Lack of satiety effect of cholecystokinin (CCK) in a new rat model not expressing the CCK-A receptor gene

Miyasaka, Kyoko; Kanai, Setsuko; Ohta, Minoru; Kawanami, Takako; Kono, Akira; Funakoshi, Akihiro

doi:10.1016/0304-3940(94)90507-x

Cited by 92 publications

(45 citation statements)

References 13 publications

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“…It is also unlikely to represent the anxiolytic-like effect of devazepide because L-365,260, which has established anxiolytic-like properties in mice (43,44), did not influence the food-suppressing effect of leptin-CCK. These results indicate that the CCK-A receptor subtype is critical for leptin-CCK-induced food intake suppression as established previously for the satiating effect of peripherally administered CCK alone (14,18,45,46). CCK-A receptors are present in vagal afferent fibers and systemic administration of CCK stimulates gastric vagal afferent discharge in rats (22,(47)(48)(49)(50)(51).…”

Section: Discussionsupporting

confidence: 82%

Synergistic interaction between leptin and cholecystokinin to reduce short-term food intake in lean mice

Barrachina

Martı́nez

Wang

et al. 1997

Proc. Natl. Acad. Sci. U.S.A.

405

256

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Leptin is a circulating protein involved in the long-term regulation of food intake and body weight. Cholecystokinin (CCK) is released postprandially and elicits satiety signals. We investigated the interaction between leptin and CCK-8 in the short-term regulation of food intake induced by 24-hr fasting in lean mice. Leptin, injected intraperitoneally (i.p.) at low doses (4-120 g͞kg), which did not influence feeding behavior for the first 3 hr postinjection, decreased food intake dose dependently by 47-83% during the first hour when coinjected with a subthreshold dose of CCK. Such an interaction was not observed between leptin and bombesin. The food-reducing effect of leptin injected with CCK was not associated with alterations in gastric emptying or locomotor behavior. Leptin-CCK action was blocked by systemic capsaicin at a dose inducing functional ablation of sensory afferent fibers and by devazepide, a CCK-A receptor antagonist but not by the CCK-B receptor antagonist, L-365,260. The decrease in food intake which occurs 5 hr after i.p. injection of leptin alone was also blunted by devazepide. Coinjection of leptin and CCK enhanced the number of Fos-positive cells in the hypothalamic paraventricular nucleus by 60%, whereas leptin or CCK alone did not modify Fos expression. These results indicate the existence of a functional synergistic interaction between leptin and CCK leading to early suppression of food intake which involves CCK-A receptors and capsaicin-sensitive afferent fibers.

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Section: Discussionsupporting

confidence: 82%

Synergistic interaction between leptin and cholecystokinin to reduce short-term food intake in lean mice

Barrachina

Martı́nez

Wang

et al. 1997

Proc. Natl. Acad. Sci. U.S.A.

405

256

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“…The contribution of each receptor to CCK-stimulated action is varied. Some pharmacological studies using CCK receptor antagonists have indicated that the CCK2 is involved in anxiety, while CCK1 has been implicated in satiety and behavior (Hughes et al 1990, Miyasaka et al 1994, Wank 1995. The gene expression and/or protein distribution of CCK1 and CCK2 have been reported (Wank 1995, Bourassa et al 1999.…”

Section: Introductionmentioning

confidence: 99%

Cholecystokinin receptors regulate sperm protein tyrosine phosphorylation via uptake of HCO3−

Zhou

Shi

et al. 2015

Reproduction

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Cholecystokinin (CCK), a peptide hormone and a neurotransmitter, was detected in mature sperm two decades ago. However, the exact role of CCK and the types of CCK receptors (now termed CCK1 and CCK2) in sperm have not been identified. Here, we find that CCK1 and CCK2 receptors are immunolocalized to the acrosomal region of mature sperm. The antagonist of CCK1 or CCK2 receptor strongly activated the soluble adenylyl cyclase/cAMP/protein kinase A signaling pathway that drives sperm capacitation-associated protein tyrosine phosphorylation in dose-and time-dependent manners. But these actions of stimulation were abolished when sperm were incubated in the medium in the absence of HCO 3 K . Further investigation demonstrated that the inhibitor of CCK1 or CCK2 receptor could accelerate the uptake of HCO 3 K and significantly elevate the intracellular pH of sperm. Interestingly, the synthetic octapeptide of CCK (CCK8) showed the same action and mechanism as antagonists of CCK receptors. Moreover, CCK8 and the antagonist of CCK1 or CCK2 receptor were also able to accelerate human sperm capacitation-associated protein tyrosine phosphorylation by stimulating the influx of HCO 3 K . Thus, the present results suggest that CCK and its receptors may regulate sperm capacitation-associated protein tyrosine phosphorylation by modulating the uptake of HCO 3 K .Reproduction (2015) 150 257-268

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“…One mechanism of obesity in OLETF rats is disruption of the cholecystokinin (CCK)-A-receptor gene (2,3). The CCK-A receptor has been implicated in satiety and a disrupted CCK-Areceptor gene induced hyperphagia (4). The characteristic features of OLETF rats are late onset of hyperglycemia at about 18 weeks of age, followed by insulin deficiency at about 65 weeks (1).…”

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confidence: 99%

A Peroxisome Proliferator-Activated Receptor γ Agonist Influenced Daily Profile of Energy Expenditure in Genetically Obese Diabetic Rats

Yoshida

Ichikawa

Ohta

et al. 2002

Japanese Journal of Pharmacology

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ABSTRACT-Otsuka Long Evans Tokushima Fatty (OLETF) rats were developed as a model of noninsulin-dependent diabetes mellitus (NIDDM) with mild obesity. We reported that the daily profiles of energy expenditure associated with two peaks (one between 05:00 and 08:00 and the other between 20:00 and 22:00) were observed at 8 weeks of age (without NIDDM), while these two peaks disappeared at 24 weeks of age with NIDDM. As a new anti-diabetic drug, a peroxisome proliferator-activated receptor C agonist pioglitazone hydrochloride has been developed, we examined whether pioglitazone normalized daily profiles of energy expenditure at 24 weeks of age. A control diet and pioglitazone (0.1%)-containing diet were fed from 6 weeks of age. The two peaks of daily profiles of energy expenditure, which disappeared in OLETF rats with the control diet at 24 weeks of age, were reproduced by administration of pioglitazone. The respiratory quotient was lower and fat derived energy used for combustion was increased by pioglitazone at both ages. The body weight, daily food intake, plasma levels of fat, insulin, leptin and the wet weight of visceral fat were not influenced, but the levels of blood hemoglobin A1c and plasma tumor necrosis factor = were decreased by pioglitazone. Administration of pioglitazone improved daily profiles of energy expenditure via affecting glucose and fat metabolisms.Keywords: Energy expenditure, Non-insulin-dependent diabetes mellitus, Obesity, Peroxisome proliferator-activated receptor C Otsuka Long Evans Tokushima Fatty (OLETF) rats were developed as a model of non-insulin-dependent diabetes mellitus (NIDDM) with mild obesity (1). One mechanism of obesity in OLETF rats is disruption of the cholecystokinin (CCK)-A-receptor gene (2, 3). The CCK-A receptor has been implicated in satiety and a disrupted CCK-Areceptor gene induced hyperphagia (4). The characteristic features of OLETF rats are late onset of hyperglycemia at about 18 weeks of age, followed by insulin deficiency at about 65 weeks (1). In an original study by Kawano et al. 1992 (1), rats were divided to three groups after an oral glucose tolerance test (OGTT) was conducted. Glucose (2 g /kg) solution was given per os, and plasma levels of glucose were measured before and at 30, 60, 90 and 120 min: 1) Diabetic type rats had a peak level of plasma glucose >16.8 mM and a level of plasma glucose at 120 min >11.2 mM, and only rats that showed both conditions by OGTT were diagnosed with clinical DM; 2) if either of the two conditions was observed in the rats, they were diagnosed with impaired glucose tolerance (IGT); and 3) normal type, where neither DM nor IGT was present. After 23 weeks of age, OLETF rats with normal type parameters were not observed (94.7% with DM and 5.2% with IGT, respectively) (1).We have previously examined the daily profile of energy expenditure in OLETF and control [Long Evans Tokushima (LETO)] rats at 8 and 24 weeks of age (5, 6). The diurnal rhythm of energy expenditure associated with the highest and lowest values for energy co...

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Lack of satiety effect of cholecystokinin (CCK) in a new rat model not expressing the CCK-A receptor gene

Cited by 92 publications

References 13 publications

Synergistic interaction between leptin and cholecystokinin to reduce short-term food intake in lean mice

Synergistic interaction between leptin and cholecystokinin to reduce short-term food intake in lean mice

Cholecystokinin receptors regulate sperm protein tyrosine phosphorylation via uptake of HCO3−

A Peroxisome Proliferator-Activated Receptor γ Agonist Influenced Daily Profile of Energy Expenditure in Genetically Obese Diabetic Rats

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