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Effect of pertussis toxin pretreated centrally on blood glucose level induced by stress

In the present study, we examined the effect of pertussis toxin (PTX) administered centrally in a variety of stress-induced blood glucose level. Mice were exposed to stress after the pretreatment of PTX (0.05 or 0.1 µg) i.c.v. or i.t. once for 6 days. Blood glucose level was measured at 0, 30, 60 an...

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Autores principales: Suh, Hong-Won, Sim, Yun-Beom, Park, Soo-Hyun, Sharma, Naveen, Im, Hyun-Ju, Hong, Jae-Seung
Formato: Online Artículo Texto
Lenguaje:English
Publicado: The Korean Physiological Society and The Korean Society of Pharmacology 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5014993/
https://www.ncbi.nlm.nih.gov/pubmed/27610033
http://dx.doi.org/10.4196/kjpp.2016.20.5.467
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author Suh, Hong-Won
Sim, Yun-Beom
Park, Soo-Hyun
Sharma, Naveen
Im, Hyun-Ju
Hong, Jae-Seung
author_facet Suh, Hong-Won
Sim, Yun-Beom
Park, Soo-Hyun
Sharma, Naveen
Im, Hyun-Ju
Hong, Jae-Seung
author_sort Suh, Hong-Won
collection PubMed
description In the present study, we examined the effect of pertussis toxin (PTX) administered centrally in a variety of stress-induced blood glucose level. Mice were exposed to stress after the pretreatment of PTX (0.05 or 0.1 µg) i.c.v. or i.t. once for 6 days. Blood glucose level was measured at 0, 30, 60 and 120 min after stress stimulation. The blood glucose level was increased in all stress groups. The blood glucose level reached at maximum level after 30 min of stress stimulation and returned to a normal level after 2 h of stress stimulation in restraint stress, physical, and emotional stress groups. The blood glucose level induced by cold-water swimming stress was gradually increased up to 1 h and returned to the normal level. The intracerebroventricular (i.c.v.) or intrathecal (i.t.) pretreatment with PTX, a Gi inhibitor, alone produced a hypoglycemia and almost abolished the elevation of the blood level induced by stress stimulation. The central pretreatment with PTX caused a reduction of plasma insulin level, whereas plasma corticosterone level was further up-regulated in all stress models. Our results suggest that the hyperglycemia produced by physical stress, emotional stress, restraint stress, and the cold-water swimming stress appear to be mediated by activation of centrally located PTX-sensitive G proteins. The reduction of blood glucose level by PTX appears to due to the reduction of plasma insulin level. The reduction of blood glucose level by PTX was accompanied by the reduction of plasma insulin level. Plasma corticosterone level up-regulation by PTX in stress models may be due to a blood glucose homeostatic mechanism.
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spelling pubmed-50149932016-09-08 Effect of pertussis toxin pretreated centrally on blood glucose level induced by stress Suh, Hong-Won Sim, Yun-Beom Park, Soo-Hyun Sharma, Naveen Im, Hyun-Ju Hong, Jae-Seung Korean J Physiol Pharmacol Original Article In the present study, we examined the effect of pertussis toxin (PTX) administered centrally in a variety of stress-induced blood glucose level. Mice were exposed to stress after the pretreatment of PTX (0.05 or 0.1 µg) i.c.v. or i.t. once for 6 days. Blood glucose level was measured at 0, 30, 60 and 120 min after stress stimulation. The blood glucose level was increased in all stress groups. The blood glucose level reached at maximum level after 30 min of stress stimulation and returned to a normal level after 2 h of stress stimulation in restraint stress, physical, and emotional stress groups. The blood glucose level induced by cold-water swimming stress was gradually increased up to 1 h and returned to the normal level. The intracerebroventricular (i.c.v.) or intrathecal (i.t.) pretreatment with PTX, a Gi inhibitor, alone produced a hypoglycemia and almost abolished the elevation of the blood level induced by stress stimulation. The central pretreatment with PTX caused a reduction of plasma insulin level, whereas plasma corticosterone level was further up-regulated in all stress models. Our results suggest that the hyperglycemia produced by physical stress, emotional stress, restraint stress, and the cold-water swimming stress appear to be mediated by activation of centrally located PTX-sensitive G proteins. The reduction of blood glucose level by PTX appears to due to the reduction of plasma insulin level. The reduction of blood glucose level by PTX was accompanied by the reduction of plasma insulin level. Plasma corticosterone level up-regulation by PTX in stress models may be due to a blood glucose homeostatic mechanism. The Korean Physiological Society and The Korean Society of Pharmacology 2016-09 2016-08-26 /pmc/articles/PMC5014993/ /pubmed/27610033 http://dx.doi.org/10.4196/kjpp.2016.20.5.467 Text en Copyright © Korean J Physiol Pharmacol http://creativecommons.org/licenses/by-nc/4.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Original Article
Suh, Hong-Won
Sim, Yun-Beom
Park, Soo-Hyun
Sharma, Naveen
Im, Hyun-Ju
Hong, Jae-Seung
Effect of pertussis toxin pretreated centrally on blood glucose level induced by stress
title Effect of pertussis toxin pretreated centrally on blood glucose level induced by stress
title_full Effect of pertussis toxin pretreated centrally on blood glucose level induced by stress
title_fullStr Effect of pertussis toxin pretreated centrally on blood glucose level induced by stress
title_full_unstemmed Effect of pertussis toxin pretreated centrally on blood glucose level induced by stress
title_short Effect of pertussis toxin pretreated centrally on blood glucose level induced by stress
title_sort effect of pertussis toxin pretreated centrally on blood glucose level induced by stress
topic Original Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5014993/
https://www.ncbi.nlm.nih.gov/pubmed/27610033
http://dx.doi.org/10.4196/kjpp.2016.20.5.467
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