Gruen R, Hietanen E, Greenwood M R
Metabolism. 1978 Dec;27(12 Suppl 2):1955-66. doi: 10.1016/s0026-0495(78)80012-2.
Lipoprotein lipase (LPL) enzyme activity in epididymal adipose tissue from obese and lean Zucker rats was measured. At 5, 10, 13, and 20 wk of age obese rats have heavier fat pads, larger fat cells, and more LPL per epididymal fat pad and per fat cell than do their lean littermate controls. Although LPL per fat cell increased as fat cell size increased in lean rats, the increased LPL activity in the obese could not be attributed solely to increased fat cell size. When obese and lean rats had similar cell sizes, LPL per fat cell was still significantly increased in the obese compared to lean. Furthermore LPL activity was increased in "preobese" (fa/fa) rats compared to either lean genotype (Fa/fa or Fa/Fa) during the second postnatal week. The data suggest that early increments in LPL activity in adipose tissue of the "pre-obese" rat may significantly contribute to the early fat cell hypertrophy seen during the development of this genetic obesity. Furthermore, early increased LPL activity may prove useful as a predictor of the onset of obesity.
测定了肥胖和瘦型 Zucker 大鼠附睾脂肪组织中的脂蛋白脂肪酶(LPL)酶活性。在 5、10、13 和 20 周龄时,肥胖大鼠的脂肪垫比其瘦型同窝对照大鼠更重,脂肪细胞更大,每个附睾脂肪垫和每个脂肪细胞中的 LPL 更多。尽管在瘦型大鼠中,每个脂肪细胞中的 LPL 随着脂肪细胞大小的增加而增加,但肥胖大鼠中 LPL 活性的增加不能仅仅归因于脂肪细胞大小的增加。当肥胖和瘦型大鼠的细胞大小相似时,与瘦型大鼠相比,肥胖大鼠每个脂肪细胞中的 LPL 仍然显著增加。此外,在出生后第二周,“肥胖前期”(fa/fa)大鼠的 LPL 活性比任一瘦型基因型(Fa/fa 或 Fa/Fa)的大鼠都有所增加。数据表明,“肥胖前期”大鼠脂肪组织中 LPL 活性的早期增加可能显著促成了这种遗传性肥胖发展过程中早期出现的脂肪细胞肥大。此外,早期 LPL 活性的增加可能被证明是肥胖发生的一个有用预测指标。