A new rat model of type 2 diabetes: the fat-fed, streptozotocin-treated rat - PubMed (original) (raw)
A new rat model of type 2 diabetes: the fat-fed, streptozotocin-treated rat
M J Reed et al. Metabolism. 2000 Nov.
Abstract
This study was initiated to develop an animal model of type 2 diabetes in a non-obese, outbred rat strain that replicates the natural history and metabolic characteristics of the human syndrome and is suitable for pharmaceutical research. Male Sprague-Dawley rats (n = 31), 7 weeks old, were fed normal chow (12% of calories as fat), or high-fat diet (40% of calories as fat) for 2 weeks and then injected with streptozotocin (STZ, 50 mg/kg intravenously). Before STZ injection, fat-fed rats had similar glucose concentrations to chow-fed rats, but significantly higher insulin, free fatty acid (FFA), and triglyceride (TG) concentrations (P < .01 to .0001). Plasma insulin concentrations in response to oral glucose (2 g/kg) were increased 2-fold by fat feeding (P < .01), and adipocyte glucose clearance under maximal insulin stimulation was significantly reduced (P < .001), suggesting that fat feeding induced insulin resistance. STZ injection increased glucose (P < .05), insulin (P < .05), FFA (P < .05), and TG (P < .0001) concentrations in fat-fed rats (Fat-fed/STZ rats) compared with chow-fed, STZ-injected rats (Chow-fed/STZ rats). Fat-fed/STZ rats were not insulin deficient compared with normal chow-fed rats, but had hyperglycemia and a somewhat higher insulin response to an oral glucose challenge (both P < .05). In addition, insulin-stimulated adipocyte glucose clearance was reduced in Fat-fed/STZ rats compared with both chow-fed and Chow-fed/STZ rats (P < .001). Finally, Fat-fed/STZ rats were sensitive to the glucose lowering effects of metformin and troglitazone. In conclusion, Fat-fed/STZ rats provide a novel animal model for type 2 diabetes, simulates the human syndrome, and is suitable for the testing of antidiabetic compounds.
Similar articles
- Effect of masoprocol on carbohydrate and lipid metabolism in a rat model of Type II diabetes.
Reed MJ, Meszaros K, Entes LJ, Claypool MD, Pinkett JG, Brignetti D, Luo J, Khandwala A, Reaven GM. Reed MJ, et al. Diabetologia. 1999 Jan;42(1):102-6. doi: 10.1007/s001250051121. Diabetologia. 1999. PMID: 10027587 - Association of insulin resistance with hyperglycemia in streptozotocin-diabetic pigs: effects of metformin at isoenergetic feeding in a type 2-like diabetic pig model.
Koopmans SJ, Mroz Z, Dekker R, Corbijn H, Ackermans M, Sauerwein H. Koopmans SJ, et al. Metabolism. 2006 Jul;55(7):960-71. doi: 10.1016/j.metabol.2006.03.004. Metabolism. 2006. PMID: 16784971 - Combination of high-fat diet-fed and low-dose streptozotocin-treated rat: a model for type 2 diabetes and pharmacological screening.
Srinivasan K, Viswanad B, Asrat L, Kaul CL, Ramarao P. Srinivasan K, et al. Pharmacol Res. 2005 Oct;52(4):313-20. doi: 10.1016/j.phrs.2005.05.004. Pharmacol Res. 2005. PMID: 15979893 - The rat models of non-insulin dependent diabetes induced by neonatal streptozotocin.
Portha B, Blondel O, Serradas P, McEvoy R, Giroix MH, Kergoat M, Bailbe D. Portha B, et al. Diabete Metab. 1989 Mar-Apr;15(2):61-75. Diabete Metab. 1989. PMID: 2525491 Review. - Challenges and issues with streptozotocin-induced diabetes - A clinically relevant animal model to understand the diabetes pathogenesis and evaluate therapeutics.
Goyal SN, Reddy NM, Patil KR, Nakhate KT, Ojha S, Patil CR, Agrawal YO. Goyal SN, et al. Chem Biol Interact. 2016 Jan 25;244:49-63. doi: 10.1016/j.cbi.2015.11.032. Epub 2015 Dec 2. Chem Biol Interact. 2016. PMID: 26656244 Review.
Cited by
- Alterations in gut microbiota during remission and recurrence of diabetes after duodenal-jejunal bypass in rats.
Zhong MW, Liu SZ, Zhang GY, Zhang X, Liu T, Hu SY. Zhong MW, et al. World J Gastroenterol. 2016 Aug 7;22(29):6706-15. doi: 10.3748/wjg.v22.i29.6706. World J Gastroenterol. 2016. PMID: 27547013 Free PMC article. - Amlodipine Ameliorates Ischemia-Induced Neovascularization in Diabetic Rats through Endothelial Progenitor Cell Mobilization.
Sun J, Xie J, Kang L, Ferro A, Dong L, Xu B. Sun J, et al. Biomed Res Int. 2016;2016:3182764. doi: 10.1155/2016/3182764. Epub 2016 May 8. Biomed Res Int. 2016. PMID: 27243031 Free PMC article. - Hyperglycemia-induced oxidative stress exacerbates mitochondrial apoptosis damage to cochlear stria vascularis pericytes via the ROS-mediated Bcl-2/CytC/AIF pathway.
Shi TF, Zhou Z, Jiang WJ, Huang TL, Si JQ, Li L. Shi TF, et al. Redox Rep. 2024 Dec;29(1):2382943. doi: 10.1080/13510002.2024.2382943. Epub 2024 Aug 2. Redox Rep. 2024. PMID: 39092597 Free PMC article. - hucMSC-sEVs-Derived 14-3-3_ζ_ Serves as a Bridge between YAP and Autophagy in Diabetic Kidney Disease.
Yin S, Liu W, Ji C, Zhu Y, Shan Y, Zhou Z, Chen W, Zhang L, Sun Z, Zhou W, Qian H. Yin S, et al. Oxid Med Cell Longev. 2022 Sep 22;2022:3281896. doi: 10.1155/2022/3281896. eCollection 2022. Oxid Med Cell Longev. 2022. PMID: 36199425 Free PMC article. - IGF-1R/β-catenin signaling axis is involved in type 2 diabetic osteoporosis.
Zhang ZD, Ren H, Wang WX, Shen GY, Huang JJ, Zhan MQ, Tang JJ, Yu X, Zhang YZ, Liang D, Yang ZD, Jiang XB. Zhang ZD, et al. J Zhejiang Univ Sci B. 2019 Oct.;20(10):838-848. doi: 10.1631/jzus.B1800648. J Zhejiang Univ Sci B. 2019. PMID: 31489803 Free PMC article.
MeSH terms
Substances
LinkOut - more resources
Full Text Sources
Other Literature Sources
Medical
Miscellaneous