Effects of Intracerebroventricular Injection of Clonidine and Neuropeptide Y on Food Intake in the Chicken.

Many studies have indicated that neuropeptide Y (NPY) stimulates and leptin inhibits food intake. In line with this, intracerebroventricular injection of NPY (10 μg) stimulated and leptin (10 μg) inhibited intake of a sucrose solution when female rats were required to obtain the solution from a bottle. However, NPY inhibited and leptin stimulated intake if the solution was infused intraorally. Thus NPY stimulates the responses used to obtain food but inhibits those used to consume food, and leptin has the opposite effects. To test the specificity of these responses the sexual behavior of male rats was examined. NPY-treated males showed minor deficits in sexual behavior but chose to ingest a sucrose solution rather than copulate with a female if offered the choice. By contrast, leptin-treated males ingested little sucrose and displayed an increase in ejaculatory frequency if given the same choice. It is suggested that NPY is not merely an orexigenic peptide, but one that directs attention toward food. Similarly, leptin may not be an anorexic peptide, but one that diverts attention away from food toward alternate stimuli.

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Influence of fasting and neuropeptide Y on the suppressive food intake induced by intracerebroventricular injection of glucagon-like peptide-1 in the neonatal chick

Brain Research ◽

10.1016/s0006-8993(97)00623-9 ◽

1997 ◽

Vol 764 (1-2) ◽

pp. 289-292 ◽

Cited By ~ 55

Author(s):

Mitsuhiro Furuse ◽

Megumi Matsumoto ◽

Ryoichi Mori ◽

Kunio Sugahara ◽

Koichiro Kano ◽

...

Keyword(s):

Food Intake ◽

Neuropeptide Y ◽

Intracerebroventricular Injection ◽

Neonatal Chick ◽

Glucagon Like Peptide ◽

Glucagon Like Peptide 1

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Faculty Opinions recommendation of Role of dorsomedial hypothalamic neuropeptide Y in modulating food intake and energy balance.

Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature ◽

10.3410/f.1147100.604223 ◽

2009 ◽

Author(s):

Julian Mercer

Keyword(s):

Energy Balance ◽

Food Intake ◽

Neuropeptide Y

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The effect of phlorizin treatment on food intake and hypothalamic neuropeptide Y in normal and diabetic rats

Regulatory Peptides ◽

10.1016/0167-0115(91)90094-w ◽

1991 ◽

Vol 35 (3) ◽

pp. 227

Author(s):

M Bose ◽

J.P.H. Wilding ◽

P.D. Lambert ◽

N Aslam ◽

M.A. Ghatei ◽

...

Keyword(s):

Food Intake ◽

Neuropeptide Y ◽

Diabetic Rats

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Neuropeptide Y1 and Y5 Receptors Mediate the Effects of Neuropeptide Y on the Hypothalamic-Pituitary-Thyroid Axis

Endocrinology ◽

10.1210/en.2002-220574 ◽

2002 ◽

Vol 143 (12) ◽

pp. 4513-4519 ◽

Cited By ~ 56

Author(s):

Csaba Fekete ◽

Sumit Sarkar ◽

William M. Rand ◽

John W. Harney ◽

Charles H. Emerson ◽

...

Keyword(s):

Thyroid Hormone ◽

Food Intake ◽

Neuropeptide Y ◽

Paraventricular Nucleus ◽

Receptor Agonist ◽

Pituitary Thyroid Axis ◽

Thyroid Axis ◽

Ad Libitum ◽

Thyroid Hormone Levels ◽

Hpt Axis

Abstract Neuropeptide Y (NPY) is one of the most important hypothalamic-derived neuropeptides mediating the effects of leptin on energy homeostasis. Central administration of NPY not only markedly stimulates food intake, but simultaneously inhibits the hypothalamic-pituitary-thyroid axis (HPT axis), replicating the central hypothyroid state associated with fasting. To identify the specific NPY receptor subtypes involved in the action of NPY on the HPT axis, we studied the effects of the highly selective Y1 ([Phe7,Pro34]pNPY) and Y5 ([chicken pancreatic polypeptide1–7, NPY19–23, Ala31, Aib32 (aminoisobutyric acid), Q34]human pancreatic polypeptide) receptor agonists on circulating thyroid hormone levels and proTRH mRNA in hypophysiotropic neurons of the hypothalamic paraventricular nucleus. The peptides were administered continuously by osmotic minipump into the cerebrospinal fluid (CSF) over 3 d in ad libitum-fed animals and animals pair-fed to artificial CSF (aCSF)-infused controls. Both Y1 and Y5 receptor agonists nearly doubled food intake compared with that of control animals receiving aCSF, similar to the effect observed for NPY. NPY, Y1, and Y5 receptor agonist administration suppressed circulating levels of thyroid hormones (T3 and T4) and resulted in inappropriately normal or low TSH levels. These alterations were also associated with significant suppression of proTRH mRNA in the paraventricular nucleus, particularly in the Y1 receptor agonist-infused group [aCSF, NPY, Y1, and Y5 (density units ± sem), 97.2 ± 8.6, 39.6 ± 8.4, 19.9 ± 1.9, and 44.6 ± 8.4]. No significant differences in thyroid hormone levels, TSH, or proTRH mRNA were observed between the agonist-infused FSanimals eating ad libitum and the agonist-infused animals pair-fed with vehicle-treated controls. These data confirm the importance of both Y1 and Y5 receptors in the NPY-mediated increase in food consumption and demonstrate that both Y1 and Y5 receptors can mediate the inhibitory effects of NPY on the HPT axis.

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Hindbrain glucagon-like peptide-1 neurons track intake volume and contribute to injection stress-induced hypophagia in meal-entrained rats

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.00243.2015 ◽

2016 ◽

Vol 310 (10) ◽

pp. R906-R916 ◽

Cited By ~ 9

Author(s):

Alison D. Kreisler ◽

Linda Rinaman

Keyword(s):

Food Intake ◽

Potential Role ◽

Liquid Diet ◽

Neural Activation ◽

Intracerebroventricular Injection ◽

Glucagon Like Peptide ◽

Glucagon Like Peptide 1 ◽

Diet Intake ◽

Published Research ◽

Diet Type

Published research supports a role for central glucagon-like peptide 1 (GLP-1) signaling in suppressing food intake in rodent species. However, it is unclear whether GLP-1 neurons track food intake and contribute to satiety, and/or whether GLP-1 signaling contributes to stress-induced hypophagia. To examine whether GLP-1 neurons track intake volume, rats were trained to consume liquid diet (LD) for 1 h daily until baseline intake stabilized. On test day, schedule-fed rats consumed unrestricted or limited volumes of LD or unrestricted volumes of diluted (calorically matched to LD) or undiluted Ensure. Rats were perfused after the test meal, and brains processed for immunolocalization of cFos and GLP-1. The large majority of GLP-1 neurons expressed cFos in rats that consumed satiating volumes, regardless of diet type, with GLP-1 activation proportional to intake volume. Since GLP-1 signaling may limit intake only when such large proportions of GLP-1 neurons are activated, a second experiment examined the effect of central GLP-1 receptor (R) antagonism on 2 h intake in schedule-fed rats. Compared with baseline, intracerebroventricular vehicle (saline) suppressed Ensure intake by ∼11%. Conversely, intracerebroventricular injection of vehicle containing GLP-1R antagonist increased intake by ∼14% compared with baseline, partly due to larger second meals. We conclude that GLP-1 neural activation effectively tracks liquid diet intake, that intracerebroventricular injection suppresses intake, and that central GLP-1 signaling contributes to this hypophagic effect. GLP-1 signaling also may contribute to satiety after large volumes have been consumed, but this potential role is difficult to separate from a role in the hypophagic response to intracerebroventricular injection.

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Regulation of food intake by neuropeptide Y in goldfish

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.2000.279.3.r1025 ◽

2000 ◽

Vol 279 (3) ◽

pp. R1025-R1034 ◽

Cited By ~ 115

Author(s):

Yuwaraj K. Narnaware ◽

Pierre P. Peyon ◽

Xinwei Lin ◽

Richard E. Peter

Keyword(s):

Food Intake ◽

Neuropeptide Y ◽

Mrna Levels ◽

Food Ration ◽

Y1 Receptor ◽

Daily Food ◽

Daily Food Ration ◽

Brain Ventricle ◽

Dose Dependent Increase ◽

Dose Dependent

In mammals, neuropeptide Y (NPY) is a potent orexigenic factor. In the present study, third brain ventricle (intracerebroventricular) injection of goldfish NPY (gNPY) caused a dose-dependent increase in food intake in goldfish, and intracerebroventricular administration of NPY Y1-receptor antagonist BIBP-3226 decreased food intake; the actions of gNPY were blocked by simultaneous injection of BIBP-3226. Goldfish maintained on a daily scheduled feeding regimen display an increase in NPY mRNA levels in the telencephalon-preoptic area and hypothalamus shortly before feeding; however, a decrease occured in optic tectum-thalamus. In both fed and unfed fish, brain NPY mRNA levels decreased after scheduled feeding. Restriction in daily food ration intake for 1 wk or food deprivation for 72 h resulted in increased brain NPY mRNA levels. Results from these studies demonstrate that NPY is a physiological brain signal involved in feeding behavior in goldfish, mediating its effects, at least in part, through Y1-like receptors in the brain.

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Neuropeptide Y increases food intake in mice

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1987.253.3.r516 ◽

1987 ◽

Vol 253 (3) ◽

pp. R516-R522 ◽

Cited By ~ 8

Author(s):

J. E. Morley ◽

E. N. Hernandez ◽

J. F. Flood

Keyword(s):

Food Intake ◽

Neuropeptide Y ◽

Water Intake ◽

Free Acid ◽

Behavioral Analysis ◽

Intracerebroventricular Administration ◽

Diabetic Mice ◽

Number Of Species ◽

Genetically Diabetic Mice ◽

Old Mice

Neuropeptide Y (NPY) stimulates eating in a number of species. In the studies reported here, intracerebroventricular administration of porcine NPY increased eating in mice. In the presence of food, NPY caused enhancement of water intake, whereas in the absence of food, NPY suppressed water intake. Behavioral analysis showed that NPY decreased the latency to eat, increased the time spent eating, and decreased grooming. Human NPY also increased food intake, whereas the free acid of NPY was inactive. Although some minor discrepancies in response were noted overall, NPY was as effective at stimulating food intake in genetically obese (ob/ob) mice compared with their lean littermates (ob/-), in genetically diabetic mice (db/db) and their nondiabetic heterozygote control (db/m), in streptozocin-induced diabetic mice and their controls, and in adult (8 mo old) compared with old (25 mo old) mice.

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