Roncari D A, Le Blanc P E
Department of Medicine, University of Calgary, Alta., Canada.
Biochem Cell Biol. 1990 Jan;68(1):238-42. doi: 10.1139/o90-032.
The process of adipose differentiation uniquely endows fat cells to accrue triacylglycerols under conditions of nutrient energy surfeit and to release fatty acids during energy deprivation. The object of this investigation was to study influences on this process in perirenal preadipocytes, grown in primary culture or first subculture and derived from male Sprague-Dawley rats, 180-200 g. Supplementation of the culture medium with 1-methyl-3-isobutylxanthine, corticosterone, and insulin induced differentiation in practically all perirenal preadipocytes, as indicated morphologically and by rising glycerophosphate dehydrogenase activity. Appreciable differentiation was induced even in the absence of methylisobutylxanthine. Transforming growth factor beta (1-1000 pM), cachectin (tumour necrosis factor alpha) (1-1000 pM), and basic fibroblast growth factor (0.063-63 nM) inhibited adipose differentiation significantly, almost completely at the higher concentrations. Direct inhibition, rather than a persisting mitogenic effect of fibroblast growth factor, was confirmed using demecolcine (Colcemid). The fact that transforming growth factor beta and cachectin inhibit differentiation in preadipocytes from postpubertal rats suggests that this effect probably also occurs in vivo, thus diverting energy from adipose depots in certain neoplastic and inflammatory states. We propose that the anterior pituitary, through fibroblast growth factor(s), modulates the pool of preadipocytes and other mesenchymal cells. The mitogenic effect would be complemented by a concerted function, inhibition of adipose differentiation, resulting in the retention of a greater number of potentially replicative cells. Then, depending on the subject's nutritional and endocrine status, extrapituitary factors would regulate the specific process of differentiation.
脂肪分化过程赋予脂肪细胞独特的能力，使其在营养能量过剩的情况下积累三酰甘油，并在能量缺乏时释放脂肪酸。本研究的目的是探讨对原代培养或首次传代培养的、取自180 - 200克雄性Sprague-Dawley大鼠的肾周前脂肪细胞这一过程的影响。向培养基中添加1-甲基-3-异丁基黄嘌呤、皮质酮和胰岛素，几乎可诱导所有肾周前脂肪细胞分化，这在形态学上以及甘油磷酸脱氢酶活性升高方面都有体现。即使在没有甲基异丁基黄嘌呤的情况下，也能诱导明显的分化。转化生长因子β（1 - 1000皮摩尔）、恶病质素（肿瘤坏死因子α）（1 - 1000皮摩尔）和碱性成纤维细胞生长因子（0.063 - 63纳摩尔）显著抑制脂肪分化，在较高浓度时几乎完全抑制。使用秋水仙胺（秋水仙酰胺）证实是直接抑制，而非成纤维细胞生长因子持续的促有丝分裂作用。转化生长因子β和恶病质素抑制青春期后大鼠前脂肪细胞分化这一事实表明，这种作用可能在体内也会发生，从而在某些肿瘤和炎症状态下使能量从脂肪库中转移出来。我们提出，垂体前叶通过成纤维细胞生长因子调节前脂肪细胞和其他间充质细胞库。促有丝分裂作用将通过协同功能，即抑制脂肪分化得到补充，从而导致保留更多潜在可复制细胞。然后，根据个体的营养和内分泌状况，垂体外因素将调节特定的分化过程。
