利用重组 DNA 技术合成人胰岛素生成因子 I(rhIGF-I)的重要价值,在于它提供了估价该激素对人体燃料代谢的作用。在正常空腹鼠,rhIGF-I 可产生低糖血症,即使是同时输入抗胰岛素血清时。有意义的是,解释这种作用的动力学机制不同于胰岛素,尽管这两种激素都可刺激周围葡萄糖摄取。rhIGF 对肝产生葡萄糖仅有微小或完全没有作用。大鼠的肝源性葡萄糖生成对 rhIGF-I 相对不敏感,与它对胰岛素的极度敏感形成显著差别。早期研究曾有力地证实,抑制葡萄糖生成所需的胰岛素比刺激周围葡萄糖摄取者要少得多。rhIGF-I 对游离脂肪酸(FFA)的作用尚不清楚。与动物相比,人体对 rhIGF-I 的代谢反应所知甚少,故作者研究 rhIGF-I 对正常人葡萄糖代谢的刺激作用,以及对 FFA、氨基酸代谢、胰岛 The important value of using recombinant DNA technology to synthesize human insulin-producing factor I (rhIGF-I) is that it provides an estimate of the effect this hormone exerts on human fuel metabolism. In normal fasting mice, rhIGF-I produces hypoglycemia even when anti-insulin serum is administered simultaneously. Significantly, the kinetic mechanism that explains this effect differs from insulin, though both of these hormones stimulate peripheral glucose uptake. rhIGF has little or no effect on the production of glucose in the liver. Rat liver-derived glucose production is relatively insensitive to rhIGF-I, which is significantly different from its sensitivity to insulin. Earlier studies have strongly demonstrated that insulin required to inhibit glucose production is much less aggressive than peripheral glucose ingestion. The effect of rhIGF-I on free fatty acids (FFA) is unclear. Compared with animals, the human body has little knowledge of the metabolic response to rhIGF-I, so the authors study the stimulating effect of rhIGF-I on normal glucose metabolism, as well as on FFA, amino acid metabolism, islet