• The Korean Journal of Physiology and Pharmacology
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• v.15 no.5
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• pp.307-312
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• 2011

It has been rereported that axons which display 5-hydroxytryptamine (5-HT) immunoreactivity are abundant in the pancreas and the majority of serotonergic axons terminate within intrapancreatic ganglia, islet and acini. This histological result strongly suggests that intrapancreatic serotonergic nerves could affect to the pancreatic endocrine and exocrine secretion. Thus, this study was aimed to investigate whether intrapancreatic serotonergic nerves could affect pancreatic exocrine secretion and an action mechanism of the intrapancreatic serotonergic nerves. The rats were anesthetized with a single injection of urethane. The median line and the abdominal aorta was carefully dissected and cannulated with PE-50 tubing just above the celiac artery, and then tightly ligated just below the superior mesenteric artery. The pancreatic duct was also cannulated with Tygon microbore tubing. With the addition of serotonin, pancreatic volume flow and amylase output were significantly inhibited electrical field stimulation (EFS). On the other hand, pancreatic volume flow and amylase output were significantly elevated in EFS with the addition of spiperone. EFS application, however, pancreatic volume flow and amylase output had no significant change in cholecystokinin (CCK) alone when serotonin was applied under a 5.6 mM glucose background. Pancreatic volume flow and amylase output under 18 mM glucose background were significantly elevated in CCK plus serotonin than in CCK alone. These data suggest that intrapancreatic serotonergic nerves play an inhibitory role in pancreatic exocrine secretion and an important role in the insulin action or release.

• Journal of Animal Science and Technology
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• v.61 no.4
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• pp.239-244
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• 2019

This study aimed to determine the effective dose of intravenous administration of L-tryptophan (L-T) on gastrointestinal hormones (GIH) secretions and melatonin using Hanwoo cattle. Three steers ($362{\pm}23kg$) fitted with indwelling jugular vein catheters were assigned in a $3{\times}3$ Latin square design. Treatments were intravenous administration of saline (control), 28.9 mg L-T/kg body weight (BW; low) and 57.8 mg L-T/kg BW (high) L-T for 1 day with 7 days of adaptation. Samples were collected after adaptation period at -60, 0, 30, 60, 90, 120, 150, 180, 240, and 300 min of sampling day. The levels of serum cholecystokinin (CCK) and secretin were higher (p < 0.05) in the high L-T group than those in the other groups. Serum Melatonin (MEL) levels were increased upon L-T administration (p < 0.05) in the high L-T group. Taken together, the effective dose of L-T administration was defined at 57.8 mg L-T/kg BW in order to stimulate increase of GIH and MEL.

• BMB Reports
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• v.57 no.3
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• pp.149-154
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• 2024

The stomach has emerged as a crucial endocrine organ in the regulation of feeding since the discovery of ghrelin. Gut-derived hormones, such as ghrelin and cholecystokinin, can act through the vagus nerve. We previously reported the satiety effect of hypothalamic clusterin, but the impact of peripheral clusterin remains unknown. In this study, we administered clusterin intraperitoneally to mice and observed its ability to suppress fasting-driven food intake. Interestingly, we found its synergism with cholecystokinin and antagonism with ghrelin. These effects were accompanied by increased c-fos immunoreactivity in nucleus tractus solitarius, area postrema, and hypothalamic paraventricular nucleus. Notably, truncal vagotomy abolished this response. The stomach expressed clusterin at high levels among the organs, and gastric clusterin was detected in specific enteroendocrine cells and the submucosal plexus. Gastric clusterin expression decreased after fasting but recovered after 2 hours of refeeding. Furthermore, we confirmed that stomachspecific overexpression of clusterin reduced food intake after overnight fasting. These results suggest that gastric clusterin may function as a gut-derived peptide involved in the regulation of feeding through the gut-brain axis.

• Journal of Ginseng Research
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• v.10 no.2
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• pp.151-158
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• 1986

On the cAMP content in isolated gastric glands from rabbit stomach, the effect of ginseng components (total saponin, diol saponin, triol saponin) with pepsinogen secretion regulatory agents (cholecystokinin, isoproterenol, carbachol, propranolol, atropine, DECAMP, DBcGMP) were studied in vitro. According to the results, ginseng components may have the effect of stimulation or inhibition on cAMP production, and both dial saponin and triol saponin may be reciprocal effect to pepsinogen secretion regulatory agents. It seemed that the ginseng components may have the normalization action to pepsinogen regulatory agents on cAMP content in isolated rabbit gastric glands.

• The Korean Journal of Pharmacology
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• v.32 no.1
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• pp.67-74
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• 1996

Cholecystokinin octapeptide (CCK-8), acetylcholine (ACh) and KCl caused a dose dependent contraction in muscle cells enzymatically digested from cat gallbladder. Maximal contraction was obtained at concentration of $10^{-9}M$ for CCK-8, $10^{-5}M$ for ACh and 20mM for KCl. CCK-8 induced contraction was unaffected in calcium free physiological salt solution (PSS) and was completely blocked by strontium substitution for calcium (p<0.001). In contrast, KCl evoked contraction was blocked in calcium free PSS (p<0.01) but was unaffected by strontium replacement of calcium. The contraction elicited by ACh was only slightly reduced in calcium free PSS (p<0.05) and was unaltered by strontium. Muscle cells permeabilized with saponin contracted in response to inositol 1,4.5-trisphosphate $(IP_3)$ and CCK-8. The contraction was blocked by the calmodulin antagonist CGS 9343B (p<0.001), whereas heparin completely blocked the effect of $IP_3$ (p<0.001). The protein kinase C (PKC) antagonist H7 had no effect on either agonist. We conclude that CCK-8 induced gallbladder muscle contraction is mediated by $IP_3$ dependent intracellular calcium release from intracellular stores and a calmodulin dependent pathway; ACh may utilize both extracellular and intracellular calcium. KCl causes muscle contracrion through influx of extracellular calcium and a calmodulin independent machanism.

• Journal of Animal Science and Technology
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• v.59 no.7
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• pp.16.1-16.6
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• 2017

Background: This study was performed to investigate the impact of exogenous ghrelin on the pancreatic ${\alpha}$-amylase outputs and responses of pancreatic proteins to ghrelin that may relate to pancreatic exocrine. Methods: Sprague-Dawley male rats (9 weeks old, $300{\pm}10g$) were injected with ghrelin via intraperitoneal (i.p.) infusion at dosage of 0, 0.1, 1.0 and $10.0{\mu}g/kg$ body weight (BW), respectively. The plasma ghrelin and cholecystokinin (CCK) level were determined using enzyme immunoassay kit; the mRNA expression of ghrelin receptor ($GHSR-1{\alpha}$) and growth hormone (GH) receptor were assessed by reverse transcription PCR; the expressions of pancreatic ${\alpha}$-amylase activity, extracellular-signal-regulated kinases (ERK), phosphorylated extracellular-signal-regulated kinases (pERK) and c-Jun N-terminal kinase (JNK) were evaluated by western blotting; moreover the responses of pancreatic proteins to ghrelin were analyzed using the two-dimensional gel electrophoresis system. Results: The exogenous ghrelin (1.0 and $10.0{\mu}g/kg\;BW$) elevated the level of plasma ghrelin (p < 0.05), and suppressed the expression of pancreatic ${\alpha}$-amylase at a dose of $10.0{\mu}g/kg\;BW$ (p < 0.05). No difference in the level of plasma CCK was observed, even though rats were exposed to any dose of exogenous ghrelin. In addition, a combination of western blot and proteomic analysis revealed exogenous ghrelin ($10.0{\mu}g/kg\;BW$) induced increasing the JNK and ERK expressions (p < 0.05) and four proteins such as Destrin, Anionic trypsin-1, Trypsinogen, and especially eukaryotic translation initiation factor 3 in rat pancreas. Conclusions: Taken together, exogenous ghrelin by i.p. infusion plays a role in the pancreatic exocrine secretion via mitogen-activated protein kinase signaling pathway.

• Korean Journal of Veterinary Research
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• v.41 no.4
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• pp.477-484
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• 2001

The regional distribution and relative frequency of neurohormonal peptides-producing cells were demonstrated in the gut of the stomachless teleost, the Prussian carp, Carassius auratus Linnaeus, using 10 types of specific antisera raised against mammalian regulatory peptides. The gut of the Prussian carp was divided into five portions from proximal to distal (Segments I~V). Most of immunoreactive cells in the epithelial lining portion, between epithelial cells, were generally spherical or spindle shape having long cytoplasmic process that reached to the lumen (open typed cell) while cells showing round in shape (close typed cell) were found in the basal portions of epithelial lining occasionally. Somatostatin-, cholecystokinin (CCK)-8- and pancreatic polypeptide (PP)- immunoreactive cells were observed in this study. However, no serotonin-, glucagon-, chromogranin A-, secretin-, vasoactive intestinal peptide (VIP)-, substance P- and bombesin-immunoreactive cells were found. Somatostatin-immunoreactive cells were restricted to most proximal segments of the gut (Segment I) with rare frequency and CCK-8-immunoreactive cells were demonstrated in the proximal segments of the gut (Segments I and II) with a few to rare frequencies. In addition, pancreatic polypeptide-immunoreactive cells were demonstrated in the proximal to middle segments (Segments I~III) with moderated to rare frequencies. In conclusion, the distribution and relative frequency of these immunoreactive cells are well corresponded to the previous reports in stomachless teleost but somewhat peculiar patterns are also detected.

• Korean Journal of Veterinary Research
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• v.42 no.3
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• pp.289-297
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• 2002

The regional distribution and relative frequency of neurohormonal peptides-producing cells were demonstrated in the gut of the stomach teleost, the Mandarin fish, Siniperca scherzeri Steindachner, using 7 types of specific antisera raised against mammalian regulatory peptides. The gastrointestinal tract of the Mandarin fish was divided into three portions from proximal to distal, stomach, small intestine and large intestine. Cells showing immunoreactivities against regulatory peptides were situated in the epithelial lining, between epithelial cells, and gastric or intestinal gland regions with various frequencies along with gastrointestinal tract. Mast of immunoreactive cells in the epithelial lining portion were generally spherical or spindle shape having long cytoplasmic process that were reached to the lumen (open type cell) while cells showing round in shape (closed type cell) were found in the gastric gland of the stomach occasionally. Serctonin-, samatostatin-, gastrin-, cholecystokinin (CCK)-8- and human pancreatic polypeptide (HPP)-immunoreactive cells were observed in this study. However, no insulin- and glucagon-immunoreactive cells were found. Serotonin- and somatostatin-immunoreactive cells were restricted to the stomach regions with moderate and numerous frequencies, respectively. Gastrin-immunoreactive cells were demonstrated in the stomach and small intestinal portions with a few and moderate frequencies, respectively and CCK-8-immunoreactive cells were restricted to the small intestinal portions with moderate frequency. In addition, HPP-immunoreactive cells were demonstrated in the stomach and small intestine with numerous frequencies, respectively. In conclusion, the distribution and relative frequency of these immunoreactive cells in the gastrointestinal tract of the Mandarin fish shows peculiar patterns compared to those of other stomach and/or stomachless teleost.

• Korean Journal of Poultry Science
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• v.16 no.4
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• pp.219-232
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• 1989

The present study was done to investigate the mechanism of Pancreatic digestive enzyme secretion in response to dietary components in chicks. A simplefied pancreatic juice collection method, useful for a short-term experiment, was developed. By wing vein injection, it was shown that the increased trypsinogen and chymotrypsinogen, while neither other single amino acids nor glucose affected the secretion of enzymes, amylase, trypsinogen and chymotrypsinogen. Cholecystokinin (CCK) had an immediate effect on pancreatic enzyme secretion and this response was in a dose dependent fashion. The injection of CCK seemed to have selective stimulation favoring the secretion of chymotrypsinosen followed by amylase and trypsinogen. Simultaneous injection of single amino acid with CCK increased digestive enzyme secretion to various extents depending on the kind of amino acids whereas the injection of glucose with CCK did not affect when compared with that of CCK'alone. By varying doses, synergetic action of CCK plus amino acid on the secretion of pancreatic digestive enzymes was observed at 0.5mM for Val and 5mM for Arg. A further attempt was made to examine the effect of combined administration of amino acids with CCK on pancreatic enzyme secretion. The injected substances were an AAs mixture and combination of selected amino acids, i.e. Thr＋Phe＋Ile, Thr＋Phe. Thr＋Ile or Phe＋Ile. When increases in enzyme outputs for the first 30 min were compared , it was shown that the responses of three enzymes, amylase, trypsinogen and chymotrypsinogen, brought about by the administration of the AAs mixture was almost entirely accounted for by the combined injection of Thr＋Phe. Thus, it was well demonstrated that CCK and amino acids had a synergetic action on the secretion of a specific pancreatic digestive enzyme depending on a kind of amino acid injected.

• The Korean Journal of Nuclear Medicine
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• v.26 no.1
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• pp.86-94
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• 1992

Quantitative analysis of gallbladder emptying is important in diagnosis of motility disorder of gallbladder and in studies of biliary physiology. However, the normal range of gallbladder ejection fraction (GBEF) has not been determined yet and the best method for stimulating the gallbladder to contract has not been elucidated adequately. The purpose of this study was to compare the gallbladder emptying effect of the fatty meal ingestion with that of the continuous infusion of cholecystokinin (CCK) and to establish the normal GBSF values of normal subjects. Quantitative hepatobiliary scan with $^{99m}Tc-DISIDA$ after a fatty meal was performed for 22 normal healthy volunteers. Among them, 10 subjects repeated the test with a fatty meal. Again, for 7 subjects quantitative heaptobiliary scan with an infusion of CCK (sincalide) at a rate of 20 ng/kg/hr for 45 minutes was performed repeatedly. The results were as follows. 1) With a fatty meal, the mean GBEF was $89.6{\pm}8.2%$ in 22 normal subjects, and there was no difference between subjects. 2) With a continuous infusion of CCK, the mean GBEF was $62.4{\pm}16.6%$ in 7 normal subjects, and there was a significant difference between subjects(p<0.05). 3) The reproducibility of GBEF by a fatty meal was significantly higher than by an infusion of CCK (p < 0.05). 4) The mean GBEF by a fatty meal was significantly higher than that by an infusion of CCK (p < 0.05). We concluded that a fatty meal is superior to a continuous infusion of CCK for inducing gall-bladder contraction because that induces more complete emptying and the response is more reproducible and constant.