Comparison of the response using ICR mice derived from three different sources to multiple low-dose streptozotocin-induced diabetes mellitus
Laboratory Animal Research volume 33, pages 150–156 (2017)
Abstract
This study was conducted to compare the multiple low-dose streptozotocin (MLDS)-induced diabetic patterns of Korl:ICR, A:ICR, and B:ICR mice obtained from three different sources. Six-week-old male ICR mice were obtained from three difference sources. Korl:ICR mice were kindly provided by the National Institute of Food and Drug Safety Evaluation (NIFDS). The other two groups of ICR mice were purchased from different vendors located in the United States (A:ICR) and Japan (B:ICR). All ICR mice that received MLDS exhibited overt diabetic symptoms throughout the study, and the incidence and development of diabetes mellitus were similar among the three ICR groups. The diabetic mice exhibited hyperglycemia, loss of body weight gain, decreased plasma insulin levels, impaired glucose tolerance, decreased number of insulin-positive cells, and decreased size of β-cells in the pancreas. The diabetes symptoms increased as the blood glucose level increased in the three ICR groups. In particular, the level of blood glucose in the STZ-treated group was higher in Korl:ICR and A:ICR mice than in B:ICR mice. The plasma insulin levels, glucose tolerance, blood chemistry, and morphological appearance of the pancreas were very similar in the ICR groups obtained from the three different sources. In conclusion, our results suggest that Korl:ICR, A:ICR, and B:ICR mice from different sources had similar overall responses to multiple low-dose STZ to induce diabetes mellitus.
References
Chia R, Achilli F, Festing MF, Fisher EM. The origins and uses of mouse outbred stocks. Nat Genet 2005; 37(11): 1181–1186.
Hubrecht RC, Kirkwood J. The UFAW Handbook on the Care and Management of Laboratory and Other Research Animals, 8th ed. Wiley-Blackwell. Oxford, 2010.
Vallender EJ, Miller GM. Nonhuman primate models in the genomic era: a paradigm shift. ILAR J 2013; 54(2): 154–165.
Fox JG, Anderson LC, Loew FM, Quimby FW. Laboratory Animal Medicine, 2nd ed, Academic Press, New York, 2002.
Cui S, Chesson C, Hope R. Genetic variation within and between strains of outbred Swiss mice. Lab Anim 1993; 27(2): 116–123.
Lehoczky JA, Cai WW, Douglas JA, Moran JL, Beier DR, Innis JW. Description and genetic mapping of Polypodia: an X-linked dominant mouse mutant with ectopic caudal limbs and other malformations. Mamm Genome 2006; 17(9): 903–913.
Al-Awar A, Kupai K, Veszelka M, Szûcs G, Attieh Z, Murlasits Z, Török S, Pósa A, Varga C. Experimental Diabetes Mellitus in Different Animal Models. J Diabetes Res 2016; 2016: 9051426.
Horton ES. NIDDM—the devastating disease. Diabetes Res Clin Pract 1995; 28 Suppl: S3–11.
Wild S, Roglic G, Green A, Sicree R, King H. Global prevalence of diabetes: estimates for the year 2000 and projections for 2030. Diabetes Care 2004; 27(5): 1047–1053.
Danaei G, Finucane MM, Lu Y, Singh GM, Cowan MJ, Paciorek CJ, Lin JK, Farzadfar F, Khang YH, Stevens GA, Rao M, Ali MK, Riley LM, Robinson CA, Ezzati M; Global Burden of Metabolic Risk Factors of Chronic Diseases Collaborating Group (Blood Glucose). National, regional, and global trends in fasting plasma glucose and diabetes prevalence since 1980: systematic analysis of health examination surveys and epidemiological studies with 370 country-years and 2·7 million participants. Lancet 2011; 378 (9785): 31–40.
Lenzen S. The mechanisms of alloxan- and streptozotocininduced diabetes. Diabetologia 2008; 51(2): 216–226.
Skovsø S. Modeling type 2 diabetes in rats using high fat diet and streptozotocin. J Diabetes Investig 2014; 5(4): 349–358.
Sakata N, Yoshimatsu G, Tsuchiya H, Egawa S, Unno M. Animal models of diabetes mellitus for islet transplantation. Exp Diabetes Res 2012; 2012: 256707.
Tesch GH, Nikolic-Paterson DJ. Recent insights into experimental mouse models of diabetic nephropathy. Nephron Exp Nephrol 2006; 104(2): e57–62.
Müller A, Schott-Ohly P, Dohle C, Gleichmann H. Differential regulation of Th1-type and Th2-type cytokine profiles in pancreatic islets of C57BL/6 and BALB/c mice by multiple low doses of streptozotocin. Immunobiology 2002; 205(1): 35–50.
Brentjens R, Saltz L. Islet cell tumors of the pancreas: the medical oncologist’s perspective. Surg Clin North Am 2001; 81(3): 527–542.
Moertel CG, Lefkopoulo M, Lipsitz S, Hahn RG, Klaassen D. Streptozocin-doxorubicin, streptozocin-fluorouracil or chlorozotocin in the treatment of advanced islet-cell carcinoma. N Engl J Med 1992; 326(8): 519–523.
Dominguez S, Denys A, Madeira I, Hammel P, Vilgrain V, Menu Y, Bernades P, Ruszniewski P. Hepatic arterial chemoembolization with streptozotocin in patients with metastatic digestive endocrine tumours. Eur J Gastroenterol Hepatol 2000; 12(2): 151–157.
Yang SJ, Je Lee W, Kim EA, Dal Nam K, Hahn HG, Young Choi S, Cho SW. Effects of N-adamantyl-4-methylthiazol-2-amine on hyperglycemia, hyperlipidemia and oxidative stress in streptozotocin-induced diabetic rats. Eur J Pharmacol 2014; 736: 26–34.
Liu Y, Sun J, Rao S, Su Y, Li J, Li C, Xu S, Yang Y. Antidiabetic activity of mycelia selenium-polysaccharide from Catathelasma ventricosum in STZ-induced diabetic mice. Food Chem Toxicol 2013; 62: 285–291.
Szkudelski T. The mechanism of alloxan and streptozotocin action in B cells of the rat pancreas. Physiol Res 2001; 50(6): 537–546.
Konrad RJ, Kudlow JE. The role of O-linked protein glycosylation in beta-cell dysfunction. Int J Mol Med 2002; 10(5): 535–539.
Chen V, Ianuzzo CD. Dosage effect of streptozotocin on rat tissue enzyme activities and glycogen concentration. Can J Physiol Pharmacol 1982; 60(10): 1251–1256.
Herold KC, Vezys V, Sun Q, Viktora D, Seung E, Reiner S, Brown DR. Regulation of cytokine production during development of autoimmune diabetes induced with multiple low doses of streptozotocin. J Immunol 1996; 156(9): 3521–3527.
Ogawa J, Takahashi S, Fujiwara T, Fukushige J, Hosokawa T, Izumi T, Kurakata S, Horikoshi H. Troglitazone can prevent development of type 1 diabetes induced by multiple low-dose streptozotocin in mice. Life Sci 1999; 65(12): 1287–1296.
Holst JJ. The physiology of glucagon-like peptide 1. Physiol Rev 2007; 87(4): 1409–1439.
Giannini EG, Testa R, Savarino V. Liver enzyme alteration: a guide for clinicians. CMAJ 2005; 172(3): 367–379.
Harris EH. Elevated liver function tests in type 2 diabetes, Clinical Diabetes. 2005; 23(3): 115–119.
Liu Y, Sun J, Rao S, Su Y, Yang Y. Antihyperglycemic, antihyperlipidemic and antioxidant activities of polysaccharides from Catathelasma ventricosum in streptozotocin-induced diabetic mice. Food Chem Toxicol 2013; 57: 39–45.
Acknowledgments
This project was supported by a grant from BIOREIN (Laboratory Animal Bio Resources Initiative) from the Ministry of Food and Drug Safety in 2015.
Author information
Authors and Affiliations
Corresponding author
Rights and permissions
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
About this article
Cite this article
Lee, D.Y., Kim, M.H., Suh, H.R. et al. Comparison of the response using ICR mice derived from three different sources to multiple low-dose streptozotocin-induced diabetes mellitus. Lab Anim Res 33, 150–156 (2017). https://doi.org/10.5625/lar.2017.33.2.150
Received:
Revised:
Accepted:
Published:
Issue Date:
DOI: https://doi.org/10.5625/lar.2017.33.2.150
Keywords
- Korl:ICR mice
- multiple low-dose streptozotocin
- diabetes mellitus
- hyperglycemia