The effects of proglumide on cholecystokinin-, bombesin-, and glucagon-induced satiety in the rat

Collins, Stephen M.; Walker, Diana L.; Forsyth, Peter; Belbeck, L.

doi:10.1016/0024-3205(83)90420-4

Cited by 63 publications

(13 citation statements)

References 14 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The failure of L364,718 to antagonize the reduction in food intake produced by another putative satiety peptide, bombesin, in fasted rats gives some indication that it is selective for the effects of CCK on food intake. This finding also provides further evidence that CCK8 and bombesin act via different mechanisms to reduce food intake, as suggested by previous studies (Smith et al, 1981c;Collins et al, 1983). Collins et al (1983) also reported that proglumide partially antagonized the effects of high doses of bombesin (4-16 jig kg-', i.p.)…”

Section: Discussionsupporting

confidence: 87%

“…If this hypothesis is correct, then a CCK receptor antagonist given alone should increase food intake. Studies using proglumide, a weak antagonist at CCK receptors, have yielded equivocal results (Collins et al, 1983;Shillabeer & Davison, 1984;Schneider et al, 1985). Thus, a reliable satiating effect of endogenous CCK remains to be demonstrated.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

The cholecystokinin receptor antagonist L364,718 increases food intake in the rat by attenuation of the action of endogenous cholecystokinin

Hewson

Leighton

Hill

et al. 1988

British J Pharmacology

153

View full text Add to dashboard Cite

To determine the role of endogenous cholecystokinin (CCK) in the regulation of food intake, the effects of the potent CCK receptor antagonist L364,718 were investigated on the intake of a palatable diet in non‐deprived rats. The effect of a single dose of proglumide was also investigated for comparative purposes. In addition, the ability of L364,718 to antagonize the reduction in food intake produced by exogenous cholecystokinin‐octapeptide (CCK8) or bombesin in food‐deprived rats was determined. L364,718 (10–100 μg kg−1, i.p.) increased the intake of palatable diet during the 30 min test period. Proglumide (300 mg kg−1, i.p.) also increased the intake of palatable diet. Conversely, CCK8 (0.5–5 μg kg−1, i.p.) produced a reduction in the intake of the diet. In fasted rats, L364,718 (100 μg kg−1, i.p.) antagonized the reduction in food intake produced by CCK8 (10 μg kg−1, i.p.) but not that produced by bombesin (50 μg kg−1, i.p.). L364,718 did not increase food intake in these animals when measured over a 6 h period. It is concluded that L364,718 is a potent, selective antagonist of the effects of CCK8 on food intake. The observation that L364,718 and proglumide increase the intake of a palatable diet provides some evidence that endogenous CCK is involved in the control of food intake in this model.

show abstract

Section: Discussionsupporting

confidence: 87%

Section: Introductionmentioning

confidence: 99%

The cholecystokinin receptor antagonist L364,718 increases food intake in the rat by attenuation of the action of endogenous cholecystokinin

Hewson

Leighton

Hill

et al. 1988

British J Pharmacology

153

View full text Add to dashboard Cite

show abstract

“…It remains to be seen whether changes in the membrane-bound receptor number jn.nutrition.org in the nodose ganglia or other tissues occurs during chronic HF diet consumption. In in vitro models, prior CCK exposure results in desensitization of pancreatic enzyme secretion (21,43) and downregulation of the receptor gene expression in pancreatic acinar cells. Therefore, changes in receptor internalization, phosphorylation, sequestration, or postreceptor transduction cascade are all possible mechanisms associated with reduced sensitivity to CCK.…”

Section: Discussionmentioning

confidence: 99%

Reduced Sensitivity to Cholecystokinin in Male Rats Fed a High-Fat Diet Is Reversible

Swartz

Savastano

Covașă

2010

The Journal of Nutrition

View full text Add to dashboard Cite

Adult rats chronically fed a high-fat (HF) diet maintain reduced sensitivity to cholecystokinin (CCK). We hypothesized that, similar to adult rats, pups fed a HF diet would also exhibit reduced sensitivity to CCK. To test this, male pups fed low-fat (LF) and HF isoenergetic (16.2 kJ/g) diets were administered CCK intraperitoneally (0.125-1 microg/kg) 1 wk following dietary adaptation. After receiving 0.5 microg/kg CCK, pups fed the HF diet suppressed food intake less (8.9 +/- 5.0%) than pups fed the LF diet (28.9 +/- 4.7%; P < 0.05) relative to intakes after saline administration. We then assessed the development and extinction of changes in CCK sensitivity by switching the diets between the groups. The HF-fed group, when switched to the LF diet, regained sensitivity by wk 4 and suppressed food intake following administration of 0.25 microg/kg CCK (33.1 +/- 5.7%; P < 0.05). The LF-fed group, when switched to the HF diet, lost sensitivity by wk 2 and did not suppress food intake after administrations of CCK compared with saline. Finally, we examined if HF-fed rats have an increased sensitivity to corn oil during brief access tests using a multibottle gustometer. At oil concentrations of 25, 75, and 100%, rats fed the HF diet sampled more oil than LF-fed rats (P < 0.05). These findings demonstrate that male rat pups fed a HF diet exhibit reduced sensitivity to CCK, the development of this reduced sensitivity is quicker than its extinction, and rats consuming a HF diet have increased oral sensitivity to oils.

show abstract

“…BBS inhibits food intake independently of CCK as evidenced by the finding that BBS, but not CCK, reduces food intake following vagotomy (200,201). Although BBS appears to utilize a nonvagal pathway unlike CCK, BBS stimulates CCK secretion (51,105), and the CCK-1R antagonist, proglumide, partially blocks the effect of high doses of BBS on food intake (42). In addition to being less sensitive to CCK, rats maintained on an Fig.…”

Section: Hf Diet Alters Sensitivity To Other Gi Peptidesmentioning

confidence: 96%

Deficits in gastrointestinal responses controlling food intake and body weight

Covașă

2010

American Journal of Physiology-Regulatory, Integrative and Comp

View full text Add to dashboard Cite

The gastrointestinal tract serves as a portal sensing incoming nutrients and relays mechanical and chemosensory signals of a meal to higher brain centers. Prolonged consumption of dietary fat causes adaptive changes within the alimentary, metabolic, and humoral systems that promote a more efficient process for energy metabolism from this rich source, leading to storage of energy in the form of adipose tissue. Furthermore, prolonged ingestion of dietary fats exerts profound effects on responses to signals involved in termination of a meal. This article reviews the effects of ingested fat on gastrointestinal motility, hormone release, and neuronal substrates. It focuses on changes in sensitivity to satiation signals resulting from chronic ingestion of high-fat diet, which may lead to disordered appetite and dysregulation of body weight.

show abstract

The effects of proglumide on cholecystokinin-, bombesin-, and glucagon-induced satiety in the rat

Cited by 63 publications

References 14 publications

The cholecystokinin receptor antagonist L364,718 increases food intake in the rat by attenuation of the action of endogenous cholecystokinin

The cholecystokinin receptor antagonist L364,718 increases food intake in the rat by attenuation of the action of endogenous cholecystokinin

Reduced Sensitivity to Cholecystokinin in Male Rats Fed a High-Fat Diet Is Reversible

Deficits in gastrointestinal responses controlling food intake and body weight

Contact Info

Product

Resources

About