高脂饮食诱导肥胖模型大鼠骨骼肌组织蛋白酪氨酸磷酸酯酶1B和胰岛素受体底物2的表达  

Expression of protein-tyrosine phosphatase 1B and insulin receptor substrate 2 in the skeletal muscle of rats with insulin resistance induced by high-fat diet

在线阅读下载全文

作  者:赵慧[1] 于苏国[1] 王令令[2] 赵艳敏[1] 

机构地区:[1]滨州医学院附属医院内分泌科,山东省滨州市256603 [2]滨州市人民医院,山东省滨州市256600

出  处:《中国组织工程研究》2012年第20期3698-3702,共5页Chinese Journal of Tissue Engineering Research

摘  要:背景:外周组织的胰岛素抵抗是2型糖尿病的主要病因。目的:观察高脂饮食诱导的肥胖大鼠骨骼肌中蛋白酪氨酸磷酸酯酶1B和胰岛素受体底物2的表达。方法:将20只SD大鼠随机等分为对照组和高脂组,分别给予常规饲料和高脂饲料喂养12周。结果和结论:与对照组相比,高脂组大鼠胰岛素敏感指数显著降低(P<0.01),大鼠葡萄糖耐量受损,胰岛素释放试验提示葡萄糖刺激的胰岛素第一时相分泌受损,骨骼肌组织中蛋白酪氨酸磷酸酯酶1B蛋白表达水平明显增加(P<0.01),骨骼肌中胰岛素诱导的胰岛素受体底物2磷酸化程度降低(P<0.01)。提示高脂饮食诱导的肥胖大鼠骨骼肌中蛋白酪氨酸磷酸酯酶1B蛋白表达量升高,使胰岛素诱导的胰岛素受体底物2磷酸化程度降低,可能是肥胖导致胰岛素抵抗的机制之一。BACKGROUND: Insulin resistance in the peripheral tissue is a major cause of type 2 diabetes mellitus. OBJECTIVE: To observe the expression of protein tyrosine phosphatase 1B (PTP-1B) and insulin receptor substrate 2 (IRS-2) in the skeletal muscle of rats with insulin resistance induced by high-fat diet. METHODS: Twenty SD rats were randomly divided into normal control group with 10 rats and high-fat diet group with 10 rats. Rats in the two groups were fed with normal diet and high-fat diet for 12 weeks, respectively. RESULTS AND CONCLUSION: The insulin sensitive index was significantly decreased in the high-fat diet rats compared with the normal rats (P 〈 0.01). In obese rats, glucose tolerance and the acute first-phase insulin secretory response to glucose were impaired. The protein level of PTP-1B in the skeletal muscle of obese rats was significantly increased compared with the control group (P 〈 0.01). Insulin-stimulated IRS-2 phosphorylation in the skeletal muscle was reduced in the obese rats (P 〈 0.01). These indicate that the increased PTP-1B level and the reduced insulin-stimulated IRS-2 phosphorylations in the skeletal muscle seem to play an important role in the insulin resistance induced by high-fat diet.

关 键 词:肥胖 蛋白酪氨酸磷酸酶1B 胰岛素受体底物2 骨骼肌 胰岛素抵抗 

分 类 号:R318[医药卫生—生物医学工程]

 

参考文献:

正在载入数据...

 

二级参考文献:

正在载入数据...

 

耦合文献:

正在载入数据...

 

引证文献:

正在载入数据...

 

二级引证文献:

正在载入数据...

 

同被引文献:

正在载入数据...

 

相关期刊文献:

正在载入数据...

相关的主题
相关的作者对象
相关的机构对象