Plasma glucose-lowering effect of β-endorphin in streptozotocin-induced diabetic rats

J. T. Cheng, I. M. Liu, T. F. Tzeng, C. C. Tsai, Tung Yuan Lai

Research output: Contribution to journalArticle

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Abstract

The effect of β-endorphin on plasma glucose levels was investigated in streptozotocin-induced diabetic rats (STZ-diabetic rats). A dose-dependent lowering of plasma glucose was observed in the fasting STZ-diabetic rat fifteen minutes after intravenous injection of β-endorphin. The plasma glucose-lowering effect of β-endorphin was abolished by pretreatment with naloxone or naloxonazine at doses sufficient to block opioid μ-receptors. Also, unlike wild-type diabetic mice, β-endorphin failed to induce its plasma glucose-lowering effect in the opioid μ-receptor knock-out diabetic mice. In isolated soleus muscle, β-endorphin enhanced the uptake of radioactive glucose in a concentration-dependent manner. Stimulatory effects of β-endorphin on glycogen synthesis were also seen in hepatocytes isolated from STZ-diabetic rats. The blockade of these actions by naloxone and naloxonazine indicated the mediation of opioid μ-receptors. In the presence of U73312, the specific inhibitor of phospholipase C (PLC), the uptake of radioactive glucose into isolated soleus muscle induced by β-endorphin was reduced in a concentration-dependent manner, but it was not affected by U73343, the negative control of U73312. Moreover, chelerythrine and GF 109203X diminished the stimulatory action of β-endorphin on the uptake of radioactive glucose at a concentration sufficient to inhibit protein kinase C (PKC). The data obtained suggest that activating opioid μ-receptors by β-endorphin may increase glucose utilization in peripheral tissues via the PLC-PKC pathway to lower plasma glucose in diabetic rats lacking insulin.

Original languageEnglish (US)
Pages (from-to)570-576
Number of pages7
JournalHormone and Metabolic Research
Volume34
Issue number10
DOIs
StatePublished - Oct 1 2002

Fingerprint

Endorphins
Streptozocin
Rats
Plasmas
Glucose
Opioid Receptors
Type C Phospholipases
Naloxone
Protein Kinase C
Muscle
Skeletal Muscle
Glycogen
Knockout Mice
Intravenous Injections
Hepatocytes
Fasting
Insulin
Tissue

Keywords

  • Hepatocytes
  • Opioid μ-Receptors
  • Phospholipase C
  • Protein Kinase C
  • Soleus Muscle
  • β-Endorphin

ASJC Scopus subject areas

  • Endocrinology, Diabetes and Metabolism
  • Biochemistry
  • Endocrinology
  • Clinical Biochemistry
  • Biochemistry, medical

Cite this

Plasma glucose-lowering effect of β-endorphin in streptozotocin-induced diabetic rats. / Cheng, J. T.; Liu, I. M.; Tzeng, T. F.; Tsai, C. C.; Lai, Tung Yuan.

In: Hormone and Metabolic Research, Vol. 34, No. 10, 01.10.2002, p. 570-576.

Research output: Contribution to journalArticle

Cheng, J. T. ; Liu, I. M. ; Tzeng, T. F. ; Tsai, C. C. ; Lai, Tung Yuan. / Plasma glucose-lowering effect of β-endorphin in streptozotocin-induced diabetic rats. In: Hormone and Metabolic Research. 2002 ; Vol. 34, No. 10. pp. 570-576.
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AB - The effect of β-endorphin on plasma glucose levels was investigated in streptozotocin-induced diabetic rats (STZ-diabetic rats). A dose-dependent lowering of plasma glucose was observed in the fasting STZ-diabetic rat fifteen minutes after intravenous injection of β-endorphin. The plasma glucose-lowering effect of β-endorphin was abolished by pretreatment with naloxone or naloxonazine at doses sufficient to block opioid μ-receptors. Also, unlike wild-type diabetic mice, β-endorphin failed to induce its plasma glucose-lowering effect in the opioid μ-receptor knock-out diabetic mice. In isolated soleus muscle, β-endorphin enhanced the uptake of radioactive glucose in a concentration-dependent manner. Stimulatory effects of β-endorphin on glycogen synthesis were also seen in hepatocytes isolated from STZ-diabetic rats. The blockade of these actions by naloxone and naloxonazine indicated the mediation of opioid μ-receptors. In the presence of U73312, the specific inhibitor of phospholipase C (PLC), the uptake of radioactive glucose into isolated soleus muscle induced by β-endorphin was reduced in a concentration-dependent manner, but it was not affected by U73343, the negative control of U73312. Moreover, chelerythrine and GF 109203X diminished the stimulatory action of β-endorphin on the uptake of radioactive glucose at a concentration sufficient to inhibit protein kinase C (PKC). The data obtained suggest that activating opioid μ-receptors by β-endorphin may increase glucose utilization in peripheral tissues via the PLC-PKC pathway to lower plasma glucose in diabetic rats lacking insulin.

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