Hollenberg C H, Vost A
J Clin Invest. 1969 Nov;47(11):2485-98. doi: 10.1172/JCI105930.
The incorporation of tritiated thymidine into the deoxyribonucleic acid (DNA) of adipose fat and stromal cells was followed under a variety of conditions. After in vitro incubation of adipose slices or up to 2 days after in vivo injection of the isotope, all DNA radioactivity was in the stromal cell fraction. From 2 to 15 days after thymidine injection total tissue DNA radioactivity was constant, while between 2 and 5 days after injection label in fat cell DNA increased markedly. Thus new labeled fat cells, initially collected in the stromal pool, required 2-5 days after completion of DNA synthesis to accumulate sufficient lipid to be harvested in the fat cell fraction. Fasting before thymidine injection practically abolished DNA synthesis in primordial fat cells and reduced less drastically formation of stromal elements. However fasting sufficient to deplete lipid stores by 50% neither destroyed mature fat cells nor impaired their capacity to reaccumulate fat with refeeding. Other studies evaluated the role of new fat cell formation in the process of lipid accretion accompanying refeeding. These experiments indicated that at least during the early phase of rapid weight gain, accumulation of fat was due to deposition of triglyceride in existing cells rather than to accelerated formation of new fat cells. Studies with hypophysectomized rats demonstrated that pituitary ablation variably affected stromal DNA synthesis and nearly abolished the formation and (or) maturation of primordial fat cells. In these animals growth hormone markedly enhanced thymidine incorporation into stromal DNA but had no effect on fat cell precursors. In intact animals the predominant effect of growth hormone was also on the stromal fraction, although an action of the hormone of lesser magnitude on fat cell precursors was also evident.
在多种条件下追踪氚标记胸腺嘧啶核苷掺入脂肪组织和基质细胞的脱氧核糖核酸（DNA）中的情况。在体外培养脂肪切片后，或在体内注射该同位素后长达2天，所有DNA放射性均存在于基质细胞部分。在注射胸腺嘧啶核苷后2至15天，总组织DNA放射性保持恒定，而在注射后2至5天，脂肪细胞DNA中的标记显著增加。因此，最初存在于基质库中的新标记脂肪细胞，在DNA合成完成后需要2至5天来积累足够的脂质，以便在脂肪细胞部分中被检测到。在注射胸腺嘧啶核苷前禁食实际上消除了原始脂肪细胞中的DNA合成，并使基质成分的形成减少，但程度较轻。然而，禁食足以使脂质储备减少50%，既不会破坏成熟脂肪细胞，也不会损害其在重新喂食时重新积累脂肪的能力。其他研究评估了新脂肪细胞形成在重新喂食伴随的脂质积聚过程中的作用。这些实验表明，至少在体重快速增加的早期阶段，脂肪的积累是由于甘油三酯在现有细胞中的沉积，而不是由于新脂肪细胞形成加速。对垂体切除大鼠的研究表明，垂体切除对基质DNA合成有不同程度的影响，几乎消除了原始脂肪细胞的形成和（或）成熟。在这些动物中，生长激素显著增强了胸腺嘧啶核苷掺入基质DNA，但对脂肪细胞前体没有影响。在完整动物中，生长激素的主要作用也在基质部分，尽管该激素对脂肪细胞前体的作用较小也很明显。
