Various pain stimulations cause an increase of the blood glucose level

Abstract

The relationship between pain stimulation and the blood glucose level was studied in ICR mice. We examined the possible change of the blood glucose level after the pain stimulation induced by acetic acid injected intraperitoneally (i.p.),, formalin injected subcutaneously (s.c.) into the hind paw, or substance P (SP), glutamate, and proinflammatory cytokines (TNF-a and IFN-g) injected intrathecally (i.t.). We found in the present study that acetic acid, formalin, SP, TNF-a, and IFN-g increased the blood glucose level. The blood glucose level reached at maximal state 30 min and returned to normal level 2 h after the pain stimulation in a fasting group. Furthermore, acetic acid, formalin, SP, TNF-a, and IFN-g caused the elevation of the blood glucose level in D-glucose-fed group only in an additive manner. However, i.t. injection of glutamate did not alter the blood glucose level in a fasting group. In contrast, i.t. injection of glutamate enhanced the blood glucose level in the D-glucose-fed group. Our results suggest that the blood glucose level appears to be differentially regulated by various pain stimulation induced by acetic acid, formalin, SP, glutamate, and pro-inflammatory cytokines.

Effect of Cholera Toxin Administered Supraspinally or Spinally on the Blood Glucose Level in Pain and D-Glucose Fed Animal Models

“…Our result is in line with the previous studies which show D-glucose feeding increases the blood glucose level [9,14]. Although supraspinal treatment with CTX alone does not affect the blood glucose level (Fig.…”

“…We recently found that the blood glucose level is elevated in acetic acid-induced writhing pain animal model as well as formalin pain model [9]. Furthermore, we recently found that pain stimulation induced by proinflammatory cytokines such as TNF-α (tumor necrosis factor-α), IFN-γ (interferon-γ) and IL-1β (inetrleukin1β) administered spinally, also causes an elevation of the blood glucose level [9,14]. Similar to the results found in D-glucose fed animal model, we found in the present study that supraspina pretreatment with CTX further enhances the blood glucose level induced by formalin-induced pain stimulation (Fig.…”

“…Recently, we have reported that various types of pain stimulation cause an elevation of the blood glucose level and differentially modulates the blood glucose level in D-glucose-fed model [9]. In addition, spinal administration with CTX differentially affects pain behaviors induced by various pro-inflammatory cytokines [10].…”

Pertussis Toxin Administered Spinally Induces a Hypoglycemic Effect on Normal and Diabetic Mice

“…For example, in an earlier clinical study, Sala et al [47] reported that a lower dose of insulin is used to regulate the BGL in patients with spinal cord injury. In addition, we recently found that substance P or several proinflammatory cytokines such as TNF-α, IFN-γ and IL-1β administered spinally cause an elevation of the BGL [48,49]. Taken together from the results of our present study and other groups, more pharmacological studies on the role of the spinal cord in the regulation of the BGL should be performed in the future.…”

Activation of spinal α2 adrenergic receptors induces hyperglycemia in mouse though activating sympathetic outflow

“…In an earlier clinical study, Sala et al (1999) have reported that less dose of insulin is used to regulate the blood glucose level in patients with spinal cord injury. In addition, we recently found that substance P or several pro-inflammatory cytokines, such as TNF-α, IFN-γ and IL-1β administered spinally causes an elevation of the blood glucose level (Sim et al, 2012a(Sim et al, , 2012b. Furthermore, our recent study has also reported that GABA receptor agonists administered spinally cause the elevation of the blood glucose level (Sim et al, 2013).…”