4-硝基喹啉1-羟色胺导致小鼠肥胖和脑损伤

T. Mizutani
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引用次数: 1

摘要

研究了单次脑内注射致癌物4-硝基喹啉1-氧化物(NQO)诱导的肥胖的生理和组织病理学,并与腹腔注射金硫葡萄糖(GTG)诱导的肥胖进行了比较。NQO-和gtg -肥胖小鼠表现出更显著的相关性。-体重比未治疗的轻?tro1,表现出食物和水的摄入量增加,以及氧气消耗增加。肥胖动物的血糖、tnl和血清胆固醇水平明显高于对照组。有n?在NQO-肥胖和gtg -肥胖的动物之间,这些代谢参数没有显著差异。然而,我们发现,nqo型肥胖动物的大脑病变主要集中在边缘系统(中隔、中隔、胼胝体和海马),gtg型肥胖动物的大脑病变主要集中在下丘脑中部。
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4-ニトロキノリン1-オキサイドによってマウスに発生した肥満と脳損傷
Obesity induced by a single intracerebral injection with the carcinogett, 4-nitroquinoline 1-oxide (NQO), was studied physiologically and histopathologically incomparison with that indtuced by intraperitoneal injection with goldthioglucose (GTG).NQO- and GTG-obese mice showed a more remarkable inc?-ease in body weight thanuntreated cou?tro1s, having exhibited an elevated intake of food and water, as well as anincreased oxygen consumption. The levels of blood glucose ;tncl serum cholesterol weresignificantly higher in fat animals than in controls. There was n?o significant differencein any of these metabolic parautteters between NQO- and GTG-obese animals. It wasevident, however, tltat cerebral lesions were mostly localized in the limbic system (septvxm, psalterium, corpus callosum and hippocampus) in the NQO-obese animals and in tltemiddle regioua of tlte hypothalamus in the GTG-obese animals.
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4-ニトロキノリン1-オキサイドによってマウスに発生した肥満と脳損傷
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