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Original communication| Volume 105, ISSUE 1, P28-35, January 1989

Characterization of insulin resistance after surgery

  • Jörgen Nordenström
    Affiliations
    From the Departments of Surgery and Medicine and the Research Center at the Huddinge Hospital Stockholm, Sweden

    From the Karolinska Institute, Stockholm, Sweden
    Search for articles by this author
  • Tomas Sonnenfeld
    Affiliations
    From the Departments of Surgery and Medicine and the Research Center at the Huddinge Hospital Stockholm, Sweden

    From the Karolinska Institute, Stockholm, Sweden
    Search for articles by this author
  • Peter Arner
    Correspondence
    Reprint requests: Peter Arner, MD, Department of Medicine, Huddinge Hospital, S-141 86 Huddinge, Sweden.
    Affiliations
    From the Departments of Surgery and Medicine and the Research Center at the Huddinge Hospital Stockholm, Sweden

    From the Karolinska Institute, Stockholm, Sweden
    Search for articles by this author
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      Abstract

      The effects of insulin on glucose utilization were investigated in seven nonobese patients before and 24 hours after elective cholecystectomy. Surgery was followed by a significant increase in the circulating levels of glucose and insulin. The hypoglycemic action of insulin was reduced by one third (p < 0.01) after surgery. In isolated fat cells after surgery there was a significant overall reduction of 35% to 50% of the effects of insulin on 3-0-methylglucose transport and lipogenesis at 1μmol/L of glucose (where hexose transport is rate-limiting for insulin action). However, there was no change in insulin sensitivity in these cells. The effects of insulin on lipogenesis in adipocytes incubated with 100 μmol/L of glucose (where glucose metabolism is rate-limiting for insulin action) and adipocyte insulin receptor binding were not influenced by surgery. Insulin action in vivo and in vitro was not altered in five nonoperated control subjects 24 hours after they were given the same type of nutritional support as the cholecystectomy patients postoperatively. It was concluded that an elective moderate surgical trauma induces a rapid and marked insulin resistance that is not the result of postoperative nutritional restriction and involves a postreceptor binding alteration of glucose transport.
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