sST2) are inflammation biomarkers linked to HF. Methods : We investigated associations between EATv, inflammation biomarkers, and the effect of metabolic control in 14 healthy controls (HCs) and 36 newly diagnosed T2D patients both before (poor glycemic control, PGC) and after 12 months of glycemic optimization (good glycemic control, GGC). EATv indexed to body surface area (iEATv) was quantified by multidetector computed tomography, and biomarker levels were measured by immunoassays. Results : PGC patients had higher iEATv (59.53 ± 21.67 vs. 36.84 ± 16.57 cm 3 /m 2 , p = 0.0017) and elevated GDF15, Galectin-3, and sST2 levels (all p < 0.05) than HC subjects. The glycemic optimization reduced iEATv ( p = 0.0232) and sST2 ( p = 0.048), while GDF15 and Galectin-3 remained unchanged. Multivariable analysis confirmed independent associations between iEATv, GDF15 (β = 0.27, p = 0.027) and sST2 (β = 0.29, p = 0.02). Conclusions : These results support the link between systemic inflammation, EAT expansion, and cardiac dysfunction, and they point to the role of epicardial fat in early HF risk of T2D patients. Background: Type 2 diabetes (T2D patients) have a 74% increased risk of heart failure (HF), but traditional HF biomarkers lack sensitivity in early disease detection. Increased epicardial adipose tissue volume (EATv) is associated with cardiovascular risk in T2D, and novel biomarkers such as growth differentiation factor 15 (GDF15), Galectin-3, and soluble suppression of tumorigenicity 2 (sST2) are inflammation biomarkers linked to HF. Methods: We investigated associations between EATv, inflammation biomarkers, and the effect of metabolic control in 14 healthy controls (HCs) and 36 newly diagnosed T2D patients both before (poor glycemic control, PGC) and after 12 months of glycemic optimization (good glycemic control, GGC). EATv indexed to body surface area (iEATv) was quantified by multidetector computed tomography, and biomarker levels were measured by immunoassays. Results: PGC patients had higher iEATv (59.53 ± 21.67 vs. 36.84 ± 16.57 cm3/m2, p = 0.0017) and elevated GDF15, Galectin-3, and sST2 levels (all p < 0.05) than HC subjects. The glycemic optimization reduced iEATv (p = 0.0232) and sST2 (p = 0.048), while GDF15 and Galectin-3 remained unchanged. Multivariable analysis confirmed independent associations between iEATv, GDF15 (β = 0.27, p = 0.027) and sST2 (β = 0.29, p = 0.02). Conclusions: These results support the link between systemic inflammation, EAT expansion, and cardiac dysfunction, and they point to the role of epicardial fat in early HF risk of T2D patients.Background: Type 2 diabetes (T2D patients) have a 74% increased risk of heart failure (HF), but traditional HF biomarkers lack sensitivity in early disease detection. Increased epicardial adipose tissue volume (EATv) is associated with cardiovascular risk in T2D, and novel biomarkers such as growth differentiation factor 15 (GDF15), Galectin-3, and soluble suppression of tumorigenicity 2 (sST2) are inflammation biomarkers linked to HF. Methods: We investigated associations between EATv, inflammation biomarkers, and the effect of metabolic control in 14 healthy controls (HCs) and 36 newly diagnosed T2D patients both before (poor glycemic control, PGC) and after 12 months of glycemic optimization (good glycemic control, GGC). EATv indexed to body surface area (iEATv) was quantified by multidetector computed tomography, and biomarker levels were measured by immunoassays. Results: PGC patients had higher iEATv (59.53 ± 21.67 vs. 36.84 ± 16.57 cm3/m2, p = 0.0017) and elevated GDF15, Galectin-3, and sST2 levels (all p < 0.05) than HC subjects. The glycemic optimization reduced iEATv (p = 0.0232) and sST2 (p = 0.048), while GDF15 and Galectin-3 remained unchanged. Multivariable analysis confirmed independent associations between iEATv, GDF15 (β = 0.27, p = 0.027) and sST2 (β = 0.29, p = 0.02). Conclusions: These results support the link between systemic inflammation, EAT expansion, and cardiac dysfunction, and they point to the role of epicardial fat in early HF risk of T2D patients. : Type 2 diabetes (T2D patients) have a 74% increased risk of heart failure (HF), but traditional HF biomarkers lack sensitivity in early disease detection. Increased epicardial adipose tissue volume (EATv) is associated with cardiovascular risk in T2D, and novel biomarkers such as growth differentiation factor 15 (GDF15), Galectin-3, and soluble suppression of tumorigenicity 2 (sST2) are inflammation biomarkers linked to HF. : We investigated associations between EATv, inflammation biomarkers, and the effect of metabolic control in 14 healthy controls (HCs) and 36 newly diagnosed T2D patients both before (poor glycemic control, PGC) and after 12 months of glycemic optimization (good glycemic control, GGC). EATv indexed to body surface area (iEATv) was quantified by multidetector computed tomography, and biomarker levels were measured by immunoassays. : PGC patients had higher iEATv (59.53 ± 21.67 vs. 36.84 ± 16.57 cm /m , = 0.0017) and elevated GDF15, Galectin-3, and sST2 levels (all < 0.05) than HC subjects. The glycemic optimization reduced iEATv ( = 0.0232) and sST2 ( = 0.048), while GDF15 and Galectin-3 remained unchanged. Multivariable analysis confirmed independent associations between iEATv, GDF15 (β = 0.27, = 0.027) and sST2 (β = 0.29, = 0.02). : These results support the link between systemic inflammation, EAT expansion, and cardiac dysfunction, and they point to the role of epicardial fat in early HF risk of T2D patients.
Audience	Academic
Author	García-Osuna, Álvaro Benitez, Sonia Gil-Millan, Pedro Julve, Josep Pérez, Antonio Viladés, David Sánchez-Quesada, José Luis Grau-Agramunt, Margarita Gich, Ignasi Rives, José Miñambres, Inka Camacho, Mercedes Genua, Idoia
AuthorAffiliation	11 CIBER of Diabetes and Metabolic Diseases (CIBERDEM), 28029 Madrid, Spain 6 CIBER of Cardiovascular Diseases (CIBERCV), 28029 Madrid, Spain; mcamacho@santpau.cat 1 Endocrinology Department, Hospital de la Santa Creu i Sant Pau, 08041 Barcelona, Spain; pedroalejandro.gil@vallhebron.cat (P.G.-M.); igenua@santpau.cat (I.G.); iminambres@santpau.cat (I.M.) 8 CIBER Epidemiología y Salud Pública (CIBERESP), 28029 Madrid, Spain 2 Department of Medicine, Universitat Autònoma de Barcelona, 08193 Barcelona, Spain 4 Department of Biochemistry and Molecular Biology, Universitat Autònoma de Barcelona, 08193 Barcelona, Spain 7 Epidemiology Department, Hospital de la Santa Creu i Sant Pau, 08041 Barcelona, Spain; igichs@santpau.cat 10 Endocrinology, Institut de Recerca Sant Pau (IR-Sant Pau), 08041 Barcelona, Spain; jjulve@santpau.cat 9 Genomic Complex Diseases, Institut de Recerca Sant Pau (IR-Sant Pau), 08041 Barcelona, Spain 3 Cardiovascular Biochemistry, Institut de Recerca Sant Pau (IR-Sant Pau), 08041
AuthorAffiliation_xml	– name: 2 Department of Medicine, Universitat Autònoma de Barcelona, 08193 Barcelona, Spain – name: 3 Cardiovascular Biochemistry, Institut de Recerca Sant Pau (IR-Sant Pau), 08041 Barcelona, Spain; jrives@santpau.cat (J.R.); agarciao@santpau.cat (Á.G.-O.); mgrauag@santpau.cat (M.G.-A.); sbenitez@santpau.cat (S.B.) – name: 8 CIBER Epidemiología y Salud Pública (CIBERESP), 28029 Madrid, Spain – name: 4 Department of Biochemistry and Molecular Biology, Universitat Autònoma de Barcelona, 08193 Barcelona, Spain – name: 9 Genomic Complex Diseases, Institut de Recerca Sant Pau (IR-Sant Pau), 08041 Barcelona, Spain – name: 11 CIBER of Diabetes and Metabolic Diseases (CIBERDEM), 28029 Madrid, Spain – name: 6 CIBER of Cardiovascular Diseases (CIBERCV), 28029 Madrid, Spain; mcamacho@santpau.cat – name: 10 Endocrinology, Institut de Recerca Sant Pau (IR-Sant Pau), 08041 Barcelona, Spain; jjulve@santpau.cat – name: 7 Epidemiology Department, Hospital de la Santa Creu i Sant Pau, 08041 Barcelona, Spain; igichs@santpau.cat – name: 1 Endocrinology Department, Hospital de la Santa Creu i Sant Pau, 08041 Barcelona, Spain; pedroalejandro.gil@vallhebron.cat (P.G.-M.); igenua@santpau.cat (I.G.); iminambres@santpau.cat (I.M.) – name: 5 Cardiology Department, Hospital de la Santa Creu i Sant Pau, 08041 Barcelona, Spain; dvilades@santpau.cat
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Keywords	heart failure (HF) GDF15 metabolic control (MC) Galectin-3 cardiovascular risk inflammatory biomarkers sST2 type 2 diabetes (T2D) epicardial adipose tissue (EAT)
Language	English
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Snippet	Background: Type 2 diabetes (T2D patients) have a 74% increased risk of heart failure (HF), but traditional HF biomarkers lack sensitivity in early disease... : Type 2 diabetes (T2D patients) have a 74% increased risk of heart failure (HF), but traditional HF biomarkers lack sensitivity in early disease detection.... Background : Type 2 diabetes (T2D patients) have a 74% increased risk of heart failure (HF), but traditional HF biomarkers lack sensitivity in early disease... Background : Type 2 diabetes (T2D patients) have a 74% increased risk of heart failure (HF), but traditional HF biomarkers lack sensitivity in early disease...
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SubjectTerms	Adipose tissues Biological markers Biomarkers Body fat Body mass index Complications and side effects Correlation analysis Creatinine Diabetes Ejection fraction Health aspects Heart failure Inflammation Insulin resistance Lipids Metabolism Optimization Oxidative stress Pericardium Risk factors Software Type 2 diabetes
Title	Association of Epicardial Adipose Tissue with Novel Inflammation and Heart Failure Biomarkers in Type 2 Diabetes Patients: Effect of Metabolic Control
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