Effect of neuropeptide Y on ingestive behaviors in the rat

Morley, J. E.; Levine, A. S.; Gosnell, Blake A.; Kneip, J.; Grace, Martha K.

doi:10.1152/ajpregu.1987.252.3.r599

Cited by 132 publications

(82 citation statements)

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“…On the other hand, high doses of NPY and PYY seemed to induce hyperactivity in guinea-pigs, and one re¯ection of this activation is the increased amount of small meals consumed (Tables 2 and 3). Indeed, injections of NPY into frontal cortex or lateral brain ventricle in rats have been shown to increase locomotion and exploration (Levine & Morley, 1984;Morley et al, 1987b;Smialowski et al, 1992), although not in all studies (Heilig et al, 1988). Our observation that increased locomotion might be connected to Y 5 receptor stimulation is in agreement with the previous ®nding showing that the Y 5 antagonist, CGP 71683A, decreases exploratory behaviour in rats (Kask et al, 2001).…”

Section: British Journal Of Pharmacology Vol 135 (8)supporting

confidence: 92%

Receptor subtypes Y₁ and Y₅ mediate neuropeptide Y induced feeding in the guinea‐pig

Lecklin

Lundell

Paananen

et al. 2002

British J Pharmacology

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1 Neuropeptide Y (NPY) is one of the most potent stimulants of food intake. It has been debated which receptor subtype mediates this response. Initially Y 1 was proposed, but later Y 5 was announced as a`feeding' receptor in rats and mice. Very little is known regarding other mammals. The present study attempts to characterize the role of NPY in feeding behaviour in the distantly related guinea-pig. When infused intracerebroventricularly, NPY dose-dependently increased food intake. 2 PYY, (Leu 31 ,Pro 34 )NPY and NPY(2 ± 36) stimulated feeding, whereas NPY(13 ± 36) had no e ect. These data suggest that either Y 1 or Y 5 receptors or both may mediate NPY induced food intake in guinea-pigs. 3 The Y 1 receptor antagonists, BIBO 3304 and H 409/22 displayed nanomolar a nity for the Y 1 receptor (K i values 1.1+0.2 nM and 5.6+0.9 nM, respectively), but low a nity for the Y 2 or Y 5 receptors. When guinea-pigs were pretreated with BIBO 3304 and H 409/22, the response to NPY was inhibited. 4 The Y 5 antagonist, CGP 71683A had high a nity for the Y 5 receptor (K i 1.3+0.05 nM) without having any signi®cant activities at the Y 1 and Y 2 receptors. When CGP 71683A was infused into brain ventricles, the feeding response to NPY was attenuated. 5 The present study shows that NPY stimulates feeding in guinea-pigs through Y 1 and Y 5 receptors. As the guinea-pig is very distantly related to the rat and mouse, this suggests that both Y 1 and Y 5 receptors may mediate NPY-induced hyperphagia also in other orders of mammals.

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Section: British Journal Of Pharmacology Vol 135 (8)supporting

confidence: 92%

Receptor subtypes Y₁ and Y₅ mediate neuropeptide Y induced feeding in the guinea‐pig

Lecklin

Lundell

Paananen

et al. 2002

British J Pharmacology

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“…These increases occurred despite the fact that NPY--infused rats were prevented from overeating by pair--feeding with controls, and that there was no increase in body weight. Adrenalectomy abolished these NPY effects, in keeping with studies showing that other adipogenic effects of NPY are completely prevented or significantly attenuated by prior adrenalectomy in rats [16,23,29,31,34,37,43,45], and restored by specific glucocorticoid replacement [31,34,45]. In adrenalectomized rats, despite significantly reduced basal plasma IGF--1 levels, central NPY infusion was still able to inhibit the somatotropic axis, indicated by further reductions in plasma IGF--1.…”

Section: Discussionsupporting

confidence: 79%

“…These effects were restored by specific glucocorticoid replacement [31,34,45]. Other studies showed that adrenalectomy or administration of type II adrenal steroid receptor antagonists significantly attenuated or abolished the hyperphagia induced by acute central NPY injection in rats [16,23,34,37], although this was not consistent in all studies [43].…”

Section: Introductionmentioning

confidence: 93%

Inhibitory effects of central neuropeptide Y on the somatotropic and gonadotropic axes in male rats are independent of adrenal hormones

Sainsbury

Herzog

2001

Peptides

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Neuropeptide Y (NPY) in the hypothalamus exerts multiple physiological functions including stimulation of adipogenic pathways such as feeding and insulin secretion as well as inhibition of the somatotropic and gonadotropic axes. Since hypothalamic NPY--ergic activity is increased by negative energy balance, NPY enables coordinated regulation of growth and reproduction in parallel with energy availability. Chronic pathological increases in central NPY--ergic activity contribute to obesity. Many of the adipogenic effects of NPY are specifically dependent on adrenal glucocorticoids. However, in the current study we show that central NPY does not require adrenal hormones to inhibit the somatotropic and gonadotropic axes in rats. Male adrenalectomized and sham--operated normal rats were intracerebroventricularly (ICV) infused with NPY (15 µg/day) or saline for 5-7 days, and plasma leptin, insulin--like growth factor (IGF--1) and testosterone were assayed, and epididymal white adipose tissue (WATe) was weighed. In normal intact rats, WATe weight and leptinemia were significantly increased by NPY, and these effects were prevented by adrenalectomy. In normal rats, NPY markedly reduced plasma IGF--1 levels (470 ± 40 versus 1260 ± 90 ng/ml) and testosterone (0.53 ± 0.28 versus 5.4 ± 0.80 nmol/l in saline--infused controls, p < 0.0001). Adrenalectomy decreased plasma IGF--1 concentrations to 290 ± 30 ( p < 0.0001 versus normal rats), which were significantly reduced further by NPY. However, adrenalectomy had no significant effect on basal nor on NPY--induced plasma testosterone concentrations. In conclusion unlike the stimulatory effects of NPY on fat mass and leptinemia, NPY--induced inhibition of the somatotropic and gonadotropic axes in male rats do not require adrenal hormones.

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“…The fiber systems from the ARC and brainstem project into various hypothalamic sites previously implicated in regulation of feeding behavior (5)(6)(7)(8). In fact, not only administration into the cerebroventricular system (3, 9, 10) but microinjection of NPY into various hypothalamic sites (11)(12)(13) rapidly elicited robust feeding responses in rats. Continuous NPY infusion into the third cerebroventricle evoked continuous episodic feeding during the infusion and postinfusion intervals (14).…”

mentioning

confidence: 99%

Neuropeptide Y secretion increases in the paraventricular nucleus in association with increased appetite for food.

Kalra

Dube

Sahu

et al. 1991

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

585

232

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Feeding in mammals is a periodic behavior; however, knowledge of how the brain signals an intermittent eating pattern is scanty. Recent indirect evidence indicates that one of the signals encoded in the structure of neuropeptide Y (NPY) is to stimulate robust feeding. Therefore, two series of experiments were undertaken to characterize NPY secretion within the paraventricular nucleus (PVN) in association with eating behavior in the rat. Dynamic changes in NPY concentration in several hypothalamic sites and release in the PVN were assessed before and during the course of food consumption in rats trained to eat daily only for 4 h. Only in the PVN were NPY concentrations elevated before the introduction of food and, thereafter, levels decreased significantly during the course ofeating. A similar temporal pattern in NPY release into the PVN interstitium was evident in samples collected by push-pull cannula perfusion in unrestrained rats. In addition, in food-deprived rats displaying a robust drive for feeding, NPY release in the PVN was also markedly enhanced in the shape of high-amplitude secretory episodes as compared to a lower release rate in rats receiving food ad libitum. The higher rate of NPY release in fasted rats returned to the control range after 24 h of ad libitum food supply. These rmdings of intense and dynamic NPY neurosecretory activity within a discrete hypothalamic site in association with an increased drive for food consumption demonstrate that NPY release in the PVN is an important orexigenic signal for periodic eating behavior. These results have important global implications for elucidating the underlying causes of the pathophysiology of eating disorders-anorexia nervosa, bulimia, and obesity-as well as constituting a specific contextual model for the formulation and testing of suitable NPY receptor agonists and antagonists for therapeutic intervention.Neural circuits that integrate metabolic, neural, and hormonal signals leading to intermittent motivation to eat reside in the hypothalamus. There is now a consensus that stimulation of hunger or appetite for food is encoded in a few specific signals in the hypothalamus. Among peptides and amines that stimulate feeding, neuropeptide Y (NPY) is found to be the most potent enhancer of consummatory behavior in a large number of species (1-4). NPY is produced in the arcuate nucleus (ARC) ofthe hypothalamus and other regions of the brain, including discrete cell groups in the brainstem. The fiber systems from the ARC and brainstem project into various hypothalamic sites previously implicated in regulation of feeding behavior (5-8). In fact, not only administration into the cerebroventricular system (3, 9, 10) but microinjection of NPY into various hypothalamic sites (11-13) rapidly elicited robust feeding responses in rats. Continuous NPY infusion into the third cerebroventricle evoked continuous episodic feeding during the infusion and postinfusion intervals (14). Multiple daily injections of NPY into the paraventricular nucleus (PVN) of the...

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Effect of neuropeptide Y on ingestive behaviors in the rat

Cited by 132 publications

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Receptor subtypes Y₁ and Y₅ mediate neuropeptide Y induced feeding in the guinea‐pig

Receptor subtypes Y₁ and Y₅ mediate neuropeptide Y induced feeding in the guinea‐pig

Inhibitory effects of central neuropeptide Y on the somatotropic and gonadotropic axes in male rats are independent of adrenal hormones

Neuropeptide Y secretion increases in the paraventricular nucleus in association with increased appetite for food.

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Effect of neuropeptide Y on ingestive behaviors in the rat

Cited by 132 publications

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Receptor subtypes Y1 and Y5 mediate neuropeptide Y induced feeding in the guinea‐pig

Receptor subtypes Y1 and Y5 mediate neuropeptide Y induced feeding in the guinea‐pig

Inhibitory effects of central neuropeptide Y on the somatotropic and gonadotropic axes in male rats are independent of adrenal hormones

Neuropeptide Y secretion increases in the paraventricular nucleus in association with increased appetite for food.

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Receptor subtypes Y₁ and Y₅ mediate neuropeptide Y induced feeding in the guinea‐pig

Receptor subtypes Y₁ and Y₅ mediate neuropeptide Y induced feeding in the guinea‐pig