THE ZUCKER RAT MODEL OF OBESITY, INSULIN RESISTANCE, HYPERLIPIDEMIA, AND RENAL INJURY

THE ZUCKER RAT MODEL OF OBESITY, INSULIN RESISTANCE, HYPERLIPIDEMIA, AND RENAL INJURY
复制标题

DOI:
10.1161/01.hyp.19.1_suppl.i110
复制
发表时间:
1992-01-01
期刊:
影响因子:
8.3
通讯作者:
KEANE, WF
KEANE, WF
中科院分区:
医学1区
文献类型:
--
作者:
KASISKE, BL;ODONNELL, MP;KEANE, WF

文献摘要

被引文献

相似文献

尽管OZR肥胖的发病机制尚不清楚,但高胰岛素血症、胰岛素抵抗和高脂血症之间的相关性表明,使用OZR进行的研究可能有助于确定许多血管疾病危险因素如何相互作用导致终末器官损伤。与其他大鼠品系一样,OZR不会自发发展动脉粥样硬化。然而,在内皮损伤模型中,OZR的动脉粥样硬化比LZR更严重。也许更有趣的是OZR发生自发性肾小球损伤的事实。虽然OZR肾小球损伤的发生和发展的重要机制仍有待澄清,脂质异常和肾小球血流动力学改变可能发挥作用。
Although the pathogenesis of obesity in OZR is unknown, the association among hyperinsulinemia, insulin resistance, and hyperlipidemia suggests that investigations using OZR may help define how a number of vascular disease risk factors interact to cause end-organ damage. Like other rat strains, OZR do not develop atherosclerosis spontaneously. Nevertheless, in an endothelial injury model, atherosclerosis was worse in OZR than in LZR. Perhaps more intriguing is the fact that OZR develop spontaneous glomerular injury. Although the mechanisms important in the development and progression of glomerular injury in OZR remain to be clarified, both lipid abnormalities and glomerular hemodynamic alterations could play a role.