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      KCI등재 SCOPUS SCIE

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

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      https://www.riss.kr/link?id=A103637264

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      다국어 초록 (Multilingual Abstract)

      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 regul...

      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.

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      참고문헌 (Reference)

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      1 Fagerholm V, "alpha2-adrenoceptor regulation of blood glucose homeostasis" 108 : 365-370, 2011

      2 Sim YB, "The modulatory role of alpha-melanocyte stimulating hormone administered spinally in the regulation of blood glucose level in d-glucose-fed and restraint stress mouse models" 48 : 207-212, 2014

      3 Hornung JP., "The human raphe nuclei and the serotonergic system" 26 : 331-343, 2003

      4 Sugimoto Y, "The effects of the serotonin1A receptor agonist buspirone on the blood glucose and pancreatic hormones in rats" 60 : 145-148, 1992

      5 Lechin F, "The effect of serotonin (5-HT) on insulin secretion" 25 : 339-346, 1975

      6 Finnegan KT, "The amine-depleting effects of 5,7-dihydroxytryptamine (5,7-DHT) in C57BL/6 mice do not increase with age" 496 : 251-256, 1989

      7 Jørgen Jensen, "The Role of Skeletal Muscle Glycogen Breakdown for Regulation of Insulin Sensitivity by Exercise" Frontiers Media SA 2 : 2011

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      9 Lin MT, "Stimulation of 5-hydroxytryptamine nerve cells in dorsal and median raphe nuclei elevates blood glucose in rats" 417 : 441-445, 1991

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      연월일 이력구분 이력상세 등재구분
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      학술지 인용정보

      학술지 인용정보
      기준연도 WOS-KCI 통합IF(2년) KCIF(2년) KCIF(3년)
      2016 0.45 0.24 0.33
      KCIF(4년) KCIF(5년) 중심성지수(3년) 즉시성지수
      0.28 0.26 0.395 0.04
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