Effect of pertussis toxin pretreated centrally on blood glucose level induced by stress.
10.4196/kjpp.2016.20.5.467
- Author:
Hong Won SUH
1
;
Yun Beom SIM
;
Soo Hyun PARK
;
Naveen SHARMA
;
Hyun Ju IM
;
Jae Seung HONG
Author Information
1. Department of Pharmacology, Institute of Natural Medicine, College of Medicine, Hallym University, Chuncheon 24252, Korea.
- Publication Type:Original Article
- Keywords:
Blood glucose;
Cold-water swimming stress;
Emotional stress-Physical stress;
Pertussis toxin-sensitive G proteins;
Restraint stress
- MeSH:
Animals;
Blood Glucose*;
Corticosterone;
GTP-Binding Proteins;
Hyperglycemia;
Hypoglycemia;
Insulin;
Mice;
Pertussis Toxin*;
Plasma;
Stress, Psychological;
Swimming;
Up-Regulation;
Whooping Cough*
- From:The Korean Journal of Physiology and Pharmacology
2016;20(5):467-476
- CountryRepublic of Korea
- Language:English
-
Abstract:
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.
