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
Department of Medical and Surgical Sciences, University Magna Graecia of Catanzaro, Catanzaro, Italy.
Research Center for the Prevention and Treatment of Metabolic Diseases (CR METDIS), University Magna Graecia of Catanzaro, Catanzaro, Italy.
Front Cardiovasc Med. 2022 Jun 29;9:924787. doi: 10.3389/fcvm.2022.924787. eCollection 2022.
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 F-FDG-PET combined with euglycemic-hyperinsulinemic clamp in three groups: a group of normal glucose tolerant individuals without metabolic syndrome ( = 10), a group of individuals with type 2 diabetes and metabolic syndrome ( = 19), and a group of subjects with type 2 diabetes without metabolic syndrome ( = 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; < 0.0001) and subjects with type 2 diabetes without metabolic syndrome (25.15 ± 4.92 μmol/min/100 g; = 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, = 0.008) and those without metabolic syndrome (2.91 ± 1.54 mg/min × Kg FFM, = 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 ( = 0.488, = 0.003), and negatively correlated with the presence of metabolic syndrome ( = -0.743, < 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.
代谢综合征是一种以代谢异常聚集为特征的病症，与2型糖尿病和心血管疾病风险增加相关。胰岛素刺激的心肌葡萄糖代谢受损已被证明是2型糖尿病患者发生心血管疾病的一个危险因素。代谢综合征患者是否存在心脏胰岛素抵抗仍不确定。为了研究这个问题，我们使用心脏动态F-FDG-PET结合正常血糖-高胰岛素钳夹技术，对三组人群的心肌葡萄糖代谢率进行了评估：一组无代谢综合征的糖耐量正常个体（n = 10），一组患有2型糖尿病和代谢综合征的个体（n = 19），以及一组患有2型糖尿病但无代谢综合征的个体（n = 6）。在调整年龄和性别后，患有2型糖尿病和代谢综合征的个体，与对照组受试者（32.9±9.7μmol/min/100g；P < 0.0001）和患有2型糖尿病但无代谢综合征的个体（25.15±4.92μmol/min/100g；P = 0.01）相比，胰岛素刺激的心肌葡萄糖代谢率显著降低（10.5±9.04μmol/min/100g）。相反，与对照组受试者（13.01±8.53mg/min×Kg FFM）相比，患有代谢综合征的糖尿病个体（3.06±1.7mg/min×Kg FFM，P = 0.008）和无代谢综合征的糖尿病个体（2.91±1.54mg/min×Kg FFM，P = 0.01）全身胰岛素刺激的葡萄糖处置均显著降低，而两组患有或不患有代谢综合征的2型糖尿病受试者之间未观察到差异。单变量相关性分析表明，心肌葡萄糖代谢与胰岛素刺激的葡萄糖处置呈正相关（r = 第0.488页，P = 0.003），与代谢综合征的存在呈负相关（r = -0.743，P < 0.0001），并与其各个组分呈负相关。总之，我们的数据表明，心肌葡萄糖代谢受损可能代表2型糖尿病和代谢综合征并存个体的一种早期心脏代谢缺陷，而与全身胰岛素抵抗无关。
