Leinsköld T, Adrian T E, Arnelo U, Larsson J, Permert J
Department of Surgery, University of Linköping, Linköping, Sweden.
J Endocrinol. 2000 Nov;167(2):331-8. doi: 10.1677/joe.0.1670331.
Insulin-like growth factor-I (IGF-I) has been demonstrated to exert a nitrogen sparing effect, both experimentally and in patients after abdominal surgery. IGF-I is a major mediator for the anabolic effects of growth hormone (GH). Whether elevated circulating IGF-I levels are the sole mediator of the anabolic effects following GH has not been clarified. IGF-I influences glucose metabolism, both through its own specific receptor and by activating the insulin receptor, and has also been proposed to influence pancreatic islet secretion directly. In the present study, the postoperative effects of IGF-I on plasma levels of other gastrointestinal and pancreatic islet hormones and growth factors were measured in patients after abdominal surgery. Fifteen patients who were candidates for large bowel resection were randomly divided into two groups: IGF-I-treated (n=8) and placebo-treated (n=7). The IGF-I group received daily two s.c. injections of human recombinant IGF-I (80 microg/kg body weight) for five days, beginning on the morning of the first postoperative day. The other group received placebo injections. Fasting plasma levels of gastrointestinal growth factors (epidermal growth factor, transforming growth factor-alpha, IGF-II), gastrointestinal hormones (gastrin, enteroglucagon, peptide YY), and islet hormones (insulin, islet amyloid polypeptide (IAPP) and pancreatic glucagon) were determined by RIA preoperatively and after five days of treatment. No significant effects of IGF-I on other growth factors or gastrointestinal hormones were seen. A marked increase in plasma insulin postoperatively compared with the preoperative levels (42+/-3 vs 61+/-5 pM, P<0.05) was seen in the placebo group, whereas the postoperative levels in the IGF-I-treated patients remained unchanged (44+/-3 vs 45+/-4 pM). A similar pattern was observed for IAPP and cortisol concentrations. No differences in glucagon concentrations were seen. In conclusion, these results suggest that IGF-I does not influence production of other gastrointestinal hormones thought to be involved in alimentary growth or pancreatic glucagon. In contrast, IGF-I caused a marked reduction of insulin and IAPP secretion. The inhibition of beta-cell secretion could be direct or, alternatively, could involve an improvement in postoperative insulin resistance, perhaps by reducing serum cortisol.
胰岛素样生长因子-I（IGF-I）已被证明在实验研究以及腹部手术后的患者中均具有氮节约效应。IGF-I是生长激素（GH）合成代谢作用的主要介质。循环中IGF-I水平升高是否是GH后合成代谢作用的唯一介质尚未明确。IGF-I通过其自身的特异性受体以及激活胰岛素受体来影响葡萄糖代谢，并且也被认为可直接影响胰岛分泌。在本研究中，对腹部手术后患者测定了IGF-I对其他胃肠和胰岛激素及生长因子血浆水平的术后影响。15名拟行大肠切除术的患者被随机分为两组：IGF-I治疗组（n = 8）和安慰剂治疗组（n = 7）。IGF-I组从术后第一天早晨开始，连续五天每日皮下注射两次重组人IGF-I（80μg/kg体重）。另一组接受安慰剂注射。术前及治疗五天后，通过放射免疫分析法测定胃肠生长因子（表皮生长因子、转化生长因子-α、IGF-II）、胃肠激素（胃泌素、肠高血糖素、肽YY）以及胰岛激素（胰岛素、胰岛淀粉样多肽（IAPP）和胰高血糖素）的空腹血浆水平。未观察到IGF-I对其他生长因子或胃肠激素有显著影响。安慰剂组术后血浆胰岛素水平较术前显著升高（42±3对61±5 pM，P<0.05），而IGF-I治疗患者的术后水平保持不变（44±3对45±4 pM）。IAPP和皮质醇浓度也观察到类似模式。胰高血糖素浓度未见差异。总之，这些结果表明IGF-I不影响其他被认为参与营养生长的胃肠激素或胰高血糖素的产生。相反，IGF-I导致胰岛素和IAPP分泌显著减少。β细胞分泌的抑制可能是直接的，或者可能涉及术后胰岛素抵抗的改善，也许是通过降低血清皮质醇来实现的。
