Adipokines,Ghrelin and Obesity‐Associated Insulin Resistance in Nondiabetic Patients with Acute Coronary Syndrome |
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| Authors: | Rocco Barazzoni Aneta Aleksova Ilaria Armellini Maria Rosa Cattin Michela Zanetti Cosimo Carriere Mauro Giacca Franca Dore Gianfranco Guarnieri Gianfranco Sinagra |
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| Institution: | 1. Clinica Medica—Department of Medical, Surgical and Health Sciences, University of Trieste, Trieste, Italy;2. Division of Cardiology, Azienda Ospedaliero‐Universitaria Ospedali Riuniti, Trieste, Italy;3. Molecular Medicine Laboratory, International Center for Genetic Engineering and Biotechnology—ICGEB, Trieste, Italy;4. Division of Nuclear Medicine, Azienda Ospedaliero‐Universitaria Ospedali Riuniti, Trieste, Italy |
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| Abstract: | Altered glucose metabolism negatively modulates outcome in acute coronary syndromes (ACS). Insulin resistance is commonly associated with increasing BMI in the general population and these associations may involve obesity‐related changes in circulating ghrelin and adipokines. We aimed at investigating interactions between BMI, insulin resistance and ACS and their associations with plasma ghrelin and adipokine concentrations. Homeostasis model assessment of insulin resistance (HOMAIR)‐insulin resistance index, plasma adiponectin, leptin, total (T‐Ghrelin), acylated (Acyl‐Ghrelin), and desacylated ghrelin (Desacyl‐Ghrelin) were measured in 60 nondiabetic ACS patients and 44 subjects without ACS matched for age, sex, and BMI. Compared with non‐ACS, ACS patients had similar HOMAIR and plasma adipokines, but lower T‐ and Desacyl‐Ghrelin and higher Acyl‐Ghrelin. Obesity (BMI > 30) was associated with higher HOMAIR, lower adiponectin, and higher leptin (P < 0.05) similarly in ACS and non‐ACS subjects. In ACS (n = 60) HOMAIR remained associated negatively with adiponectin and positively with leptin independently of BMI and c‐reactive protein (CRP) (P < 0.05). On the other hand, low T‐ and Desacyl‐Ghrelin with high Acyl‐Ghrelin characterized both obese and non‐obese ACS patients and were not associated with HOMAIR. In conclusion, in ACS patients, obesity and obesity‐related changes in plasma leptin and adiponectin are associated with and likely contribute to negatively modulate insulin resistance. ACS per se does not however enhance the negative impact of obesity on insulin sensitivity. High acylated and low desacylated ghrelin characterize ACS patients independently of obesity, but are not associated with insulin sensitivity. |
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