Barrett Karlene, McGrowder Donovan, Brown Paul, Ragoobirsingh Dalip
Department of Basic Medical Sciences (Biochemistry Section), University of the West Indies, Mona Campus, Kingston 7, Jamaica, West Indies.
Mol Cell Biochem. 2006 Dec;293(1-2):9-14. doi: 10.1007/s11010-006-0387-x. Epub 2006 Sep 4.
This study was designed to understand the cellular mechanisms responsible for defects in the insulin-stimulated signal transduction pathway in a type 2 diabetic animal model. We examined the in vitro PC-1 phosphodiesterase activity and glucose uptake in adipose tissue of streptozotocin (STZ)-induced type 2 diabetic rats. The PC-1 activity was significantly increased in adipose tissue of diabetic rats (0.54 +/- 0.08 nmol PNTP hydrolyzed/mg protein/min) compared with controls (0.29 +/- 0.05 nmol PNTP hydrolyzed/mg protein/min, p < 0.05). Upon insulin stimulation (100 nM), glucose uptake in the adipose tissue of the controls (4.17 +/- 1.28 x 10(-8) micromol/mg/min) was significantly higher than that in the diabetic rats (1.26 +/- 0.35 x 10(-8); p < 0.05). These results suggest that elevated PC-1 phosphodiesterase activity and decreased glucose uptake in adipose tissues may be acquired characteristics contributing to the development of type 2 diabetes mellitus.
本研究旨在了解2型糖尿病动物模型中胰岛素刺激信号转导通路缺陷的细胞机制。我们检测了链脲佐菌素（STZ）诱导的2型糖尿病大鼠脂肪组织中的体外PC-1磷酸二酯酶活性和葡萄糖摄取。与对照组（0.29±0.05 nmol对硝基苯磷酸酯水解/mg蛋白质/分钟，p<0.05）相比，糖尿病大鼠脂肪组织中的PC-1活性显著增加（0.54±0.08 nmol对硝基苯磷酸酯水解/mg蛋白质/分钟）。在胰岛素刺激（100 nM）后，对照组脂肪组织中的葡萄糖摄取（4.17±1.28×10⁻⁸微摩尔/mg/分钟）显著高于糖尿病大鼠（1.26±0.35×10⁻⁸；p<0.05）。这些结果表明，脂肪组织中PC-1磷酸二酯酶活性升高和葡萄糖摄取减少可能是导致2型糖尿病发生的获得性特征。
