Department of Endocrinology, Shanxi DAYI Hospital, Shanxi Medical University, Taiyuan, China.
Department of Central Laboratory, Taiyuan Central Hospital, Shanxi Medical University, Taiyuan, China.
Sci Rep. 2018 Sep 10;8(1):13542. doi: 10.1038/s41598-018-31923-3.
Insulin resistance (IR) is the main pathogenesis of metabolic syndrome and a shared pathophysiological change in conditions such as diabetes mellitus, adiposity, hypertension, and atherosclerosis. Visceral adipose tissue-derived serpin (Vaspin) is a newly discovered adipocytokine with insulin-sensitizing and anti-inflammatory effects. To examine if vaspin can improve insulin resistance in rats fed a high-fat diet via the insulin receptor substrate/phosphatidylinositol 3 kinase/protein kinase B/glucose transport (IRS/PI3K/Akt/Glut) and inhibitory κB alpha/nuclear factor-kappa B (IκBα/NF-κB) signalling pathways, thirty male Sprague-Dawley (SD) rats were randomly divided into three groups: the normal control group (NC group, n = 10), high-fat diet group (HFD group, n = 10) and vaspin intervention group (HFD + vaspin group, n = 10). Results showed that intervention with vaspin significantly decreased fasting blood glucose (FBG) and fasting insulin (FINS) concentrations in HFD - fed rats without significantly affecting body weight or triglyceride (TG) or total cholesterol (TC) levels. The areas under the intraperitoneal glucose tolerance test (IPGTT) and the insulin tolerance test (ITT) curves were significantly decreased in HFD + vaspin group compared with the HFD group, and the glucose infusion rate (GIR) showed the same trends. Western blot, real-time polymerase chain reaction (RT-PCR) and immunofluorescence staining showed that vaspin could improve insulin resistance in liver, skeletal muscle and adipose tissue by activating the IRS/PI3K/Akt/Glut signalling pathway and inhibiting the IκBα/NF-κB signalling pathway.
胰岛素抵抗（IR）是代谢综合征的主要发病机制，也是糖尿病、肥胖症、高血压和动脉粥样硬化等疾病共有的病理生理变化。内脏脂肪组织来源的丝氨酸蛋白酶抑制剂（Vaspin）是一种新发现的具有胰岛素增敏和抗炎作用的脂肪细胞因子。为了研究 Vaspin 是否可以通过胰岛素受体底物/磷酸肌醇 3 激酶/蛋白激酶 B/葡萄糖转运（IRS/PI3K/Akt/Glut）和抑制κB 激酶α/核因子-κB（IκBα/NF-κB）信号通路改善高脂肪饮食喂养的大鼠的胰岛素抵抗，将 30 只雄性 Sprague-Dawley（SD）大鼠随机分为三组：正常对照组（NC 组，n=10）、高脂肪饮食组（HFD 组，n=10）和 Vaspin 干预组（HFD+Vaspin 组，n=10）。结果显示，Vaspin 干预可显著降低高脂肪饮食喂养大鼠的空腹血糖（FBG）和空腹胰岛素（FINS）浓度，而体重或三酰甘油（TG）或总胆固醇（TC）水平无明显变化。HFD+Vaspin 组大鼠的腹腔葡萄糖耐量试验（IPGTT）和胰岛素耐量试验（ITT）曲线下面积明显低于 HFD 组，葡萄糖输注率（GIR）也有相同趋势。Western blot、实时聚合酶链反应（RT-PCR）和免疫荧光染色显示，Vaspin 通过激活 IRS/PI3K/Akt/Glut 信号通路和抑制 IκBα/NF-κB 信号通路，改善了肝脏、骨骼肌和脂肪组织的胰岛素抵抗。
