Metabolic syndrome is a condition characterized by a clustering of metabolic abnormalities associated with an increased risk of type 2 diabetes and cardiovascular disease. An impaired insulin-stimulated myocardial glucose metabolism has been shown to be a risk factor for the development of cardiovascular disease in patients with type 2 diabetes. Whether cardiac insulin resistance occurs in subjects with metabolic syndrome remains uncertain. To investigate this issue, we evaluated myocardial glucose metabolic rate using cardiac dynamic 18F-FDG-PET combined with euglycemic-hyperinsulinemic clamp in three groups: a group of normal glucose tolerant individuals without metabolic syndrome (n = 10), a group of individuals with type 2 diabetes and metabolic syndrome (n = 19), and a group of subjects with type 2 diabetes without metabolic syndrome (n = 6). After adjusting for age and gender, individuals with type 2 diabetes and metabolic syndrome exhibited a significant reduction in insulin-stimulated myocardial glucose metabolic rate (10.5 ± 9.04 μmol/min/100 g) as compared with both control subjects (32.9 ± 9.7 μmol/min/100 g; P < 0.0001) and subjects with type 2 diabetes without metabolic syndrome (25.15 ± 4.92 μmol/min/100 g; P = 0.01). Conversely, as compared with control subjects (13.01 ± 8.53 mg/min x Kg FFM), both diabetic individuals with metabolic syndrome (3.06 ± 1.7 mg/min × Kg FFM, P = 0.008) and those without metabolic syndrome (2.91 ± 1.54 mg/min × Kg FFM, P = 0.01) exhibited a significant reduction in whole-body insulin-stimulated glucose disposal, while no difference was observed between the 2 groups of subjects with type 2 diabetes with or without metabolic syndrome. Univariate correlations showed that myocardial glucose metabolism was positively correlated with insulin-stimulated glucose disposal (r = 0.488, P = 0.003), and negatively correlated with the presence of metabolic syndrome (r = -0.743, P < 0.0001) and with its individual components. In conclusion, our data suggest that an impaired myocardial glucose metabolism may represent an early cardio-metabolic defect in individuals with the coexistence of type 2 diabetes and metabolic syndrome, regardless of whole-body insulin resistance.

Metabolic Syndrome Is Associated With Impaired Insulin-Stimulated Myocardial Glucose Metabolic Rate in Individuals With Type 2 Diabetes. A Cardiac Dynamic 18F-FDG-PET Study / Succurro, Elena; Vizza, Patrizia; Papa, Annalisa; Cicone, Francesco; Monea, Giuseppe; Tradigo, Giuseppe; Fiorentino, Teresa Vanessa; Perticone, Maria; Guzzi, Pietro Hiram; Sciacqua, Angela; Andreozzi, Francesco; Veltri, Pierangelo; Cascini, Giuseppe Lucio; Sesti, Giorgio. - In: FRONTIERS IN CARDIOVASCULAR MEDICINE. - ISSN 2297-055X. - 9:(2022), pp. 1-10. [10.3389/fcvm.2022.924787]

Metabolic Syndrome Is Associated With Impaired Insulin-Stimulated Myocardial Glucose Metabolic Rate in Individuals With Type 2 Diabetes. A Cardiac Dynamic 18F-FDG-PET Study

Vizza, Patrizia;Cicone, Francesco;Sesti, Giorgio
Ultimo
Writing – Original Draft Preparation
2022

Abstract

Metabolic syndrome is a condition characterized by a clustering of metabolic abnormalities associated with an increased risk of type 2 diabetes and cardiovascular disease. An impaired insulin-stimulated myocardial glucose metabolism has been shown to be a risk factor for the development of cardiovascular disease in patients with type 2 diabetes. Whether cardiac insulin resistance occurs in subjects with metabolic syndrome remains uncertain. To investigate this issue, we evaluated myocardial glucose metabolic rate using cardiac dynamic 18F-FDG-PET combined with euglycemic-hyperinsulinemic clamp in three groups: a group of normal glucose tolerant individuals without metabolic syndrome (n = 10), a group of individuals with type 2 diabetes and metabolic syndrome (n = 19), and a group of subjects with type 2 diabetes without metabolic syndrome (n = 6). After adjusting for age and gender, individuals with type 2 diabetes and metabolic syndrome exhibited a significant reduction in insulin-stimulated myocardial glucose metabolic rate (10.5 ± 9.04 μmol/min/100 g) as compared with both control subjects (32.9 ± 9.7 μmol/min/100 g; P < 0.0001) and subjects with type 2 diabetes without metabolic syndrome (25.15 ± 4.92 μmol/min/100 g; P = 0.01). Conversely, as compared with control subjects (13.01 ± 8.53 mg/min x Kg FFM), both diabetic individuals with metabolic syndrome (3.06 ± 1.7 mg/min × Kg FFM, P = 0.008) and those without metabolic syndrome (2.91 ± 1.54 mg/min × Kg FFM, P = 0.01) exhibited a significant reduction in whole-body insulin-stimulated glucose disposal, while no difference was observed between the 2 groups of subjects with type 2 diabetes with or without metabolic syndrome. Univariate correlations showed that myocardial glucose metabolism was positively correlated with insulin-stimulated glucose disposal (r = 0.488, P = 0.003), and negatively correlated with the presence of metabolic syndrome (r = -0.743, P < 0.0001) and with its individual components. In conclusion, our data suggest that an impaired myocardial glucose metabolism may represent an early cardio-metabolic defect in individuals with the coexistence of type 2 diabetes and metabolic syndrome, regardless of whole-body insulin resistance.
2022
cardiac 18f-fdg-pet; cardiovascular disease; insulin resistance; metabolic syndrome; myocardial glucose metabolism; type 2 diabetes
01 Pubblicazione su rivista::01a Articolo in rivista
Metabolic Syndrome Is Associated With Impaired Insulin-Stimulated Myocardial Glucose Metabolic Rate in Individuals With Type 2 Diabetes. A Cardiac Dynamic 18F-FDG-PET Study / Succurro, Elena; Vizza, Patrizia; Papa, Annalisa; Cicone, Francesco; Monea, Giuseppe; Tradigo, Giuseppe; Fiorentino, Teresa Vanessa; Perticone, Maria; Guzzi, Pietro Hiram; Sciacqua, Angela; Andreozzi, Francesco; Veltri, Pierangelo; Cascini, Giuseppe Lucio; Sesti, Giorgio. - In: FRONTIERS IN CARDIOVASCULAR MEDICINE. - ISSN 2297-055X. - 9:(2022), pp. 1-10. [10.3389/fcvm.2022.924787]
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11573/1651006
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