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禁食的 Zucker(fa/fa)大鼠脂肪组织脂蛋白脂肪酶与甘油释放

Adipose tissue lipoprotein lipase and glycerol release in fasted Zucker (fa/fa) rats.

作者信息

Gruen R K, Greenwood M R

出版信息

Am J Physiol. 1981 Jul;241(1):E76-83. doi: 10.1152/ajpendo.1981.241.1.E76.

Abstract

Fat cell hypertrophy occurs in most forms of obesity. In the obese Zucker rat, fat cell hypertrophy and increased lipoprotein lipase activity (LPL) are the earliest known signs of obesity. We studied the regulation of fat cell size in the obese Zucker rat by measuring changes in fat cell LPL activity and lipolysis in response to an overnight fast in 6- and 14-wk-old lean and obese rats. At both ages, fed obese rats had significantly increased fat cell size, LPL activity, and basal glycerol release in three adipose tissue depots compared to fed lean rats. Obese rats decreased LPL activity in response to fasting, but levels always remained equal to or greater than those in fed lean rats. Obese rats also showed a reduced lipolytic response to fasting. Thus, the obese rat after an overnight fast could not produce a coordinated response to fasting similar to the lean rat, and its homeostatic adjustments to this mild stimulus favored preservation of its enlarged fat cell size.

摘要

脂肪细胞肥大在大多数肥胖类型中都会出现。在肥胖的 Zucker 大鼠中,脂肪细胞肥大和脂蛋白脂肪酶(LPL)活性增加是已知最早出现的肥胖迹象。我们通过测量 6 周龄和 14 周龄的瘦鼠和肥胖 Zucker 大鼠在禁食一夜后脂肪细胞 LPL 活性和脂肪分解的变化,研究了肥胖 Zucker 大鼠脂肪细胞大小的调节机制。在这两个年龄段,与喂食的瘦鼠相比,喂食的肥胖大鼠在三个脂肪组织库中的脂肪细胞大小、LPL 活性和基础甘油释放量均显著增加。肥胖大鼠在禁食后 LPL 活性降低,但其水平始终等于或高于喂食的瘦鼠。肥胖大鼠对禁食的脂肪分解反应也有所降低。因此,禁食一夜后的肥胖大鼠无法像瘦鼠那样对禁食产生协调反应,并且其对这种轻度刺激的稳态调节有利于维持其增大的脂肪细胞大小。

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