Effect of Sulfonylureas Administered Centrally on the Blood Glucose Level in Immobilization Stress Model

Animal Cells and Systems

Kim

et al. 2016

Self Cite

5,7-Dihydroxytryptamine (5,7-DHT) is a neurotoxin which causes the depletion of serotonin. Moreover, the serotonergic system is the regulator of the blood glucose level. However, the role of centrally located serotonergic system in blood glucose regulation after D-glucose feed and immobilization (IMO) stress was not clearly characterized yet. Thus the present study was designed to examine the effect of 5,7-DHT administered intracerebroventricularly (i.c.v.) or intrathecally (i.t.) on the blood glucose level in D-glucose-fed and immobilization stress models. Mice were pretreated once i.c.v. or i.t. with 5,7-DHT (from 10 to 40 µg) for 3 days and D-glucose (2 g/kg) was fed orally. The blood glucose level was measured at 0, 30, 60 and 120 min after Dglucose feeding and immobilization stress initiation. We found that i.c.v. or i.t. pretreatment with 5,7-DHT attenuated the blood glucose level in both animal models. D-glucose feeding causes an increase in plasma insulin level, whereas the plasma corticosterone level was downregulated in the D-glucose-fed model. The i.c.v. or i.t. pretreatment with 5,7-DHT alone slightly increased the plasma corticosterone level. In addition, the i.c.v. or i.t. pretreatment with 5,7-DHT caused a reversal of the downregulation of plasma corticosterone level induced by D-glucose feeding, whereas immobilization stress causes an increase in plasma corticosterone and insulin levels. The i.c.v or i.t. pretreatment with 5,7-DHT attenuated the immobilization stress-induced plasma corticosterone and plasma insulin levels. Our results suggest that supraspinal and spinal depletion of serotonin appears to be responsible for the downregulation of blood glucose level in both D-glucose-fed and immobilization stress models. ARTICLE HISTORY

Section: Discussionsupporting

confidence: 82%

Effects of 5,7-dihroxytryptamine administered supraspinally or spinally on the blood glucose level in D-glucose-fed and immobilization stress models

Animal Cells and Systems

Kim

et al. 2016

Self Cite

“…And also in our previous study, we similarly observed that the increase in the blood glucose level after acute IMO was accompanied by a rise in the plasma insulin level. The elevation of the insulin level appears to maintain a homeostatic regulation of the blood glucose in IMO (Sharma et al 2015). In an earlier reported study, supraspinally administration with histamine H3 receptor agonist (proxyfan) significantly decreases the glucose level compared with control mice (Henry et al 2011).…”

Section: Discussionmentioning

confidence: 87%

Effect of histamine receptors agonists or antagonists administered intracerebroventricularly and intrathecally on the blood glucose level in immobilization stress model

Sharma

Animal Cells and Systems

et al. 2015

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Effects of histamine receptors agonists or antagonists administered centrally (supraspinally or spinally) on immobilization stress-induced blood glucose levels were studied in Institute for Cancer Research mice. Mice were pretreated intracerebroventricularly (i.c.v.) or intrathecally (i.t.) with histamine (H1, H2, H3 and H4) receptor agonists or antagonists 10 min prior to immobilization stress (IMO) stimulation for 30 min. We found that the increased blood glucose level induced by IMO was attenuated by the i.c.v. pretreatment with α-methylhistamine (H3 agonist). However, H3 antagonist, H1, H2 and H4 receptor agonists and antagonists did not affect the blood glucose level. Also, i.t. pretreatment with α-methylhistamine or VUF 8430 attenuated the increased blood glucose level induced by IMO. In addition, cetirizine and carcinine enhanced the increased blood glucose level induced by IMO. However, the blood glucose level was not affected by H1 and H2 receptor agonists, H2 and H4 receptor antagonists. Corticosterone and insulin levels were also measured in α-methylhistamine (i.c.v or i.t) and with VUF 8430, carcinine and cetirizine (i.t.) treated group. We found that the corticosterone level was increased only by i.t treatment with α-methylhistamine, whereas the insulin level was attenuated by i.c.v or i.t. treatment with α-methylhistamine and i.t treatment with VUF 8430, carcinine and cetirizine. Our results suggest the active involvement of histamine receptor in blood glucose regulation in IMO.

“…In previous studies, we and others have observed that blood glucose level is increased in various types of animal stress models [ 31 32 33 34 ]. It has generally been known that the hyperglycemic effect is induced by both physical and emotional stress.…”

Section: Discussionmentioning

confidence: 99%

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

Suh

Korean J Physiol Pharmacol

et al. 2016

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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.