Searchable abstracts of presentations at key conferences in endocrinology
Endocrine Abstracts (2016) 44 P175 | DOI: 10.1530/endoabs.44.P175

SFEBES2016 Poster Presentations Obesity and Metabolism (26 abstracts)

Impaired glucose tolerance due to altered expression of INSR and GLUT4 receptors in restraint stress rat

Ayodele Morakinyo 1 , Kolawole Ajiboye 2 & Olufeyi Adegoke 1


1University of Lagos, Lagos, Nigeria; 2Babcock University, Ilishan Remo, Ogun, Nigeria.


The study investigated the potential alteration in the level of insulin and adiponectin, as well as the expression of INSR and GLUT-4 in chronic restraint stress rats. Sprague–Dawley rats were randomly divided into two groups: the control group and stress group in which the rats were exposed to one of the four different restraint stressors; 1 h, twice daily for a period of 7 days (S7D), 14 days (S14D) and 28 days (S28D). To minimize habituation, the sequence of the stressors was randomized for both the morning and afternoon sessions of the first week of exposure, and was repeated during the second week with the morning and afternoon sequences exchanged. Glucose tolerance and insulin sensitivity were evaluated following the final stress exposure. ELISA were performed to assess the level of insulin and adiponectin as well as expression of INSR and GLUT4 protein in skeletal muscle. Plasma corticosterone level was also determined a marker of stress exposure.

Restraint stress for 7 days caused transient glucose intolerance, while S14D rats demonstrated increased glucose intolerance and mild insulin insensitivity. However, restraint stress for 28 days had no effect on glucose tolerance, but did cause an increase in glucose response to insulin challenge. The serum level of adiponectin was significantly (P<0.05) lower compared with the control value while insulin remained unchanged except at in S28D rats that had a significant (P<0.05) increase. The expression of INSR and GLUT4 receptors were significantly (P<0.05) decreased in the skeletal muscle of restraint stress exposed rats. There was a significant (P<0.05) increase in the plasma corticosterone level of the stress rats compared with their control counterparts.

Restraint stress caused glucose intolerance in male Sprague–Dawley rats but becomes abated with prolonged exposure arguably due to the blunted insulin signalling in skeletal muscle.

Volume 44

Society for Endocrinology BES 2016

Brighton, UK
07 Nov 2016 - 09 Nov 2016

Society for Endocrinology 

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