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- Segersvard, R, et al.
(author)
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mRNA for pancreatic uncoupling protein 2 increases in two models of acute experimental pancreatitis in rats and mice
- 2005
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In: Cell and Tissue Research. - : Springer Science and Business Media LLC. - 1432-0878 .- 0302-766X. ; 320:2, s. 251-258
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Journal article (peer-reviewed)abstract
- Uncoupling-protein 2 (UCP2) is a mitochondrial protein that appears to be involved in cellular oxidant defense and in the regulation of oncotic cell death, both of which are important features of acute pancreatitis. However, UCP2 expression in acute pancreatitis has not been previously reported. In the current experiments, pancreatic gene expression was studied by real-time reverse-transcription/polymerase chain reaction and Northern blots. Two models of acute experimental pancreatitis were investigated: cerulein-induced pancreatitis in mice at two different time points and taurocholate-induced pancreatitis in rats at two degrees of severity. After cerulein administration, acinar injury and leukocyte infiltration was significantly higher at 24 h compared with 12 h after the first injection of cerulein (P < 0.05, P < 0.005, respectively). UCP2 mRNA was unchanged at 12 h but was nearly 12-fold greater than control levels after 24 h (P < 0.001). UCP2 gene expression correlated with acinar injury (r=0.69; P < 0.001). By 72 h after taurocholate administration, the severe group had more necrosis than the mild group (P < 0.005). Pancreatic UCP2 mRNA was increased fourfold in the severe group compared with controls (P < 0.01). UCP2 expression correlated with parenchymal necrosis (r=0.61; P < 0.01). Thus, pancreatic UCP2 mRNA increased in two models of acute pancreatitis. The increase in UCP2 gene expression was correlated with the severity of the disease. Up-regulation of UCP2 in the pancreas may be a protective response to oxidative stress, but this increase may also have a negative influence on cellular energy metabolism. Therefore, acinar UCP2 may be an important modifier of the severity of acute pancreatitis.
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- Strommer, L, et al.
(author)
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Early impairment of insulin secretion in rats after surgical trauma
- 2002
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In: European journal of endocrinology. - : Oxford University Press (OUP). - 0804-4643 .- 1479-683X. ; 147:6, s. 825-833
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Journal article (peer-reviewed)abstract
- 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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