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肥胖 Zucker 大鼠棕色脂肪氧消耗存在缺陷。

Defective brown adipose oxygen consumption in obese Zucker rats.

作者信息

Levin B E, Finnegan M B, Marquet E, Sullivan A C

出版信息

Am J Physiol. 1984 Jul;247(1 Pt 1):E94-100. doi: 10.1152/ajpendo.1984.247.1.E94.

DOI:10.1152/ajpendo.1984.247.1.E94
PMID:6331192
Abstract

The thermogenic capacity and morphologic characteristics of interscapular brown adipose tissue (IBAT) were assessed in 3- to 4-mo-old male, lean and obese Zucker rats. Pads from obese rats were threefold heavier and contained similar numbers of cells but an average of 50% fewer multilocular cells than pads from lean rats and 40% less mitochondrial protein per pad. The maximal number of beta-adrenoreceptor binding sites, as assessed by [125I]iodocyanopindolol binding to isolated brown adipocytes from obese rats was 50% of that in lean rats on a per cell and per pad basis. Basal and norepinephrine (NE)-stimulated in vitro oxygen consumption in isolated brown adipocytes from lean rats correlated directly with the proportion of mutilocular cells present. This correlation was not seen in cells from obese rats that had a 50% decrease in their basal respiratory rates and could not be further stimulated by excess NE or fatty acid. Electron micrographs of IBAT from obese rats revealed distorted mitochondrial shapes and cristae patterns and the presence of numerous inclusion bodies. Because NE-stimulated lipolysis had previously been shown to be normal in the obese Zucker rat, these data suggest that defective BAT thermogenesis in the obese rat is due to an inability of mitochondria to utilize free fatty acids for the production of enhanced oxygen consumption.

摘要

在3至4月龄的雄性、瘦型和肥胖型Zucker大鼠中评估了肩胛间棕色脂肪组织(IBAT)的产热能力和形态特征。肥胖大鼠的脂肪垫重量是瘦型大鼠的三倍,细胞数量相似,但与瘦型大鼠的脂肪垫相比,多泡性细胞平均少50%,每个脂肪垫的线粒体蛋白少40%。通过[125I]碘氰吲哚洛尔与肥胖大鼠分离的棕色脂肪细胞结合来评估,β-肾上腺素能受体结合位点的最大数量在每个细胞和每个脂肪垫的基础上是瘦型大鼠的50%。瘦型大鼠分离的棕色脂肪细胞中,基础和去甲肾上腺素(NE)刺激的体外氧消耗与多泡性细胞的比例直接相关。在肥胖大鼠的细胞中未观察到这种相关性,这些细胞的基础呼吸速率降低了50%,并且不能被过量的NE或脂肪酸进一步刺激。肥胖大鼠IBAT的电子显微镜照片显示线粒体形状和嵴模式扭曲,并且存在大量包涵体。因为之前已证明肥胖型Zucker大鼠中NE刺激的脂肪分解是正常的,这些数据表明肥胖大鼠棕色脂肪组织产热缺陷是由于线粒体无法利用游离脂肪酸来增加氧消耗。

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