Investigations of the mechanism of the reduction of plasma glucose by cold-stress in streptozotocin-induced diabetic rats

Liu, I.M.; Niu, Chiang Shan; Chi, Tzong‐Cherng; Kuo, Daih‐Huang

doi:10.1016/s0306-4522(99)00068-8

Cited by 31 publications

(35 citation statements)

References 33 publications

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“…It has been reported that blood glucose level was increased by the exposure to cold stress for 60 min in normal rat (25) but there is another report showing no…”

Section: Discussionmentioning

confidence: 92%

Mice Lacking Cav2.3 (α1E) Calcium Channel Exhibit Hyperglycemia

Matsuda

Saegusa

Zong

et al. 2001

Biochemical and Biophysical Research Communications

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“…It has been reported that blood glucose level was increased by the exposure to cold stress for 60 min in normal rat (25) but there is another report showing no…”

Section: Discussionmentioning

confidence: 92%

Mice Lacking Cav2.3 (α1E) Calcium Channel Exhibit Hyperglycemia

Matsuda

Saegusa

Zong

et al. 2001

Biochemical and Biophysical Research Communications

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“…In healthy volunteers and insulin-dependent diabetic patients, infusion of β-endorphin increased plasma glucagon with an increase of plasma glucose [23]. However, injection of β-endorphin decreased plasma glucose in STZ-diabetic rats [24]. This difference might be due to the purity and/or concentration of synthetic peptides used, which might affect the variable subtype of opioid receptors.…”

Section: Discussionmentioning

confidence: 99%

Activation of imidazoline receptors in adrenal gland to lower plasma glucose in streptozotocin-induced diabetic rats

et al. 2005

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Our results suggest that agmatine may activate I(2)-imidazoline receptors in the adrenal gland. This enhances secretion of beta-endorphin, which can activate opioid mu-receptors to increase GLUT4 gene expression and/or suppress hepatic PEPCK gene expression, resulting in a lowering of plasma glucose in diabetic rats lacking insulin. The results provide a potential new target for intervention in type 1 diabetes.

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“…The short half-life of peptide (31) limited its clinical development. Actually, injection of exogenous ␤-endorphin produced only a transient lowering of plasma glucose in STZ-induced diabetic rats (6). Otherwise, tramadol decreased the plasma glucose in normal rats at a dose of 1-5 mg/kg, a level that was higher than that required to be effective in diabetic rats.…”

Section: Discussionmentioning

confidence: 99%

“…However, the effect of opioids on glucose homeostasis does not depend entirely on insulin. In our previous study (6), we found that ␤-endorphin is also responsible for the reduction of plasma glucose during cold exposure in streptozotocin (STZ)-induced diabetic rats, which were used as a type 1 diabetes model. Actually, injection of exogenous ␤-endorphin lowered plasma glucose in STZ-induced diabetic rats (6).…”

mentioning

confidence: 99%

“…In our previous study (6), we found that ␤-endorphin is also responsible for the reduction of plasma glucose during cold exposure in streptozotocin (STZ)-induced diabetic rats, which were used as a type 1 diabetes model. Actually, injection of exogenous ␤-endorphin lowered plasma glucose in STZ-induced diabetic rats (6). Moreover, we demonstrated that loperamide, an agonist of opioid -receptors, could lower plasma glucose in STZ-induced diabetic rats (7).…”

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confidence: 99%

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Plasma Glucose–Lowering Effect of Tramadol in Streptozotocin-Induced Diabetic Rats

et al. 2001

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The effect of tramadol on the plasma glucose level of streptozotocin (STZ)-induced diabetic rats was investigated. A dose-dependent lowering of plasma glucose was seen in the fasting STZ-induced diabetic rats 30 min after intravenous injection of tramadol. This effect of tramadol was abolished by pretreatment with naloxone or naloxonazine at doses sufficient to block opioid -receptors. However, response to tramadol was not changed in STZ-induced diabetic rats receiving p-chlorophenylalanine at a dose sufficient to deplete endogenous 5-hydroxytrptamine (5-HT). Therefore, mediation of 5-HT in this action of tramadol is ruled out. In isolated soleus muscle, tramadol enhanced the uptake of radioactive glucose in a concentration-dependent manner. The stimulatory effects of tramadol on glycogen synthesis were also seen in hepatocytes isolated from STZ-induced diabetic rats. The blockade of these actions by naloxone and naloxonazine indicated the mediation of opioid -receptors. The mRNA and protein levels of the subtype 4 form of glucose transporter in soleus muscle were increased after repeated treatments for 4 days with tramadol in STZ-induced diabetic rats. Moreover, similar repeated treatments with tramadol reversed the elevated mRNA and protein levels of phosphoenolpyruvate carboxykinase in the liver of STZinduced diabetic rats. These results suggest that activation of opioid -receptors by tramadol can increase the utilization of glucose and/or decrease hepatic gluconeogenesis to lower plasma glucose in diabetic rats lacking insulin. Diabetes 50: [2815][2816][2817][2818][2819][2820][2821] 2001 U nlike the analgesic effects of opioids, their effects on glucose metabolism in diabetes have received little attention. In diabetic patients, ␤-endorphin stimulates insulin secretion (1). Also, ␤-endorphin is known to be involved in plasma glucose homeostasis (2,3). Opioid receptors in the pancreas have been investigated for this regulation of plasma glucose (4,5). However, the effect of opioids on glucose homeostasis does not depend entirely on insulin. In our previous study (6), we found that ␤-endorphin is also responsible for the reduction of plasma glucose during cold exposure in streptozotocin (STZ)-induced diabetic rats, which were used as a type 1 diabetes model. Actually, injection of exogenous ␤-endorphin lowered plasma glucose in STZ-induced diabetic rats (6). Moreover, we demonstrated that loperamide, an agonist of opioid -receptors, could lower plasma glucose in STZ-induced diabetic rats (7). Thus, it has been shown that activation of opioid -receptors may produce a plasma glucose-lowering effect in diabetic rats lacking insulin. Clinically, tramadol has widely been used as an analgesic through activation of opioid -receptors (8 -11) and others (9). In the present study, we investigated the effect of tramadol on plasma glucose and characterized the role of opioid -receptors in the action of tramadol during the absence of insulin, both in vivo and in vitro. We also examined the influence of repeated treatmen...

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Investigations of the mechanism of the reduction of plasma glucose by cold-stress in streptozotocin-induced diabetic rats

Cited by 31 publications

References 33 publications

Mice Lacking Cav2.3 (α1E) Calcium Channel Exhibit Hyperglycemia

Mice Lacking Cav2.3 (α1E) Calcium Channel Exhibit Hyperglycemia

Activation of imidazoline receptors in adrenal gland to lower plasma glucose in streptozotocin-induced diabetic rats

Plasma Glucose–Lowering Effect of Tramadol in Streptozotocin-Induced Diabetic Rats

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