CCK enhances response to gastric distension by acting on capsaicin-insensitive vagal afferents

Wall, Esther H.E.M. van de; Duffy, Peter H.; Ritter, Robert C.

doi:10.1152/ajpregu.00809.2004

Cited by 46 publications

(28 citation statements)

References 47 publications

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“…Sham-vagotomized control rats (n ϭ 8) were prepared by surgically approaching the vagi, but not sectioning them. These procedures have previously been described in detail (42,48). Briefly, rats were anesthetized with a mixture containing ketamine (50 mg/kg), acepromazine (2 mg/kg), and xylazine (25 mg/kg) (0.1 ml mixture/100 g body wt).…”

Section: Surgeries and Capsaicin Treatmentmentioning

confidence: 99%

Circulating GLP-1 and CCK-8 reduce food intake by capsaicin-insensitive, nonvagal mechanisms

Zhang

Ritter

2012

American Journal of Physiology-Regulatory, Integrative and Comp

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Zhang J, Ritter RC. Circulating GLP-1 and CCK-8 reduce food intake by capsaicin-insensitive, nonvagal mechanisms. Am J Physiol Regul Integr Comp Physiol 302: R264 -R273, 2012. First published October 26, 2011 doi:10.1152/ajpregu.00114.2011.-Previous reports suggest that glucagon-like peptide (GLP-1), a peptide secreted from the distal small intestine, is an endocrine satiation signal. Nevertheless, there are conflicting reports regarding the site where circulating GLP-1 acts to reduce food intake. To test the hypothesis that vagal afferents are necessary for reduction of food intake by circulating GLP-1, we measured intake of 15% sucrose during intravenous GLP-1 infusion in intact, vagotomized, and capsaicin-treated rats. We also measured sucrose intake during intravenous infusion of cholecystokinin, a peptide known to reduce food intake via abdominal vagal afferents. We found that reduction of intake by GLP-1 was not diminished by capsaicin treatment or vagotomy. In fact, reduction of sucrose intake by our highest GLP-1 dose was enhanced in vagotomized and capsaicin-treated rats. Intravenous GLP-1 induced comparable increases of hindbrain c-Fos immunoreactivity in intact, capsaicin-treated, and vagotomized rats. Plasma concentrations of active GLP-1 in capsaicin-treated rats did not differ from those of controls during the intravenous infusions. Finally, capsaicin treatment was not associated with altered GLP-1R mRNA in the brain, but nodose ganglia GLP-1R mRNA was significantly reduced in capsaicin-treated rats. Although reduction of food intake by intraperitoneal cholecystokinin was abolished in vagotomized and capsaicin-treated rats, reduction of intake by intravenous cholecystokinin was only partially attenuated. These results indicate that vagal or capsaicin-sensitive neurons are not necessary for reduction of food intake by circulating (endocrine) GLP-1, or cholecystokinin. Vagal participation in satiation by these peptides may be limited to paracrine effects exerted near the sites of their secretion.

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Section: Surgeries and Capsaicin Treatmentmentioning

confidence: 99%

Circulating GLP-1 and CCK-8 reduce food intake by capsaicin-insensitive, nonvagal mechanisms

Zhang

Ritter

2012

American Journal of Physiology-Regulatory, Integrative and Comp

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“…Recently, van De Wall et al (47) reported that lorglumide did not diminish the expression of Fos induced by 2-ml distension; however, it completely reversed the enhancement of distension-induced Fos expression by CCK. This suggests that lorglumide specifically reduces the response of vagal afferents to distension.…”

Section: Discussionmentioning

confidence: 97%

“…Our final experiment addressed whether the diminished feeding response to gastric distension in OLETF rats could be explained, at least partially, through decreased vagal activation of distension signals. Gastric distension induces Fos within the NTS region of the DVC (19,47), an area established as the primary termination site for vagal afferent input from the stomach (50). Furthermore, distension-induced Fos expression in the NTS is abolished via vagotomy (21,25).…”

Section: Discussionmentioning

confidence: 99%

“…Eight rats (n ϭ 4 rats/strain) had their stomachs distended with 8 ml of warmed water for a period of 90 min, whereas six rats (n ϭ 3 rats/strain) underwent all procedures as described above except that no inflation of the catheter occurred (sham distension). These methods have been previously described by van de Wall and colleagues with slight modifications (47).…”

Section: Analysis Of C-fos Expression In the Hindbrain Of Oletf And Lmentioning

confidence: 99%

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Decreased gastric mechanodetection, but preserved gastric emptying, in CCK-1 receptor-deficient OLETF rats

Jonghe¹,

Hajnal²,

Covașă³

2006

American Journal of Physiology-Gastrointestinal and Liver Physi

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creased gastric mechanodetection, but preserved gastric emptying, in CCK-1 receptor-deficient OLETF rats. Am J Physiol Gastrointest Liver Physiol 291: G640 -G649, 2006. First published May 25, 2006 doi:10.1152/ajpgi.00109.2006.-Obese CCK-1 receptor-lacking Otsuka Long Evans Tokushima fatty (OLETF) rats are hyperphagic relative to control, nonmutant Long Evans Tokushima Otsuka (LETO) rats. This study sought to assess whether the overeating observed in OLETF rats is associated with changes in gastric emptying rates or detection of gastric volume. We performed experiments in both 12-and 29-wk-old OLETF and LETO rats to address possible alterations in gastric functions during the development of increased body weight and blood glucose abnormalities in OLETF rats. Gastric emptying of a 5-g solid chow test meal was not significantly different between strains at either 1, 2, or 4 h postmeal. When rats with ad libitum access to chow were tested, there were no significant differences in gastric emptying between strains at any time period despite OLETF rats consuming significantly more chow than LETO rats. Similar to solid food, 5-min gastric emptying of a 5-ml isosmotic and hyperosmotic saline or glucose load was not significantly different between strains. When the stomach was distended with a 15-ml semisolid chow load, there was no significance difference in emptying at either 1 or 2 h. No significant differences in gastric emptying were detected between 12-and 29-wk-old rats under any conditions. Both young and old OLETF rats, however, reduced sham intake significantly less compared with LETO rats during a brief period of gastric distension by 5-or 10-ml balloon inflation. Finally, OLETF rats showed decreased Fos expression in the nucleus of the solitary tract relative to LETO rats after an 8-ml gastric distension. These findings demonstrate that OLETF rats do not express deficits in controlling gastric emptying rates; however, they exhibit decreased behavioral and vagal responsiveness to gastric distension that may contribute to the increased meal size in these animals.cholecystokinin; hyperphagia; cholecystokinin-1 receptor; c-Fos; gastric distension; sucrose; sham feeding THE OTSUKA LONG-EVANS TOKUSHIMA FATTY (OLETF) rat is an outbred mutant strain of the Long Evans Tokushima Otsuka (LETO) rat that lacks CCK-1 receptor expression entirely due to a spontaneous 6.8-kb mutation spanning the promoter and first two exon regions of the CCK-1 receptor gene (46). In addition to the use of these animals as a model of insulin resistance, due to their natural manifestation of hyperglycemia and non-insulin-dependent diabetes mellitus relative to agematched LETO rats (16), OLETF rats are also currently under investigation as a model of obesity. OLETF rats exhibit an increased rate of weight gain relative to controls across their lifespan, with a marked elevation in body weight seen as early as 2-4 postnatal days (2, 27, 43). It is also known that OLETF rats are hyperphagic via increased meal size. This behavior has been attribu...

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“…CCK also increases satiation via CCK-A receptors on vagal afferents which signal via the nucleus of the solitary tract (NTS) in the brainstem (van de Wall et al, 2005). LCFAs also stimulate the release of the anorectic gut hormones peptide YY (PYY) and glucagon-like peptide-1 (GLP-1) from human enteroendocrine cells (Stoeckel et al, 2008).…”

Section: Lipid Sensingmentioning

confidence: 99%

The effect of L-cysteine on appetite in humans

Amin¹,

Agahi²,

Martin³

et al. 2014

EJEA

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CCK enhances response to gastric distension by acting on capsaicin-insensitive vagal afferents

Cited by 46 publications

References 47 publications

Circulating GLP-1 and CCK-8 reduce food intake by capsaicin-insensitive, nonvagal mechanisms

Circulating GLP-1 and CCK-8 reduce food intake by capsaicin-insensitive, nonvagal mechanisms

Decreased gastric mechanodetection, but preserved gastric emptying, in CCK-1 receptor-deficient OLETF rats

The effect of L-cysteine on appetite in humans

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