Feldman J M, Blalock J A
Res Commun Chem Pathol Pharmacol. 1979 Dec;26(3):479-93.
The purpose of this study was to determine if the elevated concentration of norepinephrine in the hypothalamus of the obese-hyperglycemic mouse plays a role in the development of this syndrome. We treated normal and obese mice with the monoamine oxidase inhibitors pargyline or clorgyline for 25 weeks. This resulted in significant inhibition of monoamine oxidase in their hypothalamus, cerebral cortex, kidney, heart and epididymal fat. There was a significant increase in the norepinephrine concentration of the hypothalamus of the normal mice and the cerebral cortex of the obese mice. The obese mice receiving clorgyline had an increase in plasma glucose (313 +/- 9 mg/dl). However, the increase in tissue norepinephrine concentration did not result in increased weight gain or alterations in organ weights in the mice. Thus, the elevated hypothalamic norepinephrine concentration in obese mice is probably not the cause of their obesity.
本研究的目的是确定肥胖高血糖小鼠下丘脑去甲肾上腺素浓度升高是否在该综合征的发展中起作用。我们用单胺氧化酶抑制剂帕吉林或氯吉兰对正常和肥胖小鼠进行了25周的治疗。这导致它们的下丘脑、大脑皮层、肾脏、心脏和附睾脂肪中的单胺氧化酶受到显著抑制。正常小鼠下丘脑和肥胖小鼠大脑皮层中的去甲肾上腺素浓度显著增加。接受氯吉兰治疗的肥胖小鼠血糖升高（313±9mg/dl）。然而，组织中去甲肾上腺素浓度的增加并未导致小鼠体重增加或器官重量改变。因此，肥胖小鼠下丘脑去甲肾上腺素浓度升高可能不是其肥胖的原因。
