title: Gastrointestinal growth factors and pancreatic islet hormones during postoperative IGF-I supplementation in man.
abstract: 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.
authors.affiliation: Department of Surgery, University of Linköping, Linköping, Sweden.
authors.forename: T
authors.initials: T
authors.lastname: Leinsköld
authors.forename: T E
authors.initials: TE
authors.lastname: Adrian
authors.forename: U
authors.initials: U
authors.lastname: Arnelo
authors.forename: J
authors.initials: J
authors.lastname: Larsson
authors.forename: J
authors.initials: J
authors.lastname: Permert
mesh_terms: D000368:Aged; D000682:Amyloid / Q000097:blood; D001786:Blood Glucose / Q000378:metabolism; D004311:Double-Blind Method; D005260:Female; D006133:Growth Substances / Q000378:metabolism*; D006801:Humans; D007328:Insulin / Q000097:blood; D007334:Insulin-Like Growth Factor I / Q000378:metabolism / Q000627:therapeutic use*; D058228:Islet Amyloid Polypeptide; D008297:Male; D008875:Middle Aged; D010187:Pancreatic Hormones / Q000378:metabolism*; D011182:Postoperative Care / Q000379:methods*
chemical_list: D000682:Amyloid; D001786:Blood Glucose; D006133:Growth Substances; D007328:Insulin; D058228:Islet Amyloid Polypeptide; D010187:Pancreatic Hormones; D007334:Insulin-Like Growth Factor I