Johnson P R, Goldstein A L
Int J Obes. 1981;5(6):563-70.
One of several hypotheses concerning the nature of the genetic lesion which produces obesity in the Zucker fatty rat is that a defect in control of cellular proliferation in adipose tissue leads to hypercellular-hypertrophic obesity with all its metabolic and behavioral sequalae. Three lines of evidence are presented which render this hypothesis untenable: (1) maximal cell enlargement precedes maximum rate of cell addition in adipose tissue; (2) lipectomized obese rats do not regenerate subcutaneous adipocytes; and (3) cultured adipocyte precursors from obese rat adipose tissue grow at the same rate as do cells cultured from lean tissue. An alternative hypothesis that an alteration in hepatic lipid metabolism may be the locus of the genetic lesion is presented along with evidence from in-vivo and in-vitro studies of hepatic lipogenesis in the Zucker rat.
关于导致Zucker肥胖大鼠肥胖的基因损伤本质的几种假说之一是，脂肪组织中细胞增殖控制缺陷会导致细胞增多性-肥大性肥胖及其所有代谢和行为后果。本文提供了三条证据，使该假说站不住脚：（1）脂肪组织中细胞最大程度的增大先于细胞增加的最大速率；（2）脂肪切除的肥胖大鼠不会再生皮下脂肪细胞；（3）来自肥胖大鼠脂肪组织的培养脂肪细胞前体与来自瘦组织培养的细胞生长速率相同。本文还提出了另一种假说，即肝脏脂质代谢改变可能是基因损伤的部位，并提供了来自对Zucker大鼠肝脏脂肪生成的体内和体外研究的证据。
