谷氨酸诱导肥胖大鼠不同器官胰岛素结合的体内评价。

P Nenoff, H Remke, F Müller, T Arndt, T Mothes
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引用次数: 5

摘要

新生wistar大鼠注射na - l -谷氨酸(2mg /g body mass s.c);出生后第1-5天)引起下丘脑病变,随后出现发育不良-肥厚性肥胖。与其他肥胖动物模型不同,这些大鼠在外周正常胰岛素水平下发生肥胖。然而,从2月龄(生长大鼠)开始,外周胰岛素浓度逐渐升高,6月龄(成年大鼠)高胰岛素血症开始显现。令人惊讶的是,成年大鼠表现出正常的血糖,这表明胰岛素敏感性发生了变化。在之前工作的基础上,利用Whitcomb等人在1985年描述的体内放射受体测定法,研究了生长和成年大鼠不同器官的胰岛素结合。与体外方法相比,该方法在瘦鼠和肥胖鼠血浆中的真实代谢和激素条件下有效。肝脏、胰腺、肾上腺、胃、十二指肠、脾脏和心肌的胰岛素结合在两个年龄组的瘦鼠和肥胖鼠之间没有统计学差异。因此,肝脏胰岛素结合在生长湿器官为6323 +/- 458 pg/g,在成年瘦大鼠为7586 +/- 959 pg/g。肥胖大鼠相应值分别为5755 +/- 445 pg/g和7830 +/- 526 pg/g。在肥胖大鼠中没有检测到胰岛素结合的器官特异性下调,表明胰岛素敏感性没有改变。由此可见,成年谷氨酸诱导的肥胖大鼠高胰岛素血症不能通过胰岛素结合减少和器官特异性胰岛素清除率降低来解释。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
In vivo assessment of insulin binding in different organs of growing and adult glutamate-induced obese rats.
Injection of Na-L-glutamate into neonate Wistar-rats (2 mg/g body mass s.c.; day 1-5 of life) induces hypothalamic lesions, which are followed by hypoplastic-hypertrophic obesity despite normophagia. In contrast to other animal models of obesity, these rats develop obesity under peripheral normoinsulinemic conditions. However, beginning at an age of 2 months (growing rats), peripheral insulin concentration rises gradually and at an age of 6 months (adults rats) hyperinsulinemia becomes manifest. Surprisingly, adult rats show normoglycemia, pointing to alterations in insulin sensitivity. In continuation to previous work, insulin binding of different organs of growing and adult rats was investigated using the in vivo radioreceptor assay described by Whitcomb et al. in 1985. In contrast to in vitro methods, this assay works under real metabolic and hormonal conditions in plasma of lean and obese rats. Insulin binding of liver, pancreas, adrenals, stomach, duodenum, spleen, and heart muscles was found to be not statistically different between lean and obese rats of both age groups. Thus, liver insulin binding was 6323 +/- 458 pg/g wet organ in growing, and 7586 +/- 959 pg/g in adult lean rats. Corresponding values for obese rats were 5755 +/- 445 pg/g and 7830 +/- 526 pg/g, respectively. Organ specific down regulation of insulin binding in obese rats was not detected, suggesting unalterated insulin sensitivity. It is concluded that hyperinsulinemia of adult glutamate-induced obese rats cannot be explained by diminished insulin binding and reduced organ specific insulin clearance.
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