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

Azita Parvaneh Tafreshi; Razieh jalal; Shamila Darvishalipoor; Hoori Sepehri; Khosrow Adeli

International Journal of Endocrinology and Metabolism

Research Institute for Endocrine Sciences

Current Issue All Issues In Press Search

Journal Information Boards and Committees Indexing and Listing Sources Journal Metrics Open Peer Review (OPR)Publication Ethics and Malpractice Statement Contact Us Support Reviewer and AE Registration Form

APC

Authors Guide Submit Manuscript

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

Author(s):

Azita Parvaneh Tafreshi¹,

Razieh jalal²,

Shamila Darvishalipoor^1,*,

Hoori Sepehri³,

Khosrow Adeli⁴

1Department of Basic Sciences in Biotechnology, The National Research Institute of Genetic Engineering and Biotechnology, Tehran, IR.Iran

2Department of Chemistry, Ferdowsi University, Mashad, Tehran, IR.Iran

3Department of Physiology, Faculty of Sciences, Tehran, IR.Iran

4Department 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:Aug 31, 2010

Article type:Research Article

Received:May 29, 2019

Accepted:Aug 31, 2010

How to Cite:Azita Parvaneh TafreshiRazieh jalalShamila DarvishalipoorHoori SepehriKhosrow AdeliInvestigation on the expression of IGF-I protein in insulin-resistant rat brain.Int J Endocrinol Metab.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.

Keywords

Diabetes Insulin Resistance Brain IGF-I

Fulltext

This part is available in the PDF file.

References

1.
The references are available in the PDF file.

comments