1996 Fiscal Year Final Research Report Summary
The role of opioid agonist and cytokine in metabolic changes mediated by central nervous system
| Project/Area Number |
06671321
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Digestive surgery
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| Research Institution | Kurume University |
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Principal Investigator |
YOSHIDA Shogo Faculty of Medicine, Kurume University, assistant., 医学部, 助手 (30191589)
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| Co-Investigator(Kenkyū-buntansha) |
ISHIBASHI Nobuya Faculty of Medicine, Kurume University, assistant., 医学部, 助手 (90248427)
KAIBARA Atsushi Faculty of Medicine, Kurume University, assistant., 医学部, 助手 (20204315)
SHIROUZU Yuichirou Faculty of Medicine, Kurume University, assistant., 医学部, 助手 (20258429)
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| Project Period (FY) |
1994 – 1996
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| Keywords | cytokine / surgical stress / protein turnover / gluconeogenesis / stress hormone / opioid |
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| Research Abstract |
The objective of theses series of experiment was to determine whether opioid receptor was involved in cytokine mediated metabolic change. Male SD rats were catheterized into the cerebroventricular and jugular vein. The treatment was performed 6 days after the surgery. Glucose production and protein turnover were measured by a constant infusion method of 1-^<13> C-leucine and 6-^3 H-glucose. Morphine levels in the brain were determined, using coulometry analysis. Intra-cerebroventicular (ICV) injection of TNFalpha (600ng) caused an increase in both glucose production and whole body protein breakdown rate, and a decrease in muscle protein synthesis rate. This metabolic change was associated with an increase in serum corticosterone and catecholamine levels. In the contrary, these were no differences in metabolic and hormonal changes with systemic administration of TNF compared to the control group, suggesting that there is a significant pathway to facilitate metabolic changes mediated by cytokine via central nervous system.
Metabolic alteration induced by intra-cerebral injection of TNF was inhibited by prophylactic administration of fentanyl citrate (50mu/g/kg). Furthermore, systemic administration of fentanyl inhibited an increase in the serum stress hormone levels induced by ICV injection of TNF.These results suggested that opioid receptor was involved in cytokine mediated metabolic alteration via central nervous system.
Morphine levels in the brain were increased with ICV injection of TNF,but no increase was found with systemic injection of TNF.Furthermore, prophylactic administration of fentany prevented an increase in the brain morphine levels induced by ICV THF.
We concluded that metabolic change induced by cytokine was partially mediated via central nervous system and opioid receptor was involved in this pathway.
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