• 대한약리학회:학술대회논문집
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• 대한약리학회 2006년도 58th Annual Meeting of The Korean Society of Pharmacology
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• pp.63-63
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• 2006

• 대한수의학회지
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• 제32권3호
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• pp.321-331
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• 1992

The regional distribution and relative frequency of gastrointestinal endocrine cells were studied immunohistochemically in the gastrointestinal mucosa and pancreas of the fresh water turtle. Ten kinds of endocrine cells were identified in the gastrointestinal tract. Cholecystokinin-8-, bovine pancreatic polypetide-and glucagon-immunoreactive cells were seen throughout the gastrointestinal tract, also among them cholecystokinin-8-immunoreactive cells were most predominant in segment III. Although gastrin- and gastrin/cholecystokinin-immunoreactive cells were found from segment III to VI and X, respectively, they were numerous in segment III. Somatostatin-immunoreactive cells were observed from segment I to VII. 5-hydroxytryptamine- immunoreactive cells were detected in segment I, III, VIII, IX and X. Human pancreatic polypeptide-immunoreactive cells were demonstrated in segment V, VI, VIII, IX and X. Insulin-immunoreactive cells were found from segment III to X except for segment VIII, but rare in segment VII. Neurotensin-immunoreactive cells were found to be restricted to segment VIII, IX and X. No porcine chromogranin-, substance P- and bombesin-immunoreactive cells were detected throughout the gastrointestinal tract of the fresh water turtle. Although typical mammalian pancreatic islets encapsulated by connective tissue were not present in this species, five kinds of endocrine cells-glucagon, insulin, somatostatin, bovine pancreatic polypeptide and 5-hydroxytryptamine-were found in forming small or large groups and scattered in the exocrine gland region. However porcine chromogranin- and motilin-immunoreactive cells could not be demonstrated in the pancreas.

• Nutrition Research and Practice
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• 제8권2호
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• pp.146-150
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• 2014

BACKGROUND/OBJECTIVES: Cholecystokinin (CCK), a hormone or neuropeptide, is secreted in response to intraluminal nutrients by enteroendocrine I-cells of the intestine and has important physiological actions related to appetite regulation and satiety. The stimulation on CCK secretion from the intestine is of potential relevance for body weight management. Naringenin (4',5,7-trihydroxyflavanone) and its glycoside naringin (naringenin 7-rhamnoglucoside) have been reported to have many biological functions. In the current study, we investigated the question of whether naringenin and naringin could stimulate CCK secretion and then examined the mechanisms involved in CCK release. MATERIALS/METHODS: STC-1 cells were used as a model of enteroendocrine cells. CCK release and changes in intracellular $Ca^{2+}$ ($[Ca^{2+}]_i$) were measured after incubation of cells with naringenin and naringin for 1 h. RESULTS: Naringenin caused significant (P < 0.05) stimulation of CCK secretion, but naringin did not. In addition, regarding the secretory mechanisms, naringenin-induced CCK secretion involved increases in $[Ca^{2+}]_i$, influx of extracellular $Ca^{2+}$, at least in part, and activation of TRP channels, including TRPA1. CONCLUSION: Findings of this study suggest that naringenin could have a role in appetite regulation and satiety.

• The Korean Journal of Physiology and Pharmacology
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• 제4권4호
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• pp.275-281
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• 2000

Cholecystokinin (CCK) is a gastrointestinal hormone which plays an important role in satiety and gastric motility. It is also widely distributed throughout the central nervous system, where it appears to be involved in the central control of anxiety, feeding behavior and nociception. Two distinct CCK receptor types, $CCK_A$ and $CCK_B,$ have been found in the brain. Both CCK receptors coexist in the rat nucleus tractus solitarius (NTS), which is the primary center for the coordination of peripheral and central activities related to gastrointestinal, cardiovascular and respiratory functions. In order to study ionic actions of CCK on each type of receptor, we investigated the effects of CCK-8S on neurons located in the NTS of the rat using whole-cell patch-clamp recordings in brainstem slices. Application of CCK-8S, under current clamp, produced a membrane depolarization accompanied by action potential firing. This CCK-evoked excitation was dose-dependent $(10\;nM{\sim}10\;{\mu}M)$ and observed in more than 60% of NTS neurons. Under voltage clamp conditions, CCK-8S induced an inward current with a notably increased spontaneous excitatory synaptic activity. However, CCK-8S did not significantly change the amplitude of pharmacologically isolated and evoked EPSP(C)s. Using selective $CCK_A$ and $CCK_B$ receptor antagonists, we observed two different effects of CCK-8S, which suggest $CCK_A$ receptor-mediated inhibitory and $CCK_B$ receptor-mediated excitatory effects in the NTS. These results may help to explain the ability of CCK to modulate gastrointestinal and other reflex systems in the NTS.

• 대한약리학회지
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• 제31권1호
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• pp.11-15
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• 1995

연수의 세로토닌 신경계는 내재성 하행성 동통 억제계 (endogenous descending pain inhibitory system) 에 있어서 중추적인 역할을 하고 있다. 연수의 세로토닌 신경세포에 대한 cholecystokinin (CCK) 및 second messenger systems에 작용하는 약물들의 작용을 알아보기 위하여, 쥐의 태자 (태생 14일) 로부터 연수를 분리하여 10동안 배양한 후 5-hydroxytryptamine (5-HT)의 분비에 대한 cholecystokinin (CCK) 및 second messenger systems에 작용하는 약물의 영향을 연구하였다. 배양 10일된 세포에 여러 neuropeptide들을 $10{\mu}M$ 농도로 48 시간동안 자극한 결과, CCK 와 substance P에 의하여 5-HT의 분비가 증가됨을 관찰하였다. Somatostatin, proctolin, thyrotropin releasing hormone, 및 interleukin-6 은 5-HT의 분비에 있어서 아무런 영향이 없었다. 어떠한 second messenger가 CCK에 의한 5-HT 분비에 연관되어 있나를 알아보기 위하여 calcium channel 봉쇄제인 nimodipine, 그리고 calmodulin 길항제인 calmidazolium의 영향을 살펴본 결과 nimodipine ($1{\mu}M$)은 거의 완전하게, 그리고 calmidazolium ($1{\mu}M$)은 부분적으로 유의하게 CCK에 의한 5-HT의 분비를 억제하였다. 또한 adenyl cyclase의 활성도를 높이는 forskolin ($5{\mu}M$)은 5-HT의 분비를 증가시켰지만 protein kinase C(PKC)를 활성화시키는 phorbol myristate acetate (PMA)는 $2{\mu}M$ 농도에서 5-HT의 분비에 아무런 영향을 미치지 아니하였다. 이상의 연구결과, calcium channel을 통한 calcium influx와 세포내 calmodulin이 CCK에 의한 5-HT분비 증가에 있어서 중요한 역할을 함을 제시한다. 또한, 5-HT의 분비에 있어서 cyclic AMP system이 중요한 역할을 하나, PKC system은 5-HT의 분비에 연관이 없음을 제시하고 있다.

• Biomolecules & Therapeutics
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• 제7권2호
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• pp.138-144
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• 1999

Recent studies have suggested that Panax ginseng saponins may stimulate pancreaticobiliary secretion. However, the precise mechanisms underlying the alterations in pancreaticobiliary function associated with ginseng saponins remain uncertain. We studied the effects of ginseng saponins and devazepide, cholecys-tokinin receptor antagonist, on pancreaticobiliary secretion in male Sprague-Dawley rats. The saponins tested were crude saponin (TS) and panaxatriol saponin (PTS). After single or two weeks administration of saponins, pancreaticobiliary juice of rats was collected for 8hrs. Single administration of TS and PTS did not change the volume of pancreaticobiliary juice compared with control group. In contrast, the pretreatment of devazepide significantly increased the volume of pancreaticobiliary juice. The amylase activity was significantly increased by acute TS treatment, but this increase was inhibited by devazepide pretreatment. In animals with two weeks administration of TS and PTS, the volume of pancreaticobiliary juice was not increased as compared to the control group. However, the volume of pancreaticobiliary juice was significantly increased by devazepide treatment. The amylase activity was significantly increased by two weeks administration TS and PTS respectively. This increase was inhibited by devazepide treatment. Our findings suggest that ginseng saponins, especially panaxatriol, increase the amylase activity in pancreaticobiliary juice, and this is, in part, caused by release of endogenous cholecystokinin.

• Archives of Pharmacal Research
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• 제18권6호
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• pp.434-439
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• 1995

In pancreatic cells, NO formation is associated with increased levels of cGMP and endocrine/exocrine secretion. In the present study, the role of NO in the regulation of exocrine secretion was investigated in rat pancreatic tissues. Treatment of rat pancreatic tissue with sholecystokinin-pancreozymin (CCK-PZ) resulted in an significant increase in arginine conversion to citruline, the amount of nitrite/nitrate, the release of amylase, and the level of cGMP. Furthermore, CCK-PZ stimulated increase of amylase release and conversion of arginine to citrulline transformation were counteracted by the inhibitor of NO synthase, $N^G-nitro-L-arginine$ methyl ester. The results on the time course of CCK-PZ-induced citrulline formation within the first seconds of simulation. The kinetics of citrulline accumulation correlate well with those of cGMP rise, which further confirms the conclusion that NO mediates the response to CCK-PZ by cGMP.

• Journal of Acupuncture Research
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• 제24권2호
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• pp.101-112
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• 2007

목적 : CCK는 현재까지 가장 많이 연구된 식후의 포만신호 전달물질로, 음식섭취를 감소하고, 캡사이신 반응성의 미주신경에 의해 위장운동과 위내의 공복감을 억제시킨다 전침의 진통효과 발현기전에 영향을 미치는 항아편양 단백물질로서, 내인성 CCK와 그 수용체(CCK-A와 CCK-B)의 역할은 기존의 연구에서 이미 보고되어 왔다. 이에 착안하여， 본 연구에서는 포만감의 측면에서 전침자극이 내인성 CCK의 발현에 어떠한 영향을 미치는가를 살펴보고자 한다. 방법 : 48시간 절식 쥐 모델을 이용하여, 전침자극 후 30분과 60분 동안, 먹이 섭취량 변화를 측정하고, 먹이섭취량에 영향을 주는 신경전달경로에서 CCK가 관여하는지를 확인하기 위해 미주신경절제술을 시행한 쥐와 비교하였다. 한편 48시간 절식 쥐 모델을 대상으로하여 침자극 후 시상하부의 CCK mRNA 발현변화를 관찰하였다. 결과 : 전침군에서 30분과 60분 뒤의 먹이 섭취가 대조군에 비해 현저히 낮게 관찰되었는데, 포만감에 관련된 침의 이와 같은 효과는 CCK 수용체에 길항작용이 있는 lorglumide와 미주신경절제술에 의해 차단됨을 알 수 있었다. 시상하부의 CCK mRNA의 발현되는 대조군에 비하여 전침군에서 증가하는 경향이 관찰되었으나, 통계학적인 유의성은 확인 할 수 없었다. 결론 : 위의 결과에서, 전침은 포만감에 영향을 미치는 내인성 CCK 메카니즘을 활성화시키는 것을 알수 있었다.

• International Journal of Oral Biology
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• 제31권4호
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• pp.127-133
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• 2006

[ $H_2O_2$ ], a member of reactive oxygen species (ROS), is known to be involved in the mediation of physiological functions in a variety of cell types. However, little has been known about the physiological role of $H_2O_2$ in exocrine cells. Therefore, in the present study, the effect of $H_2O_2$ on cholecystokinin (CCK)-evoked $Ca^{2+}$ mobilization and amylase release was investigated in rat pancreatic acinar cells. Stimulation of the acinar cells with sulfated octapeptide form of CCK (CCK-8S) induced biphasic increase in amylase release. Addition of $30\;{\mu}M\;H_2O_2$ enhanced amylase release caused by 10 pM CCK-8S, but inhibited the amylase release induced by CCK-8S at concentrations higher than 100 pM. An ROS scavenger, $10\;{\mu}M$ Mn(III)tetrakis(4-benzoic acid)porphyrin chloride, increased amylase release caused by CCK-8S at concentrations higher than 100 pM, although lower concentrations of CCK-8S-induced amylase release was not affected. To examine whether the effect of $H_2O_2$ on CCK-8S-induced amylase release was exerted via modulation of intracellular $Ca^{2+}$ signaling, we measured the changes in intracellular $Ca^{2+}$ concentration $([Ca^{2+}]_i)$ in fura-2 loaded acinar cells. Although $30\;{\mu}M\;H_2O_2$ did not induce any increase in $[Ca^{2+}]_i$ by itself, it increased the frequency and amplitude of $[Ca^{2+}]_i$ oscillations caused by 10 pM CCK-8S. However, $30\;{\mu}M\;H_2O_2$ had little effect on 1 nM CCK-8S-induced increase in $[Ca^{2+}]_i$. ROS scavenger, 1 mM N-acetylcysteine, did not affect $[Ca^{2+}]_i$ changes induced by 10 pM or 1 nM CCK-8S. Therefore, it was concluded that $30\;{\mu}M\;H_2O_2$ enhanced low concentration of CCK-8S-induced amylase release probably by increasing $[Ca^{2+}]_i$ oscillations while it inhibited high concentration of CCK-8S-induced amylase release.

• The Korean Journal of Physiology and Pharmacology
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• 제5권1호
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• pp.71-78
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• 2001

Capsaicin, a pungent ingredient of hot pepper, elicits an intense burning pain when applied cutaneously and intradermally. Activation of capsaicin-gated channel in C-type dorsal root ganglion (DRG) neurons produces nonselective cationic currents. Although electrophysiological and biochemical properties of capsaicin-activated current $(I_{CAP})$ were studied, the regulatory mechanism and intracellular signaling pathway are still unclear. In the present study, we investigated the modulations of $I_{CAP}$ by DAMGO $({\mu}-opioid\;agonist)$ and cholecystokinin octapeptide (CCK-8). In 18 out of 86 cells, the amplitude of $I_{CAP}$ was significantly increased by DAMGO and completely reversed after washout, while $I_{CAP}$ was decreased by DAMGO in 25 cells. In 43 cells, DAMGO had no effect on $I_{CAP}$. Mean action potential duration was significantly different between 'increased-by-DAMGO' group and 'decreased-by-DAMGO' group. Mean amplitudes of $I_H$ were not significantly different between both groups. CCK-8 reversibly enhanced the amplitude of $I_{CAP}$ (5/13). DAMGO also increased $I_{CAP}$ amplitude significantly in the same cells. The amplitude of $I_{CAP}$ was increased in additive manner by combined applications of DAMGO and CCK-8 in these cells. These results suggest that DAMGO and CCK-8 can either increase or decrease $I_{CAP}$ presumably depending on the subtypes of DRG cells and classified by electrophysiological properties.