Investigation on the expression of IGF-I protein in insulin-resistant rat brain

authors:

avatar Azita Parvaneh Tafreshi 1 , avatar Razieh jalal 2 , avatar Shamila Darvishalipoor 1 , * , avatar Hoori Sepehri 3 , avatar Khosrow Adeli 4

Department of Basic Sciences in Biotechnology, The National Research Institute of Genetic Engineering and Biotechnology, Tehran, IR.Iran
Department of Chemistry, Ferdowsi University, Mashad, Tehran, IR.Iran
Department of Physiology, Faculty of Sciences, Tehran, IR.Iran
Department of Clinical Biochemistry, Hospital for Sick Children, University of Toronto, Toronto, Ontario, Canada
International Journal of Endocrinology and Metabolism: Vol.8, issue 3; e94645
published online: August 31, 2010
article type: Research Article
received: May 29, 2019
accepted: August 31, 2010

How To Cite Parvaneh Tafreshi A, jalal R, Darvishalipoor S, Sepehri H, Adeli K. Investigation on the expression of IGF-I protein in insulin-resistant rat brain. Int J Endocrinol Metab. 2010;8(3):e94645. 

Abstract

Diabetes Insulin Resistance Brain IGF-I Background: In insulin-resistance animal models, insulin uptake from the periphery to the brain is impaired. Although brain insulin is not involved in glucose transfer to the neurons, it is required for neuron survival and function, mediated by binding to insulin receptors. Furthermore, an insulin homologue called insulin-like growth factor (IGF-I), which is abundantly expressed in mature neurons and acts in parallel with insulin in the brain, has the ability to bind to the insulin receptor and trigger the signal transduction pathway. Objectives: Although reduced levels of brain insulin and serum IGF-I have been reported during insulin resistance, no data is available on IGF-I levels in the brain. In this study, we sought to investigate if the expression of IGF-I is also altered in brains of insulin-resistant rats. Materials and Methods: Wistar rats were given 10% fructose in their drinking water for up to 4 months to induce insulin resistance. The rats were then killed and perfused with PFA 4%; then, there brains were excised, sectioned, and examined for immunoreactivity of IGF-I. Results: Our results showed an increased intensity of IGF-I in most brain areas of the insulin-resistant rats. Conclusions: Altogether, an increased expression of IGF-I in the brain could be a compensatory mechanism and substitute for low levels or lack of insulin in the brains of insulin-resistant animals.

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References

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