Biopolym. Cell. 1999; 15(2):103-108.
Reviews
Different models of the diabetes mellitus in experimental research on animals
- Institute of Molecular Biology and Genetics, NAS of Ukraine
150, Akademika Zabolotnoho Str., Kyiv, Ukraine, 03680
Abstract
This review describe the established models of the diabetes in rodents. They mver different forms of the disease concerned with the natural mutations occurred, with genetic engineering manipulations and with the induction using different chemicals agents like as alloksan and streptozotocin (STZ). It was shown that mice response to the subdiabetogemc STZ doses is influenced by animal age. It was also shown the subsequent injection sensibilizes mice response.
Full text: (PDF, in Russian)
References
[1]
Zaitsev TI. Inbred and mutant animals in diabetes and obesity research. Vestn Akad Med Nauk SSSR. 1983;(9):51-7.
[2]
Yefremov AS, Bezrodnyy YU.V. Structure and function of insulin receptors. Kiev: Naukova Dumka, 1987. 186 p.
[3]
Tarantul VZ. Targeting of genes as a modern method for studying their functions. Mol Gen Mikrobiol Virusol. 1996;(2):3-13.
[4]
Grupe A, Hultgren B, Ryan A, Ma YH, Bauer M, Stewart TA. Transgenic knockouts reveal a critical requirement for pancreatic beta cell glucokinase in maintaining glucose homeostasis. Cell. 1995;83(1):69-78.
[5]
Tamemoto H, Kadowaki T, Tobe K, Yagi T, Sakura H, Hayakawa T, Terauchi Y, Ueki K, Kaburagi Y, Satoh S, et al. Insulin resistance and growth retardation in mice lacking insulin receptor substrate-1. Nature. 1994;372(6502):182-6.
[6]
Araki E, Lipes MA, Patti ME, Brüning JC, Haag B 3rd, Johnson RS, Kahn CR. Alternative pathway of insulin signalling in mice with targeted disruption of the IRS-1 gene. Nature. 1994;372(6502):186-90.
[7]
Leiter EH, Prochazka M, Coleman DL. The non-obese diabetic (NOD) mouse. Am J Pathol. 1987;128(2):380-3.
[8]
Naji A, Silvers WK, Bellgrau D, Barker CF. Spontaneous diabetes in rats: destruction of islets is prevented by immunological tolerance. Science. 1981;213(4514):1390-2.
[9]
Hattori M, Buse JB, Jackson RA, Glimcher L, Dorf ME, Minami M, Makino S, Moriwaki K, Kuzuya H, Imura H, et al. The NOD mouse: recessive diabetogenic gene in the major histocompatibility complex. Science. 1986;231(4739):733-5.
[10]
Prochazka M, Leiter EH, Serreze DV, Coleman DL. Three recessive loci required for insulin-dependent diabetes in nonobese diabetic mice. Science. 1987;237(4812):286-9.
[11]
Wicker LS, Miller BJ, Coker LZ, McNally SE, Scott S, Mullen Y, Appel MC. Genetic control of diabetes and insulitis in the nonobese diabetic (NOD) mouse. J Exp Med. 1987;165(6):1639-54.
[12]
Lund T, O'Reilly L, Hutchings P, Kanagawa O, Simpson E, Gravely R, Chandler P, Dyson J, Picard JK, Edwards A, et al. Prevention of insulin-dependent diabetes mellitus in non-obese diabetic mice by transgenes encoding modified I-A beta-chain or normal I-E alpha-chain. Nature. 1990;345(6277):727-9.
[13]
Faustman D, Li XP, Lin HY, Fu YE, Eisenbarth G, Avruch J, Guo J. Linkage of faulty major histocompatibility complex class I to autoimmune diabetes. Science. 1991;254(5039):1756-61.
[14]
Gaskins HR, Monaco JJ, Leiter EH. Expression of intra-MHC transporter (Ham) genes and class I antigens in diabetes-susceptible NOD mice. Science. 1992;256(5065):1826-8; author reply 1830-1.
[15]
Georgiou HM, Mandel TE. Induction of insulitis in athymic (nude) mice. The effect of NOD thymus and pancreas transplantation. Diabetes. 1995;44(1):49-59.
[16]
Gorus FK, Malaisse WJ, Pipeleers DG. Selective uptake of alloxan by pancreatic B-cells. Biochem J. 1982;208(2):513-5.
[17]
Grankvist K, Marklund SL, Taljedal IB. CuZn-superoxide dismutase, Mn-superoxide dismutase, catalase and glutathione peroxidase in pancreatic islets and other tissues in the mouse. Biochem J. 1981;199(2):393-8.
[18]
Blokh KO, Poltorak VV, Poverennyy AM. Molecular mechanisms of damage beta cells of the pancreas by the action of diabetogenic factors. Usp Sovrem Biol. 1987; 103(1):96-108.
[19]
Weiss RB. Streptozotocin: a review of its pharmacology, efficacy and toxicy. Cancer Treat Rep. 1982; 66 :427—438.
[20]
Like AA, Rossini AA. Streptozotocin-induced pancreatic insulitis: new model of diabetes mellitus. Science. 1976;193(4251):415-7.
[21]
Kim YT, Steinberg C. Immunologic studies on the induction of diabetes in experimental animals. Cellular basis for the induction of diabetes by streptozotocin. Diabetes. 1984;33(8):771-7.
[22]
Cockfield SM, Ramassar V, Urmson J, Halloran PF. Multiple low dose streptozotocin induces systemic MHC expression in mice by triggering T cells to release IFN-gamma. J Immunol. 1989;142(4):1120-8.
[23]
Schnedl WJ, Ferber S, Johnson JH, Newgard CB. STZ transport and cytotoxicity. Specific enhancement in GLUT2-expressing cells. Diabetes. 1994;43(11):1326-33.
[24]
Herold KC, Montag AG, Fitch FW. Treatment with anti-T-lymphocyte antibodies prevents induction of insulitis in mice given multiple doses of streptozocin. Diabetes. 1987;36(7):796-801.
[25]
Herold KC, Bloch TN, Vezys V, Sun Q. Diabetes induced with low doses of streptozotocin is mediated by V beta 8.2+ T-cells. Diabetes. 1995;44(3):354-9.
[26]
Klinkhammer C, Popowa P, Gleichmann H. Specific immunity to streptozocin. Cellular requirements for induction of lymphoproliferation. Diabetes. 1988;37(1):74-80.