Ramos M P, Crespo-Solans M D, del Campo S, Cacho J, Herrera E
Facultad de Ciencias Experimentales y de la Salud, Universidad San Pablo-CEU, Ctra. Boadilla del Monte km.5,3, E-28668, Madrid, Spain.
Am J Physiol Endocrinol Metab. 2003 Aug;285(2):E318-28. doi: 10.1152/ajpendo.00456.2002. Epub 2003 Apr 15.
Insulin sensitivity has been implicated in the variation of fat accumulation in early gestation by as-yet-unknown mechanisms. In the present study, we analyzed the insulin sensitivity of lipolysis and lipogenesis in lumbar adipocytes from rats at 0, 7, 14, and 20 days of gestation. In adipocytes of 7-day pregnant rats, we found a twofold decrease in both beta-agonist (isoproterenol and BRL-37344)-stimulated lipolysis and beta3-adrenoceptor protein but not in lipolysis initiated by forskolin or isobutylmethylxanthine, suggesting a modification of the lipolytic pathway at the receptor level. Whereas adipocytes from 7-day pregnant rats showed a twofold increase in fatty acid synthesis from glucose, those from 20-day pregnant animals displayed a decreased lipogenic activity. Insulin responsiveness of the lipolytic and lipogenic pathways was analyzed by dose-response experiments, giving evidence for the involvement of improved insulin responsiveness in the enhanced lipogenic and reduced lipolytic activities of adipocytes in early pregnancy. In contrast, insulin resistance is responsible for lower antilipolytic and lipogenic actions of insulin in late pregnant animals. In conclusion, the present study shows that enhanced adipose tissue insulin responsiveness during early pregnancy contributes to maternal fat accumulation, whereas decreased insulin responsiveness during late gestation modulates fat breakdown.
胰岛素敏感性通过尚未明确的机制与妊娠早期脂肪堆积的变化有关。在本研究中，我们分析了妊娠0、7、14和20天大鼠腰椎脂肪细胞中脂肪分解和脂肪生成的胰岛素敏感性。在妊娠7天的大鼠脂肪细胞中，我们发现β-激动剂（异丙肾上腺素和BRL-37344）刺激的脂肪分解和β3-肾上腺素能受体蛋白均降低了两倍，但由福斯高林或异丁基甲基黄嘌呤引发的脂肪分解未降低，这表明在受体水平上脂肪分解途径发生了改变。妊娠7天的大鼠脂肪细胞中，葡萄糖合成脂肪酸的能力增加了两倍，而妊娠20天的动物脂肪细胞的脂肪生成活性降低。通过剂量反应实验分析了脂肪分解和脂肪生成途径的胰岛素反应性，结果表明胰岛素反应性的改善参与了妊娠早期脂肪细胞脂肪生成增强和脂肪分解减少的过程。相反，胰岛素抵抗导致妊娠后期动物胰岛素的抗脂肪分解和脂肪生成作用降低。总之，本研究表明，妊娠早期脂肪组织胰岛素反应性增强有助于母体脂肪堆积，而妊娠后期胰岛素反应性降低则调节脂肪分解。
