Clinica Medica-Department of Medical, Surgical and Health Sciences, University of Trieste, Trieste, Italy.
Obesity (Silver Spring). 2012 Dec;20(12):2348-53. doi: 10.1038/oby.2012.121. Epub 2012 May 4.
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 (HOMA(IR))-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 HOMA(IR) and plasma adipokines, but lower T- and Desacyl-Ghrelin and higher Acyl-Ghrelin. Obesity (BMI > 30) was associated with higher HOMA(IR), lower adiponectin, and higher leptin (P < 0.05) similarly in ACS and non-ACS subjects. In ACS (n = 60) HOMA(IR) 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 HOMA(IR). 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.
葡萄糖代谢改变可使急性冠状动脉综合征（ACS）患者的预后恶化。在一般人群中，胰岛素抵抗通常与 BMI 的增加有关，这些关联可能涉及与肥胖相关的循环 ghrelin 和脂肪因子的变化。我们旨在研究 BMI、胰岛素抵抗与 ACS 之间的相互作用及其与血浆 ghrelin 和脂肪因子浓度的关系。在 60 名非糖尿病 ACS 患者和 44 名年龄、性别和 BMI 匹配的无 ACS 患者中，测量了胰岛素抵抗的稳态模型评估（HOMA(IR))-胰岛素抵抗指数、血浆脂联素、瘦素、总（T-Ghrelin）、酰化（Acyl-Ghrelin）和去酰化 ghrelin（Desacyl-Ghrelin）。与非 ACS 患者相比，ACS 患者的 HOMA(IR)和血浆脂肪因子相似，但 T-Ghrelin 和 Desacyl-Ghrelin 水平较低，Acyl-Ghrelin 水平较高。肥胖（BMI>30）与 ACS 和非 ACS 患者的 HOMA(IR)升高、脂联素降低和瘦素升高有关（P<0.05）。在 ACS 患者（n=60）中，HOMA(IR)与脂联素呈负相关，与瘦素呈正相关，与 BMI 和 C 反应蛋白（CRP）独立相关（P<0.05）。另一方面，低 T-Ghrelin 和 Desacyl-Ghrelin 伴高 Acyl-Ghrelin 特征在肥胖和非肥胖 ACS 患者中均存在，且与 HOMA(IR)无关。总之，在 ACS 患者中，肥胖和肥胖相关的血浆瘦素和脂联素变化与胰岛素抵抗呈负相关，并可能导致其恶化。然而，ACS 本身并不能增加肥胖对胰岛素敏感性的负面影响。高酰化和低去酰化 ghrelin 特征在 ACS 患者中与肥胖无关，但与胰岛素敏感性无关。
