In This Issue of Diabetes

Edited by Helaine E. Resnick, PhD, MPH

Insulin Resistance Directly Impacts Islet Cell Morphology in Nondiabetic Humans

Based on data from pancreatic tissue samples collected from nondiabetic patients undergoing pancreatoduodenectomy, a new study in this issue of Diabetes (p. 994) suggests that even in the absence of frank diabetes, insulin resistance has a direct impact on islet cell biology. The article describes pre- and postoperative data from 18 nondiabetic patients (9 men and 9 women) who underwent pancreatoduodenectomy for treatment of tumor of the ampulla of Vater. The new study uses tissue samples taken from the downstream edge of the surgical cut. In this procedure, the volume of removed pancreas is constant at 50% and includes removal of the head of the pancreas, which contains 50% of β-cell mass. Another notable feature of the new study is that no participants were diabetic by established criteria, thereby allowing a critical examination of islet biology prior to disease onset. The investigators divided the patients into two groups—insulin resistant and insulin sensitive—based on preoperative assessments. Among the striking findings was that patients who were insulin sensitive before their pancreatoduodenectomy retained their glucose tolerance, but seven of nine insulin-resistant patients developed diabetes in response to the same procedure. In addition, although the surgery resulted in a reduction in insulin secretion for all patients regardless of their preoperative insulin sensitivity, insulin-resistant patients in the postoperative follow-up period also had decrements in all phases of insulin secretion and increased glucagon secretion in response to a mixed meal. Examination of the tissue samples collected during surgery indicated that insulin-resistant patients had greater average islet cell size, a finding that suggests that these patients’ preoperative insulin resistance impacted islet cell …

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This Article

  1. doi: 10.2337/db14-ti03 Diabetes vol. 63 no. 3 817-818
  1. Free via Open Access: OA