OBJECTIVE:Streptozotocin (STZ)-induced diabetes in Wistar rats results in severe hyperlipidemia and a characteristic cardiomyopathy. However, Wistar-Kyoto (WKY) rats made diabetic with a similar dose of STZ did not develop heart dysfunction or hypertriglyceridemia at 12 weeks post-STZ. We investigated whether an apparent resistance of the WKY strain to develop diabetic cardiomyopathy and hypertriglyceridemia following chronic diabetes could be due to a reduced susceptibility to the diabetogenic effects of STZ.

METHODS:Adult male WKY and Wistar rats were made diabetic with a moderate (55 mg/kg) or high (75 mg/kg) dose of STZ. At 6 weeks of diabetes, glucose tolerance, cardiac function, pancreatic insulin content and basal and post-heparin plasma lipolytic activity were determined.

RESULTS:Administration of a moderate dose of STZ produced cardiac dysfunction in Wistar but not WKY rats at 6 weeks after diabetes induction. The same dose of STZ in WKY rats also resulted in a lesser degree of hyperglycemia and glucose intolerance, and significantly higher pancreatic insulin content relative to Wistar rats. Following a high dose of STZ, the apparent resistance to developing cardiomyopathy was lost in the WKY rats. As well, the WKY rats demonstrated an equal degree of hyperglycemia and glucose intolerance as Wistar rats. However, unlike the Wistar strain, WKY rats did not demonstrate either hypertriglyceridemia or a reduced heparin-releasable plasma lipoprotein lipase (LPL) activity following a high dose of STZ.

CONCLUSIONS:These results suggest that the incidence of diabetes-related cardiomyopathy and hypertriglyceridemia in rats may be independently influenced by strain-dependent susceptibilities to the beta-cytotoxic effects of STZ. The absence of hypertriglyceridemia in severely diabetic WKY rats may be linked to the maintenance of a critical level of plasma LPL activity.

译文

目标:链脲佐菌素(STZ)诱导的Wistar大鼠糖尿病会导致严重的高脂血症和典型的心肌病。但是,在STZ后12周,使用相似剂量的STZ患糖尿病的Wistar-Kyoto(WKY)大鼠并未出现心脏功能障碍或高甘油三酯血症。我们调查了WKY菌株对慢性糖尿病后糖尿病性心肌病和高甘油三酯血症的明显抵抗是否可能是由于对STZ的致糖尿病作用的敏感性降低所致。

方法:成年男性用中度(55 mg / kg)或高(75 mg / kg)剂量的STZ使WKY和Wistar大鼠患糖尿病。在糖尿病的6周时,测定了葡萄糖耐量,心脏功能,胰腺胰岛素含量以及肝素基础和血浆中的脂解活性。

结果:服用中等剂量的STZ诱导糖尿病后6周,Wistar大鼠出现心脏功能障碍,但WKY大鼠没有。与Wistar大鼠相比,WKY大鼠中相同剂量的STZ还导致较低的高血糖和葡萄糖耐受不良,以及显着较高的胰腺胰岛素含量。服用高剂量的STZ后,WKY大鼠失去了明显的对发展性心肌病的抵抗力。同样,WKY大鼠表现出与Wistar大鼠相同程度的高血糖和葡萄糖耐受不良。但是,与Wistar菌株不同,WKY大鼠在高剂量的STZ后既未表现出高甘油三酸酯血症或肝素释放性血浆脂蛋白脂肪酶(LPL)活性降低。

结论:这些结果表明,大鼠与糖尿病有关的心肌病和高甘油三酯血症的发生可能受到STZ的β细胞毒性作用的应变依赖性敏感性的独立影响。严重糖尿病WKY大鼠缺乏高甘油三酸酯血症可能与维持血浆LPL活性临界水平有关。

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