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Early impairment of insulin secretion in rats after surgical trauma
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- Strommer, L (author)
- Karolinska Institutet
- Wickbom, M (author)
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- Wang, F (author)
- Karolinska Institutet
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- Herrington, MK (author)
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- (creator_code:org_t)
- Oxford University Press (OUP), 2002
- 2002
- English.
- In: European journal of endocrinology. - : Oxford University Press (OUP). - 0804-4643 .- 1479-683X. ; 147:6, s. 825-833
- Journal article (peer-reviewed)
Abstract
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- OBJECTIVE: Hyperglycaemia associated with insulin resistance is common after trauma and surgical procedures. Both reduced insulin sensitivity and altered insulin secretion may contribute to the impaired glucose homeostasis. We have demonstrated that skeletal muscle insulin resistance is present 2 h after small intestinal resection in rats. In this study, the aim was to investigate insulin secretion in the same experimental model. DESIGN: Small intestinal resection (5 cm) was performed in adult rats. The control animals underwent anaesthesia only. METHODS: The intravenous glucose tolerance test (IVGTT), the hyperglycaemic clamp and in vitro studies in isolated pancreatic islets were performed after surgery. Concentrations of blood glucose, plasma insulin, corticosterone and interleukin-6 (IL-6) were determined 0-5 h postoperatively. RESULTS: The insulin response in the IVGTT was attenuated 2 h (P<0.05) but not 4 h or during the hyperglycaemic clamp (3.5-4.5 h) postoperatively. Insulin secretion in response to glucose in vitro was decreased 2 h after the surgery (P<0.05), but no change was seen in arginine-stimulated secretion. Plasma levels of corticosterone were increased 3.5-5 h postoperatively (P<0.001-0.05). Increases in IL-6 were also seen postoperatively. CONCLUSION: We demonstrate that glucose-induced, but not arginine-induced, insulin secretion is temporarily impaired after intestinal resection in rats. The later appearance of elevated corticosterone and IL-6 levels, as well as the preservation of the beta-cell inhibition in vitro, argues against the possibility that these two circulating factors are causally responsible for reduced insulin release seen after surgery in this model.
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