Rapid communicationEvidence that decreased feeding induced by systemic injection of cholecystokinin is mediated by CCK-A receptors
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A new potent and selective non-peptide gastrin antagonist and brain cholecystokinin receptor (CCK-B) ligand: L-365,260
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Cited by (119)
The expression of the gastrin/cholecystokinin (GAST/CCK) family and their receptors (CCKAR/CCKBR) in the chicken changes in response to quantitative restriction and reveals a functional role of CCK in the crop
2022, General and Comparative EndocrinologyCitation Excerpt :The GAST/CCK family also has roles in the central nervous system including the control of behaviour (Ballaz, 2017) and notably in cockerels, crowing (Shimmura et al., 2019). In mammals CCK acts as a satiety hormone as evidenced by reductions in food intake after intra peritoneal injection with its action through CCKAR (Dourish et al., 1989), an observation which has also been replicated in avian species including the chicken (Covasa and Forbes, 1994; Dunn et al., 2013; Rodriguez-Sinovas et al., 1997). CCK was first recognised and named for its role in the release of bile from the gall bladder in mammals and this is also true in the chicken (Dimaline and Lee, 1990).
Cholecystokinin (CCK) and related adjunct peptide therapies for the treatment of obesity and type 2 diabetes
2018, PeptidesCitation Excerpt :Similar appetite suppressive effects were later demonstrated in pigs [30], rhesus monkeys [31] as well as in humans [32]. To delineate the specific receptor subtypes involved in CCK-mediated appetite suppressive effects, studies have utilised the CCK-1 receptor antagonist, devazepide, and CCK-2 receptor antagonist, L-365,260, in rodents and humans [33,34]. Current understanding suggests that CCK stimulates CCK-1 receptors on a subgroup of visceral afferent nerves that send satiety signals to the hypothalamus [35].
Neuroendocrine Control of Energy Stores
2015, Williams Textbook of EndocrinologyCannabinoid Receptors and Cholecystokinin in Feeding Inhibition
2013, Vitamins and HormonesCitation Excerpt :Vagal nerve afferents within the gastrointestinal tract and hepatoportal regions are stimulated by mechanical distension, chemical stimulation, and local production of gut hormones (Schwartz, 2000). The satiety action of CCK appears to be mediated by activation of peripheral CCK1 receptors located in the vagus nerve (Corp et al., 1993; Dourish, Ruckert, Tattersall, & Iversen, 1989). CCK is rapidly released from I-cells in the upper intestine (the duodenum and jejunum) in response to the intraluminal presence of the digestive products of fats and proteins (Cummings & Overduin, 2007), and its binding and axonal transport are evident in all abdominal vagal branches (Moran, Smith, Hostetler, & McHugh, 1987).
The CCK<inf>B</inf> antagonist CI988 reduces food intake in fasted rats via a dopamine mediated pathway
2013, PeptidesCitation Excerpt :The present study provides evidence that the CCKB receptor antagonist CI988 reduces food intake in fasted rats after ICV administration, an effect that was blocked by the dopamine receptor antagonist, flupentixol. Various studies indicate that peripheral CCK is involved in the regulation of food intake via the CCKA receptor system [11,25,34]. However, it has also been shown that ICV injection of the CCKB receptor antagonist L365,260 reduces food intake, suggesting that central CCKB signaling may play a role in the modulation of food intake [6].
Neuroendocrine Control of Energy Stores
2011, Williams Textbook of Endocrinology, Twelfth Edition