Celiac and the cranial mesenteric arteries supply gastrointestinal sites that regulate meal size and intermeal interval length via cholecystokinin-58 in male rats

Sayegh, Ayman I.; Washington, Martha C.; Johnson, Ruth E.; Johnson-Rouse, Tanisha; Freeman, Corren; Harrison, Anthony; Lucas, Jennifer B.; Shelby, Mandy; Fisher, Brittley; Willis, William L.; Reeve, Joseph J.

doi:10.1016/j.yhbeh.2014.11.011

Cited by 18 publications

(16 citation statements)

References 34 publications

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“…The active forms of CCK differ in the number of amino acids in their structure and are found in the plasma, gastrointestinal tract, and brain [6-8]. They act at these sites by means of specific receptors, such as type 1 CCK receptor (CCK-1R or CCKAR) in the gastrointestinal tract, and type 2 CCK receptor (CCK-2R or CCKBR) in the brain [9].…”

Section: Introductionmentioning

confidence: 99%

Satietogenic Protein from Tamarind Seeds Decreases Food Intake, Leptin Plasma and CCK-1r Gene Expression in Obese Wistar Rats

et al. 2018

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Objective: This study evaluated the effect of a protein, the isolated Trypsin Inhibitor (TTI) from Tamarindus indica L. seed, as a CCK secretagogue and its action upon food intake and leptin in obese Wistar rats. Methods: Three groups of obese rats were fed 10 days one of the following diets: Standard diet (Labina®) + water; High Glycemic Index and Load (HGLI) diet + water or HGLI diet + TTI. Lean animals were fed the standard diet for the 10 days. Food intake, zoometric measurements, plasma CCK, plasma leptin, relative mRNA expression of intestinal CCK-related genes, and expression of the ob gene in subcutaneous adipose tissue were assessed. Results: TTI decreased food intake but did not increase plasma CCK in obese animals. On the other hand, TTI treatment decreased CCK-1R gene expression in obese animals compared with the obese group with no treatment (p = 0.027). Obese animals treated with TTI presented lower plasma leptin than the non-treated obese animals. Conclusion: We suggest that TTI by decreasing plasma leptin may improve CCK action, regardless of its increase in plasma from obese rats, since food intake was lowest.

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Section: Introductionmentioning

confidence: 99%

Satietogenic Protein from Tamarind Seeds Decreases Food Intake, Leptin Plasma and CCK-1r Gene Expression in Obese Wistar Rats

et al. 2018

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“…One catheter was implanted in each rat, as described previously (Sayegh, et al, 2014; Washington, et al, 2014). Catheters (Micro-Renathane R-ITC-SP 9.5, Braintree Scientific, Braintree MA) were 24 cm long.…”

Section: Methodsmentioning

confidence: 99%

“…In addition to the better anatomical specificity, this technique permits the use of smaller doses of GLP-1 than necessary in intraperitoneal-injection tests, which may minimizes possible side effects. We previously used this intra-arterial catheterization technique to test CA and CMA infusions of cholecystokinin (CCK) and gastrin releasing peptide (GRP) (Sayegh, et al, 2015; Washington, Aglan, & Sayegh, 2014). …”

Section: Introductionmentioning

confidence: 99%

Exogenous glucagon-like peptide-1 acts in sites supplied by the cranial mesenteric artery to reduce meal size and prolong the intermeal interval in rats

et al. 2016

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Three experiments were done to better assess the gastrointestinal (GI) site(s) of action of GLP-1 on food intake in rats. First, near-spontaneous nocturnal chow meal size (MS), intermeal intervals (IMI) length and satiety ratios (SR = MS/IMI) were measured after infusion of saline, 0.025 or 0.5 nmol/kg GLP-1 into the celiac artery (CA, supplying the stomach and upper duodenum), cranial mesenteric artery (CMA, supplying small and all of the large intestine except the rectum), femoral artery (FA, control) or portal vein (PV, control). Second, infusion of 0.5 nmol/kg GLP-1 was tested after pretreatment with the GLP-1 receptor (GLP-1R) antagonist exendin-4(3–39) via the same routes. Third, the regional distribution of GLP-1R in the rat GI tract was determined using rtPCR. CA, CMA and FA GLP-1 reduced first MS relative to saline, with the CMA route more effective than the others. Only CMA GLP-1 prolonged the IMI. None of the infusions affected second MS or later eating. CA and CMA GLP-1 increased the SR, with the CMA route more effective than the CA route. CMA exendin-4 (3–39) infusion reduced the effect of CMA GLP-1. Finally GLP-1R expression was found throughout the GI tract. The results suggest that exogenous GLP-1 acts in multiple GI sites to reduce feeding under our conditions and that GLP-1R in the area supplied by the CMA, i.e., the small and part of the large intestine, plays the leading role.

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“…This powerful approach was also applied to selective infusions into the celiac artery (supplying splenic, left gastric and common hepatic arteries) and the more distal cranial mesenteric artery (supplying pancreatico-duodenal, jejunal, and ileocolic arteries), with the former responsible for regulating meal size, while the latter was responsible for regulating inter-meal interval [31, 32]. CCK1R-bearing vagal afferent neurons are present in both vascular distributions, but it is fascinating that regulation of meal size is an event that appears to be regulated higher in the gut than regulation of the inter-meal interval.…”

Section: Ligand-directed Bias In Signalingmentioning

confidence: 99%

“…Indeed, CCK affects all these events, with impact on pylorus to slow gastric emptying if too much food is entering the small bowel, with a stimulatory impact on gallbladder emptying to contribute to micelle formation critical for fat emulsification, and with stimulatory effects on secretion of pancreatic zymogens for digestion of complex nutrients. Of particular interest, recent studies reviewed above [31, 32] suggest that even within the “proximal gut,” CCK may include spatial differences in action, with the most proximal events stimulated by CCK acting at CCK1Rs contributing to limiting meal size, and the more distal events stimulated by this same hormone and receptor contributing to extending the inter-meal interval. In evolution, it has been more of a challenge to ensure adequate nutrition, than to prevent excessive feeding.…”

Section: Benefits Of Combination Therapiesmentioning

confidence: 99%

Metabolic Actions of the Type 1 Cholecystokinin Receptor: Its Potential as a Therapeutic Target

Miller

Desai

2016

Trends in Endocrinology & Metabolism

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Cholecystokinin regulates appetite and reduces food intake by activating the type 1 CCK receptor (CCK1R). Attempts to develop CCK1R agonists for obesity have yielded active agents that have not reached clinical practice. In this review we discuss why, along with new strategies to target CCK1R more effectively. We examine signaling events and the possibility of developing agents that exhibit ligand-directed bias, to dissociate satiety activity from undesirable side effects. Potential allosteric sites of modulation are also reviewed, along with desired properties of a positive allosteric modulator without intrinsic agonist action as another strategy to treat obesity. These new types of CCK1R-active drugs could be useful as stand-alone agents or as part of a rational drug combination for management of obesity.

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Celiac and the cranial mesenteric arteries supply gastrointestinal sites that regulate meal size and intermeal interval length via cholecystokinin-58 in male rats

Cited by 18 publications

References 34 publications

Satietogenic Protein from Tamarind Seeds Decreases Food Intake, Leptin Plasma and <b><i>CCK-1r</i></b> Gene Expression in Obese Wistar Rats

Satietogenic Protein from Tamarind Seeds Decreases Food Intake, Leptin Plasma and <b><i>CCK-1r</i></b> Gene Expression in Obese Wistar Rats

Exogenous glucagon-like peptide-1 acts in sites supplied by the cranial mesenteric artery to reduce meal size and prolong the intermeal interval in rats

Metabolic Actions of the Type 1 Cholecystokinin Receptor: Its Potential as a Therapeutic Target

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