Insulin receptor and glucose transporter-4 expression in the skeletal muscle of chronically stressed rats
Date
2016
Authors
Morakinyo, AO
Iranloye, BO
Samuel, TA
Mofolorunso, AM
Adegoke, OA
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Abstract
Background: Stress defined as a disruption in the normal homeostatic functions of an organism caused by stressor (a physiological or psychological challenge) is an unavoidable normal component of life. Previous studies suggest that stress hormones have acute adverse effects on glycaemic control. The aim of this study was to assess the effect of chronic psychological and physical stress on the expression of insulin receptor and GLUT4 transporters in male Sprague-Dawley rats. Methods: Male rats (12 weeks old) were randomly distributed into 3 groups: control, water avoidance stress (WAS), forced swimming stress (FSS). The stress procedures were performed between 9:00 and 11:00 am to minimize the effect of circadian rhythm and lasted for 28 consecutive days. Levels of insulin and corticosterone in the blood were determined using enzyme-linked immunosorbent assay. Glucose metabolism was assessed by glucose tolerance test (GTT) and insulin tolerance test (ITT), and expression of insulin receptor (INSR) and glucose transporter-4 (GLUT4) in skeletal muscle. Results: The FSS rats had decreased food intake as well as final body weight and without adverse changes in GTT, stress worsened insulin sensitivity in FSS rats and increased insulin in the blood. Stress also increased corticosterone, decreased INSR and GLUT4 in the skeletal muscle of both groups. Conclusion: Chronic stress evokes insulin insensitivity and impairs glucose metabolism through the down-regulation of INSR and GLUT4 in skeletal muscles.
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Keywords
Chronic stress , Glucose tolerance , Glucose transporter , Insulin sensitivity , Corticosterone
Citation
Morakinyo AO, Iranloye BO, Samuel TA, Mofolorunso AM and Adegoke OA. (2016). Insulin receptor and glucose transporter-4 expression in the skeletal muscle of chronically stressed rats. Journal of African Association of Physiological Sciences 4: 21-31