Division of Endocrinology and Metabolism, Department of Internal Medicine, Korea University Guro Hospital, Seoul 152-050, Korea.
J Clin Endocrinol Metab. 2011 Aug;96(8):E1325-9. doi: 10.1210/jc.2011-0620. Epub 2011 Jun 15.
The dysregulation of hepatokines may be associated with the pathogenesis of insulin resistance and type 2 diabetes. A recent study has suggested that selenoprotein P (SeP), a novel hepatokine, may play a role in the regulation of glucose metabolism and insulin sensitivity. We examined the relationship between circulating SeP levels and clinical parameters associated with insulin resistance in humans.
We compared serum SeP concentrations in 100 subjects with diverse glucose tolerance statuses. Furthermore, we evaluated the relationship between SeP and cardiometabolic risk factors including insulin resistance, high-sensitivity C-reactive protein, and carotid intima-media thickness.
Serum SeP concentrations were significantly higher in patients with type 2 diabetes or prediabetes than those with normal glucose tolerance (all P < 0.01) and decreased in a stepwise manner [1032.4 (495.9-2149.4) vs. 867.3 (516.3-1582.7) vs. 362.0 (252.5-694.5), P = 0.004]. In addition, overweight and obese subjects had significantly increased SeP levels compared with lean subjects (P = 0.002). Spearman's partial correlation analysis adjusted for age and gender showed a significant relationship between SeP and cardiometabolic factors including body mass index, waist circumference, systolic blood pressure, triglycerides, glucose, hemoglobin A1c, aspartate aminotransferase, and insulin resistance. Furthermore, in multiple regression analyses, SeP showed an independent association with carotid intima-media thickness as well as high-sensitivity C-reactive protein, even after adjustment for other confounding factors.
Circulating SeP concentrations were elevated in patients with glucose metabolism dysregulation and were related to various cardiometabolic parameters including insulin resistance, inflammation, and atherosclerosis.
肝源激素的失调可能与胰岛素抵抗和 2 型糖尿病的发病机制有关。最近的一项研究表明，新型肝源激素硒蛋白 P（SeP）可能在调节葡萄糖代谢和胰岛素敏感性方面发挥作用。我们研究了循环 SeP 水平与人类胰岛素抵抗相关的临床参数之间的关系。
我们比较了 100 例葡萄糖耐量状态不同的受试者的血清 SeP 浓度。此外，我们评估了 SeP 与包括胰岛素抵抗、高敏 C 反应蛋白和颈动脉内膜中层厚度在内的心血管代谢危险因素之间的关系。
血清 SeP 浓度在 2 型糖尿病或糖尿病前期患者中明显高于糖耐量正常者（均 P < 0.01），且呈逐渐降低趋势[1032.4（495.9-2149.4）比 867.3（516.3-1582.7）比 362.0（252.5-694.5），P = 0.004]。此外，超重和肥胖者的 SeP 水平明显高于非肥胖者（P = 0.002）。经年龄和性别调整的 Spearman 偏相关分析显示，SeP 与心血管代谢因素（包括体重指数、腰围、收缩压、甘油三酯、血糖、糖化血红蛋白、天冬氨酸氨基转移酶和胰岛素抵抗）呈显著相关。此外，在多元回归分析中，SeP 与颈动脉内膜中层厚度和高敏 C 反应蛋白呈独立相关，即使在调整其他混杂因素后也是如此。
循环 SeP 浓度在葡萄糖代谢失调的患者中升高，并与包括胰岛素抵抗、炎症和动脉粥样硬化在内的各种心血管代谢参数相关。
