Development of Wistar rat model of insulin resistance

doi:10.3748/wjg.v11.i24.3675

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Jun 28, 2005 (publication date) through Nov 27, 2024

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World Journal of Gastroenterology

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1007-9327

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Baishideng Publishing Group Inc, 7041 Koll Center Parkway, Suite 160, Pleasanton, CA 94566, USA

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World J Gastroenterol. Jun 28, 2005; 11(24): 3675-3679
Published online Jun 28, 2005. doi: 10.3748/wjg.v11.i24.3675

Development of Wistar rat model of insulin resistance

Jing Ai, Ning Wang, Mei Yang, Zhi-Min Du, Yong-Chun Zhang, Bao-Feng Yang

Jing Ai, Ning Wang, Mei Yang, Yong-Chun Zhang, Bao-Feng Yang, Department of Pharmacology, Harbin Medical University, Bio-Pharmaceutical Key Laboratory of Heilongjiang Province, Harbin 150086, Heilongjiang Province, China

Zhi-Min Du, State Base for Drug Clinical Trial, Harbin Medical University, Harbin 150086, Heilongjiang Province, China

Author contributions: All authors contributed equally to the work.

Supported by the Key Found of the Technological Office of Heilongjiang Province, No. 20010101001-00, the National Natural Science Foundation of China, No. 30371647, Foundation of Educational Office of Heilongjiang Province, No. 10531094

Correspondence to: Professor Bao-Feng Yang, Department of Pharmacology, Harbin Medical University, Harbin 150086, Heilongjiang Province, China. yangbf@ems.hrbmu.edu.cn

Telephone: +86-451-86671354 Fax: +86-451-86669482

Received: June 28, 2004
Revised: June 29, 2004
Accepted: August 5, 2004
Published online: June 28, 2005

Abstract

AIM: To establish a simplified and reliable animal model of insulin resistance with low cost in Wistar rats.

METHODS: Wistar rats were treated with a high fat emulsion by ig for 10 d. Changes of the diets, drinking and body weight were monitored every day and insulin resistance was evaluated by hyperinsulinemic-euglycemic clamp techniques and short insulin tolerance test using capillary blood glucose. Morphologic changes of liver, fat, skeletal muscles, and pancreatic islets were assessed under light microscope. mRNA expressions of GLUT2 and α-glucosidase in small intestine epithelium, GLUT4 in skeletal muscles and Kir6.2 in beta cell of islets were determined by in situ hybridization.

RESULTS: K_ITT was smaller in treated animals (4.5±0.9) than in untreated control Wistar rats (6.8±1.5), and so was glucose injection rate. Both adipocyte hypertrophy and large pancreatic islets were seen in high fat fed rats, but no changes of skeletal muscles and livers were observed. mRNA levels of GLUT2, α-glucosidase in small intestinal epithelium and Kir6.2 mRNA in beta cells of islets increased, whereas that of GLUT4 in skeletal muscles decreased in high fat fed group compared with normal control group.

CONCLUSION: An insulin resistance animal model in Wistar rats is established by ig special fat emulsion.

Keywords: Wistar rat; Insulin resistance; Model