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Polyamines pp 143-158 | Cite as

Transgenic Rodents with Altered SSAT Expression as Models of Pancreatitis and Altered Glucose and Lipid Metabolism

  • Anne Uimari
  • Mervi T. Hyvönen
  • Eija Pirinen
  • Leena AlhonenEmail author
Protocol
Part of the Methods in Molecular Biology book series (MIMB, volume 720)

Abstract

Depletion of pancreatic acinar cell polyamines in response to activation of polyamine catabolism is associated with the development of acute pancreatitis in experimental rodent models. The disease is characterized by general hallmarks seen also in human pancreatitis, such as accumulation of intraperitoneal ascites, acinar cell necrosis, and pancreatic as well as remote organ edema and inflammation. Thus, these animals make useful models for the human disease. Determination of these hallmarks can be used to assess the severity of the disease and to evaluate the efficacy of any therapy applied. The metabolic changes seen in genetically modified mice with either accelerated or inactivated polyamine catabolism have revealed that polyamine catabolism is involved in the regulation of glucose and lipid metabolism. The simplest method to determine the metabolic phenotype of the animal is to assess the concentrations of blood metabolites. Fasting blood glucose level is an indicator of overall glucose homeostasis, whereas fasting insulin level is a useful marker of insulin sensitivity. A more detailed analysis of glucose homeostasis and insulin sensitivity can be obtained by intraperitoneal glucose and insulin tolerance tests. Blood lipid levels mainly reflect triglyceride, free fatty acid, and cholesterol metabolism. Altered blood glucose and/or lipid levels are associated with several diseases, e.g., diabetes, Cushing’s syndrome, hyperthyroidism, atherosclerosis, pancreatitis, and dysfunction of the liver and kidneys.

Key words

Acute pancreatitis Edema Myeloperoxidase Histological damage Glucose metabolism Insulin sensitivity Glucose tolerance Lipid metabolism Lipoproteins Cholesterol Free fatty acids Triglycerides 

Notes

Acknowledgements

The authors thank Riitta Sinervirta and Sisko Juutinen for technical assistance and Taina Roiha for the photography of material for Fig. 1. This work was supported by the Academy of Finland.

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Copyright information

© Springer Science+Business Media, LLC 2011

Authors and Affiliations

  • Anne Uimari
    • 1
  • Mervi T. Hyvönen
    • 2
  • Eija Pirinen
    • 1
  • Leena Alhonen
    • 3
    Email author
  1. 1.A.I. Virtanen Institute for Molecular Sciences, Biocenter KuopioUniversity of KuopioKuopioFinland
  2. 2.Department of Biotechnology and Molecular Medicine, A.I. Virtanen Institute for Molecular Sciences, Biocenter KuopioUniversity of KuopioKuopioFinland
  3. 3.A.I. Virtanen Institute for Molecular Sciences, Biocenter KuopioUniversity of Eastern finlandKuopioFinland

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