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Cholecystokinin

No cross-reactivity with Gastrin

Cholecystokinin is a peptide hormone of the gastrointestinal system responsible for stimulating the digestion of fat and protein. Cholecystokinin, previously called pancreozymin, is synthesised by I-cells in the mucosal epithelium of the small intestine and secreted in the duodenum, the first segment of the small intestine, and causes the release of digestive enzymes and bile from the pancreas and gallbladder, respectively. It also acts as a hunger suppressant. Recent evidence has suggested that it also plays a major role in inducing drug tolerance to opioids like morphine and heroin, and is partly implicated in experiences of pain hypersensitivity during opioid withdrawal.

Hindbrain Response Model

Hindbrain Response Model 

Model for regulation of the hindbrain response to satiety signals by hormonal input from the ARC. Adiposity signals such as insulin and leptin circulate in proportion to body fat mass and act on hypothalamic ARC neurons that project to hypothalamic areas such as the LHA (not shown) and PVN. In turn, these “second order” neurons project to hindbrain autonomic centers such as the NTS that process afferent input from satiety signals such as CCK. Input from descending, leptin-sensitive hypothalamic projections is integrated in the NTS with vagally mediated input from CCK, such that the timing of meal termination is regulated by changes in body fat content. Modified with permission from Nature GI, gastrointestinal.

Morton G.J., et al. J Clin Invest. 2005 March 1; 115(3):703–710.

Neurocentric model

Neurocentric Model 

Neurocentric model depicting sites where defects in the negative feedback regulation of energy balance and glucose production predispose to weight gain and insulin resistance. Defects in the secretion of insulin or leptin (1), in the hypothalamic sensing of adiposity- or nutrient related signals (2), or in the neuronal responsiveness to these inputs (3) predispose to both positive energy balance and increased glucose production. If sustained, these will result in pathological weight gain and insulin resistance.

Schwartz MW, Porte D Jr. Diabetes, obesity, and the brain. Science. 2005 Jan 21;307(5708):375-9

 

Weaning and Feed Intake Alter Pancreatic Enzyme Activities and Corresponding mRNA Levels in 7-d-Old Piglets

We investigated the changes in the capacity for synthesis of the exocrine pancreas of piglets during the 2 wk after weaning at 7 d of age (trial 1) by measuring the expression of digestive enzymes at mRNA and activity levels in pancreas homogenates, and the effects of high and low feed intakes during the 1st wk postweaning (trial 2) on these measures. The trypsin mRNA level was transiently decreased 43% 3 d postweaning (P < 0.05). Thereafter, trypsin and lipase mRNAs linearly increased (P < 0.05). During the 1st wk postweaning, trypsin- and lipase-specific activities were reduced 44 and 79% (P < 0.05), respectively, whereas 14 d after weaning, trypsin was at the preweaning value and lipase was at a low level. Amylase-specific activity did not change with weaning. Plasma cholecystokinin (CCK) and gastrin concentrations decreased 1 d postweaning and increased afterward up to 3 and 5 d postweaning, respectively. By 3 d after weaning, the mRNA level of trypsin was twofold higher (P < 0.05) in piglets that consumed more feed than in those that consumed less, whereas 7 d after weaning, the groups did not differ. By 7 d after weaning, the specific activity of amylase was higher, and lipase-specific activity was lower, in piglets that consumed more feed than in those that consumed less. Plasma CCK and gastrin concentrations measured 7 d after weaning were correlated with feed intake (r = +0.56 and r = +0.68, P < 0.05, respectively). In conclusion, by 3 d postweaning, pancreatic exocrine function was adapting to the new diet. Afterward, the expression of specific genes coding digestive enzymes and the levels of pancreatic enzyme activities were restored or stimulated, except for lipase-specific activity. Therefore, the pancreas can adjust to weaning and dry food intake as early as wk 2 of life.

Marion et al. J. Nutr 2003; 133:362-368

Effects of intracerebroventricular administration of the CCK(1) receptor antagonist devazepide on food intake in rats.

The effects of intracerebroventricular administration of devezapide, a CCK(1) receptor antagonist, was investigated on food intake in rats. In the first experiment, rats (n=5) were deprived of food for 17 h and injected intracerebroventricularly with either vehicle or devazepide (1, 10, 25 or 100 ng). Five minutes after vehicle or drug administration, the animals were presented with food and intake measured for 60 min. Devazepide produced a dose-related increase in food intake. Doses of 1, 10 and 25 ng significantly increased consumption (at least P<0.01 in each case). A second experiment was subsequently undertaken to investigate whether systemic administration of the intracerebroventricular doses used in the first experiment would affect food intake. Rats (n=8) that have been deprived of food for 17 h were injected intraperitoneally with either vehicle or devazepide (3, 30, 75 or 300 ng/kg). Five minutes after vehicle or drug administration, the animals were presented with food and intake was measured for 60 min. Devazepide (3-300 ng/kg, i.p.) had no significant effects on food consumption. The results show that central administration of low doses of devazepide increase food intake in rats, while similar doses, given systemically, do not affect consumption. These findings suggest the possibility that endogenous cholecystokinin (CCK), acting at central CCK(1) receptors, may play a physiological role in the control of feeding behaviour in the rat.

Ebenezer IS. Eur J Pharmacol 2002 Apr 19;441(1-2):79-82

Daily CCK injection enhances reduction of body weight by chronic intracerebroventricular leptin infusion.

In the present study, we tested the hypothesis that a single daily injection of the gut peptide CCK, together with continuous leptin infusion, would produce significantly greater loss of body weight than leptin alone. We found that a single daily intraperitoneal injection of CCK-8 (0.5 microg/kg) significantly enhanced the weight-reducing effects of 0.5 microg/day leptin infused continuously into the lateral ventricle of male Sprague-Dawley rats by osmotic minipump. However, CCK and leptin together did not enhance reduction of daily chow intake. Furthermore, there was no synergistic reduction of 30-min sucrose intake, although a significant main effect of both leptin and CCK was observed on sucrose intake. These results 1) confirm our previous reports of synergy between leptin and CCK on body weight, 2) demonstrate that enhancement of leptin-induced weight loss does not require bolus administration of leptin, and 3) suggest that enhanced body weight loss following leptin and CCK does not require synergistic reduction of food intake by leptin and CCK.

Matson et al. Am J Physiol Regul Integr Comp Physiol 2002 May;282(5):R1368-73 

Effects of peripheral CCK receptor blockage on gastric emptying in rats

Type A CCK receptor (CCKAR) antagonists differing in blood-brain barrier permeability [devazepide penetrates; the dicyclohexylammonium salf of Na-3-quinolinoyl-D-Glu-N,N-dipentylaminde (A-70104) does not] were used to test the hypothesis that duodenal nutrient-induced inhibition of gastric emptying is mediated by CCKARs located peripheral to the blood-brain barrier. Rats received A-70104 (700 or 3,000 nmol . kg-1. h-1) or devazepide (2.5 umol/kg iv) and either a 15-min intravenous infusion of CCK-8 (3nmol.kg-1.h-1) or duodenal infusion of casein, peptone, Intralipid, or maltose. Gastric emptying of saline was measured during the last 5 min of each infusion. A-70104 and devazepide abolished the gastric emptying response to a madximal inhibitory dose of CCK-8. Each of the macronutrients inhibited gastric emptying. A-70104 and devazepide attenuated inhibitory responses to each macronutrient. Intravenous injection of a CCK antibody to immunoneutralize circulating CCK had no effect on peptone or Intralipid-induced responses. Thus endogenous CCK appears to act in part by a paracrine or neurocrine mechanism at CCKARs peripheral to the blood-brain barrier to inhibit gastric emptying.

Reidelberger et al. Am J Physiol Regul Integr Comp Physiol 2003; 284: R66-R75

Effects of fat digestion on appetite, APD motility, and gut hormones in response to duodenal fat infusion in humans

The presence of nutrients in the small intestine slows gastric emptying and suppresses appetite and food intake; these effects are partly mediated by the release of gut hormones, including CCK. We investigated the hypothesis that the modulation of antropyloroduodenal motility, suppression of appetite, and stimulation of CCK and glucagon-like peptide-1 secretion by intraduodenal fat are dependent on triglyceride hydrolysis by lipase. Sixteen healthy, young, lean men were studied twice in double-blind, randomized, crossover fashion. Ratings for appetite-related sensations, antropyloroduodenal motility, and plasma CCK and glucagon-like peptide-1 concentrations were measured during a 120-min duodenal infusion of a triglyceride emulsion (2.8 kcal/min) on one day with, on the other day without, 120 mg tetrahydrolipstatin, a potent lipase inhibitor. Immediately after the duodenal fat infusion, food intake at a buffet lunch was quantified. Lipase inhibition with tetrahydrolipstatin was associated with reductions itonic and phasic pyloric pressures, increased numbers of isolated antral and duodenal pressure waves, and stimulation of antropyloroduodenal pressure-wave sequences (all P < 0.05). Scores for prospective consumption and food intake at lunch were greater, and nausea scores were slightly less, and the rises in plasma CCK and glucagon-like peptide-1 were abolished (all P < 0.05). In conclusion, lipase inhibition attenuates the effects of duodenal fat on antropyloroduodenal motility, appetite, and CCK and glucagon-like peptide-1 secretion.

Feinle C et al. Am J Physiol Gastrointest Liver Physiol 284: G798-G807, 2003

Effects of intravenous infusion of amylin on feeding patterns

Effects of intravenous infusion of amylin on feeding patterns

Reidelberger et al. Am J Physiol Regul Integr Comp Physiol 280: R605-R611, 2001

Mapping in Human Colon Tissue (H-069-02)

  

  

Protocol for antibody staining

Tissue Sample

Human colon and colon cancer tissues

Fixative

10% formalin

Embedding

Paraffin

Negative Control

No primary antibody

Pretreatment

N/A

Blocking

3% H2O2, 2% Normal Goat Serum

Primary Antibody

rabbit anti-CCK-33 (Human, Rat) antibody (Cat. No.: H-069-02)

Optimal Dilution

1: 500

Secondary Antibody

Goat Anti-Rabbit IgG, Biotinylated (1:400), 30 min

Amplification

Streptavidin-HRP (Vector), 1:400, 30 min

Detection System

HRP

Substrate

DAB (Sigma), 3 min

Counterstained

Hematoxylin, 30 sec

 

Mapping in Human Colon Tissue and Colon Cancer (H-069-04)

  

  

Protocol for antibody staining

Tissue Sample

Human colon and colon cancer tissues

Fixative

10% formalin

Embedding

Paraffin

Negative Control

No primary antibody

Pretreatment

N/A

Blocking

3% H2O2, 2% Normal Goat Serum

Primary Antibody

rabbit anti-CCK (26-33) (H,R,M) antibody (Cat. No.: H-069-04)

Optimal Dilution

1: 500

Secondary Antibody

Goat Anti-Rabbit IgG, Biotinylated (1:400), 30 min

Amplification

Streptavidin-HRP (Vector), 1:400, 30 min

Detection System

HRP

Substrate

DAB (Sigma), 3 min

Counterstained

Hematoxylin, 30 sec

Mapping in Human Colon Cancer Tissue (H-069-27)

Protocol for antibody staining

Tissue Sample

Human colon cancer tissues

Fixative

10% formalin

Embedding

Paraffin

Negative Control

No primary antibody

Pretreatment

N/A

Blocking

3% H2O2, 2% Normal Goat Serum

Primary Antibody

rabbit anti-CCK (46-69) (Human) antibody (Cat. No.: H-069-27)

Optimal Dilution

1: 500

Secondary Antibody

Goat Anti-Rabbit IgG, Biotinylated (1:400), 30 min

Amplification

Streptavidin-HRP (Vector), 1:400, 30 min

Detection System

HRP

Substrate

DAB (Sigma), 3 min

Counterstained

Hematoxylin, 30 sec

 

Mapping in Rat Intestine Tissue (H-069-04)

Rabbit Anti CCK Serum H-069-04 

Protocol for antibody staining

Tissue Sample

Rat intestine tissues

Fixative

10% formalin

Embedding

Paraffin

Negative Control

No primary antibody

Pretreatment

N/A

Blocking

3% H2O2, 2% Normal Goat Serum

Primary Antibody

rabbit anti-CCK (26-33) (H,R,M) antibody (Cat. No.: H-069-04)

Optimal Dilution

1: 500

Secondary Antibody

Goat Anti-Rabbit IgG, Biotinylated (1:400), 30 min

Amplification

Streptavidin-HRP (Vector), 1:400, 30 min

Detection System

HRP

Substrate

DAB (Sigma), 3 min

Counterstained

Hematoxylin, 30 sec

 See more publications using our CCK kits in reference section

Cholecystokinin-33 Human EIA Kit (EK-069-02) and Fluorescent EIA Kit (FEK-069-02)

 

Cholecystokinin Octapeptide (Non-Sulfated)
EIA kit (EK-069-04), FEIA Kit (FEK-069-04), CEIA Kit (CEK-069-04) and Extraction Free (EKE-069-04)

Linear Range: 0.11-2.33 ng/ml

Linear Range 15-333 pg/ml
7 times more sensitive than normal EIA kits

 

Linear Range: 2.36 - 90 pg/ml
Over 47 times more sensitive than normal EIA kits

Linear Range: 0.11-2.33 ng/ml

 

Cholecystokinin Octapeptide (1-21) Human (EK-069-19)

CCK EIA Kit References

Links to publications that use EK-069-04:

Bercik et al. Role of gut-brain axis in persistent abnormal feeding behavior in mice following eradication of Helicobacter pylori infection.
Am J Physiol Regul Integr Comp Physiol. 2009 Mar;296(3):R587-94.

Jeon et al. SREBP-2 regulates gut peptide secretion through intestinal bitter taste receptor signaling in mice.
J Clin Invest. 2008 Nov;118(11):3693-700. 

Hira et al. Calcium-sensing receptor mediates phenylalanine-induced cholecystokinin secretion in enteroendocrine STC-1 cells.
FEBS J. 2008 Sep;275(18):4620-6. 

Tanaka et al. Free fatty acids induce cholecystokinin secretion through GPR120.
Naunyn Schmiedebergs Arch Pharmacol. 2008 Jun;377(4-6):523-7.

Guijarro et al. Sustained weight loss after Roux-en-Y gastric bypass is characterized by down regulation of endocannabinoids and mitochondrial function.
Ann Surg. 2008 May;247(5):779-90.

Katanyutanon et al. The effect of whole-body radiation on blood levels of gastrointestinal peptides in the rat.
Int J Clin Exp Med. 2008;1(4):332-7.

Zhang et al. Effects of active immunization against cholecystokinin 8 on performance, contents of serum hormones, and expressions of CCK gene and CCK receptor gene in pigs.
Endocrine. 2007 Dec;32(3):338-44.

Guijarro et al. Characterization of weight loss and weight regain mechanisms after Roux-en-Y gastric bypass in rats.
Am J Physiol Regul Integr Comp Physiol. 2007 Oct;293(4):R1474-89. 

Bogunovic et al. Enteroendocrine cells express functional Toll-like receptors
Am J Physiol Gastrointest Liver Physiol. 2007 Jun;292(6):G1770-83.

Choi et al. GPR93 activation by protein hydrolysate induces CCK transcription and secretion in STC-1 cells
Am J Physiol Gastrointest Liver Physiol. 2007 May;292(5):G1366-75.

Leidy et al. Effects of acute and chronic protein intake on metabolism, appetite, and ghrelin during weight loss.
Obesity (Silver Spring). 2007 May;15(5):1215-25.

Tieken et al. Effects of solid versus liquid meal-replacement products of similar energy content on hunger, satiety, and appetite-regulating hormones in older adults.
Horm Metab Res. 2007 May;39(5):389-94. 

Palazzo et al. Activation of Enteroendocrine Cells via TLRs Induces Hormone, Chemokine, and Defensin Secretion
J Immunol. 2007 Apr 1;178(7):4296-303.

Sufian et al. Pork peptone stimulates cholecystokinin secretion from enteroendocrine cells and suppresses appetite in rats.
Biosci Biotechnol Biochem. 2006 Aug;70(8):1869-74.

Fushimi et al. Dietary acetic acid reduces serum cholesterol and triacylglycerols in rats fed a cholesterol-rich diet.
Br J Nutr. 2006 May;95(5):916-24. 

Di Francesco et al. Delayed Postprandial Gastric Emptying and Impaired Gallbladder Contraction Together With Elevated Cholecystokinin and Peptide YY Serum Levels Sustain Satiety and Inhibit Hunger in Healthy Elderly Persons
J Gerontol A Biol Sci Med Sci. 2005 Dec;60(12):1581-5.

Suzuki et al. Changes in GI hormones and their effect on gastric emptying and transit times after Roux-en-Y gastric bypass in rat model
Surgery. 2005 Aug;138(2):283-90.

Chen et al. Delayed Liquid Gastric Emptying in Patients With Hepatocellular Carcinoma
Am J Gastroenterol. 2000 Nov;95(11):3230-7.

Höcherl et al. Effect of tropisetron on circulating catecholamines and other putative biochemical markers in serum of patients with fibromyalgia.
Scand J Rheumatol Suppl. 2000;113:46-8.

CCK RIA Kit References

Links to publications that use this RK-069-04:

Reynolds et al. Effect of the glycemic index of carbohydrates on day-long (10 h) profiles of plasma glucose, insulin, cholecystokinin and ghrelin.
Eur J Clin Nutr. 2008 Oct 29. [Epub ahead of print]

Fogel et al. Satiety signalling histaminergic system and brain-gut peptides in regulation of food intake in rats with portocaval anastomosis.
J Physiol Pharmacol. 2008 Aug;59 Suppl 2:135-44.

Xu et al. Effects of gastric electric stimulation on gastric distention responsive neurons and expressions of CCK in rodent hippocampus.
Obesity (Silver Spring). 2008 May;16(5):951-7.

Li et al. Does chronic ethanol intake cause chronic pancreatitis?: evidence and mechanism.
Pancreas. 2008 Aug;37(2):189-95.

Keenan et al. Effects of resistant starch, a non-digestible fermentable fiber, on reducing body fat.
Obesity (Silver Spring). 2006 Sep;14(9):1523-34.

Kierson et al. Ghrelin and cholecystokinin in term and preterm human breast milk.
Acta Paediatr. 2006 Aug;95(8):991-5.

Kalmar et al. Postprandial gastrointestinal hormone production is different, depending on the type of reconstruction following total gastrectomy.
Ann Surg. 2006 Apr;243(4):465-71.

Cullen et al. Gastric emptying of liquids and postprandial pancreatobiliary secretion are temporarily impaired during endotoxemia.
Dig Dis Sci. 1999 Nov;44(11):2172-7.

Chiu et al. Somatic electrical nerve stimulation regulates the motility of sphincter of Oddi in rabbits and cats: evidence for a somatovisceral reflex mediated by cholecystokinin.
Dig Dis Sci. 1999 Sep;44(9):1759-67.

 

%CCK%;%069-10%;%069-08%


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