Horwitz B A, Inokuchi T, Wickler S J, Stern J S
Metabolism. 1984 Apr;33(4):354-7. doi: 10.1016/0026-0495(84)90198-7.
The genetically obese adult Zucker rat (fafa) exhibits reduced thermogenesis when stimulated by physiological agents (cold, catecholamines). Recent evidence suggests that this thermogenic defect may be important in the manifestation of the animal's obesity and that it reflects a reduced thermogenic contribution from brown adipose tissue, the major nonshivering thermogenic site in many mammals. The present study describes the effects of the obese genotype on brown (and white) adipocyte size, number, and lipid content and tissue lipoprotein lipase (LPL) activity. In the obese rats, brown fat depots were increased in mass. This increase could be accounted for by brown fat hypertrophy (due primarily to an increase in the amount of triglyceride present in each cell) rather than hyperplasia (there being no increase in the number of brown fat cells). In addition, unlike the situation in white fat, the brown fat from the obese rats did not exhibit higher LPL activity than did the brown fat from their lean littermates. This absence of an increased capacity for triglyceride uptake, coupled with the greater amount of triglyceride per brown adipocyte, is consistent with a reduction of triglyceride oxidation (and, thus, heat production) in the cells from the obese (v the lean) rats.
遗传性肥胖的成年 Zucker 大鼠(fafa)在受到生理因素(寒冷、儿茶酚胺)刺激时,产热减少。最近的证据表明,这种产热缺陷可能在该动物肥胖的表现中起重要作用,并且它反映了棕色脂肪组织(许多哺乳动物主要的非寒战产热部位)产热贡献的减少。本研究描述了肥胖基因型对棕色(和白色)脂肪细胞大小、数量、脂质含量以及组织脂蛋白脂肪酶(LPL)活性的影响。在肥胖大鼠中,棕色脂肪库的质量增加。这种增加可归因于棕色脂肪肥大(主要是由于每个细胞中甘油三酯含量增加)而非增生(棕色脂肪细胞数量没有增加)。此外,与白色脂肪的情况不同,肥胖大鼠的棕色脂肪与它们瘦的同窝仔鼠的棕色脂肪相比,LPL 活性并未更高。甘油三酯摄取能力没有增加,再加上每个棕色脂肪细胞中甘油三酯含量更高,这与肥胖(相对于瘦)大鼠细胞中甘油三酯氧化(进而产热)减少是一致的。