肥胖 Zucker 大鼠的局部脂肪垫生长与细胞构成：热量限制的调节作用

Regional fat pad growth and cellularity in obese zucker rats: modulation by caloric restriction.

作者信息

Hausman Dorothy B, Fine Jacqueline B, Tagra Krishna, Fleming Shea S, Martin Roy J, DiGirolamo Mario

机构信息

Department of Foods and Nutrition, University of Georgia, Athens, Georgia 30602, USA.

出版信息

Obes Res. 2003 May;11(5):674-82. doi: 10.1038/oby.2003.96.

DOI:10.1038/oby.2003.96

PMID:12740458

Abstract

OBJECTIVE

To investigate, in young obese male Zucker rats, the effects of chronic food restriction and subsequent refeeding on: 1). parameters of nonadipose and adipose growth, 2). regional adipose depot cellularity [fat cell volume (FCV) and number], and 3). circulating leptin levels.

RESEARCH METHODS AND PROCEDURES

Obese (fa/fa) and lean (Fa/?) male Zucker rats were studied from age 5 to 19 weeks. After baseline food intake monitoring, 10 obese rats were subjected to 58 days of marked caloric restriction from ad libitum levels [obese-restricted (OR)], followed by a return to ad libitum feeding for 22 days. Ten lean control rats and 10 obese control rats were fed ad libitum for the entire experiment. All rats were fed using a computer-driven automated feeding system designed to mimic natural eating patterns.

RESULTS

After food restriction, OR rats weighed significantly less than did lean and obese rats and showed a significant diminution in body and adipose growth as compared with obese rats. Relative adiposity was not different between obese and OR rats and was significantly higher than that of lean rats. The limitation in growth of the adipose tissue mass in OR rats was due mostly to suppression of fat cell proliferation because the mean FCV in each of the four depots was not affected. Serum leptin levels of OR and obese rats were not different from each other but were significantly higher than those of lean rats.

DISCUSSION

Marked caloric restriction affects obese male Zucker rats in a manner different from that of nongenetic rodent models (i.e., Wistar rats). In comparison with the response to caloric deprivation of Wistar rats, these calorically restricted obese male Zucker rats appeared to defend their relative adiposity and mean FCV at the expense of fat cell number. These findings indicate that genetic and/or tissue-specific controls override the general consequences of food restriction in this genetic model of obesity.

摘要

目的

研究在年轻肥胖雄性 Zucker 大鼠中，长期食物限制及随后再喂养对以下方面的影响：1）非脂肪组织和脂肪组织生长参数；2）局部脂肪储存细胞构成[脂肪细胞体积（FCV）和数量]；3）循环瘦素水平。

研究方法与步骤

对肥胖（fa/fa）和瘦（Fa/?）雄性 Zucker 大鼠从 5 周龄至 19 周龄进行研究。在监测基线食物摄入量后，10 只肥胖大鼠从随意进食水平开始进行 58 天的显著热量限制[肥胖限制组（OR）]，随后恢复随意进食 22 天。10 只瘦对照大鼠和 10 只肥胖对照大鼠在整个实验过程中均随意进食。所有大鼠均使用计算机驱动的自动喂食系统进行喂养，该系统旨在模拟自然进食模式。

结果

食物限制后，OR 组大鼠体重显著低于瘦大鼠和肥胖大鼠，且与肥胖大鼠相比，其身体和脂肪组织生长显著减少。肥胖大鼠和 OR 组大鼠的相对肥胖程度无差异，且显著高于瘦大鼠。OR 组大鼠脂肪组织质量生长受限主要是由于脂肪细胞增殖受到抑制，因为四个储存部位中每个部位的平均 FCV 未受影响。OR 组大鼠和肥胖大鼠的血清瘦素水平彼此无差异，但显著高于瘦大鼠。

讨论

显著热量限制对肥胖雄性 Zucker 大鼠的影响方式与非基因啮齿动物模型（即 Wistar 大鼠）不同。与 Wistar 大鼠对热量剥夺的反应相比，这些热量受限的肥胖雄性 Zucker 大鼠似乎以脂肪细胞数量为代价来维持其相对肥胖程度和平均 FCV。这些发现表明在这种肥胖基因模型中，遗传和/或组织特异性控制优先于食物限制的一般后果。