CCK-8 and CCK-58 differ in their effects on nocturnal solid meal pattern in undisturbed rats

Goebel-Stengel, Miriam; Stengel, Andreas; Wang, Lixin; Ohning, Gordon V.; Taché, Yvette; Reeve, Joseph R.

doi:10.1152/ajpregu.00365.2011

Cited by 23 publications

(21 citation statements)

References 63 publications

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“…This robust observation, made during a scheduled feeding regimen is in line with the earlier reported IMI extension by CCK-58 (but not by CCK-8) during ad-libitum chow feeding [22]. Additionally, CCK-58’s actions are consistent with earlier reported IMI effects of endogenous CCK signaling [7, 36, 41], and stronger reductions of food intake by larger CCK forms than by CCK-8 [61].…”

Section: Discussionsupporting

confidence: 90%

“…Indeed, recently, one of us (JRR) reported no differences in the occurrence of grooming and locomotion in rats following administration of an anorexigenic dose of CCK-58 and vehicle [22]. In the current, second study we aimed to extend this observation by examining effects on the microstructure of licking during the first meal after CCK-58 administration.…”

Section: Introductionmentioning

confidence: 86%

“…Generally, satiation or satiety actions of exogenous doses of peptides such as CCK are validated by observations that meal-size reduction is accompanied by natural prandial and post-prandial motor behaviors and the absence of signs of malaise [22, 34, 63]. Indeed, recently, one of us (JRR) reported no differences in the occurrence of grooming and locomotion in rats following administration of an anorexigenic dose of CCK-58 and vehicle [22].…”

Section: Introductionmentioning

confidence: 99%

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CCK-58 elicits both satiety and satiation in rats while CCK-8 elicits only satiation

Overduin¹,

Gibbs²,

Cummings³

et al. 2014

Peptides

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Reduction of food intake by exogenous cholecystokinin (CCK) has been demonstrated primarily for its short molecular form, CCK-8. Mounting evidence, however, implicates CCK-58 as a major physiologically active CCK form, with different neural and exocrine response profiles than CCK-8. In three studies, we compared meal-pattern effects of intraperitoneal injections CCK-8 vs. CCK-58 in undeprived male Sprague-Dawley rats consuming sweetened condensed milk. In study one, rats (N=10) received CCK-8, CCK-58 (0.45, 0.9, 1.8 and 3.6 nmole/kg) or vehicle before a 4-hour test-food presentation. At most doses, both CCK-8 and CCK-58 reduced meal size relative to vehicle. Meal-size reduction prompted a compensatory shortening of the intermeal interval (IMI) after CCK-8, but not after CCK-58, which uniquely increased the satiety ratio (IMI/size of the preceding meal). In the second study, lick patterns were monitored after administration of 0.9nmole/kg CCK-58, CCK-8 or vehicle. Lick cluster size, lick efficiency and interlick-interval distribution remained unaltered compared to vehicle, implying natural satiation, rather than illness, following both CCK forms. In study 3, threshold satiating doses of the two CCK forms were given at 5 and 30 minutes after meal termination, respectively. CCK 58, but not CCK-8 increased the intermeal interval and satiety ratio compared to vehicle. In conclusion, while CCK 58 and CCK-8 both stimulate satiation, thereby reducing meal size, CCK-58 consistently exerts a satiety effect, prolonging IMI. Given the physiological prominence of CCK-58, these results suggest that CCK’s role in food intake regulation may require reexamination.

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Section: Discussionsupporting

confidence: 90%

Section: Introductionmentioning

confidence: 86%

Section: Introductionmentioning

confidence: 99%

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CCK-58 elicits both satiety and satiation in rats while CCK-8 elicits only satiation

Overduin¹,

Gibbs²,

Cummings³

et al. 2014

Peptides

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“…However, with the use of techniques that minimize CCK peptide degradation, CCK-58 is the only circulating form of CCK in the rat (19,76). CCK-58 produces a prolonged inhibition of food intake compared with CCK-8, inhibiting food intake for as long as 60 min, and a longer latency to first meal and intermeal interval (27,28). However, CCK-58 is not commercially available, which explains the more common use of the octapeptide form in most research.…”

Section: Discussionmentioning

confidence: 99%

The subfornical organ: a novel site of action of cholecystokinin

Ahmed

Dai

et al. 2014

American Journal of Physiology-Regulatory, Integrative and Comp

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The subfornical organ (SFO) is an important sensory circumventricular organ implicated in the regulation of fluid homeostasis and energy balance. We investigated whether the SFO is activated by the hormone cholecystokinin (CCK). CCK₁ and CCK₂ receptors were identified in the SFO by RT-PCR. Dissociated SFO neurons that responded to CCK (40/77), were mostly depolarized (9.2 ± 0.9 mV, 30/77), but some were hyperpolarized (-7.3 ± 1.1 mV, 10/77). We next examined the responses of SFO neurons in vivo to CCK (16 μg/kg ip), in the presence and absence of CCK₁ or CCK₂ receptor antagonists (devazepide; 600 μg/kg and L-365,260; 100 μg/kg, respectively), using the functional activation markers c-Fos and phosphorylated extracellular signal-related kinase (p-ERK). The nucleus of the solitary tract (NTS) served as a control for CCK-induced activity. There was a significant increase in c-Fos expression in the NTS (259.2 ± 20.8 neurons) compared with vehicle (47.5 ± 2.5). Similarly, in the SFO, c-Fos was expressed in 40.5 ± 10.6 neurons in CCK-treated compared with 6.6 ± 2.7 in vehicle-treated rats (P < 0.01). Devazepide significantly reduced the effects of CCK in the NTS but not in SFO. L-365,260 blocked the effects of CCK in both brain regions. CCK increased the number of p-ERK neurons in NTS (27.0 ± 4.0) as well as SFO (18.0 ± 4.0), compared with vehicle (8.0 ± 2.6 and 4.3 ± 0.6, respectively; P < 0.05). Both devazepide and L-365,260 reduced CCK-induced p-ERK in NTS, but only L-365,260 reduced it in the SFO. In conclusion, the SFO represents a novel brain region at which circulating CCK may act via CCK₂ receptors to influence central autonomic control.

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“…53 Part of these actions are different between species with CCK being an inhibitor of gastric motility in humans 58 and rats 59 In addition to the functions described above CCK reduces food intake. 57,62 The peptide is released from intestinal I cells after food intake with the most potent stimulation by lipids and proteins, 63,64 binds to the CCK A on vagal afferents and leads to an activation of cells in the NTS that ultimately induce a reduction of food intake. 65,66 In humans, stimulation of the CCK A with the orally-active CCK A agonist, GI181771X did not induce a reduction of body weight, while gastrointestinal side effects and effects on gallbladder and bile duct were observed.…”

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confidence: 99%

Control of Food Intake by Gastrointestinal Peptides: Mechanisms of Action and Possible Modulation in the Treatment of Obesity

Prinz

Stengel

2017

J Neurogastroenterol Motil

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This review focuses on the control of appetite by food intake-regulatory peptides secreted from the gastrointestinal tract, namely cholecystokinin, glucagon-like peptide 1, peptide YY, ghrelin, and the recently discovered nesfatin-1 via the gut-brain axis. Additionally, we describe the impact of external factors such as intake of different nutrients or stress on the secretion of gastrointestinal peptides. Finally, we highlight possible conservative--physical activity and pharmacotherapy--treatment strategies for obesity as well as surgical techniques such as deep brain stimulation and bariatric surgery also altering these peptidergic pathways.

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CCK-8 and CCK-58 differ in their effects on nocturnal solid meal pattern in undisturbed rats

Abstract: . CCK-8 and CCK-58 differ in their effects on nocturnal solid meal pattern in undisturbed rats.

Cited by 23 publications

References 63 publications

CCK-58 elicits both satiety and satiation in rats while CCK-8 elicits only satiation

CCK-58 elicits both satiety and satiation in rats while CCK-8 elicits only satiation

The subfornical organ: a novel site of action of cholecystokinin

Control of Food Intake by Gastrointestinal Peptides: Mechanisms of Action and Possible Modulation in the Treatment of Obesity

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