Neuropeptide Y is associated with changes in appetite-associated hypothalamic nuclei but not food intake in a hypophagic avian model

2013 ◽  
Vol 236 ◽  
pp. 327-331 ◽  
Author(s):  
Brandon A. Newmyer ◽  
Wint Nandar ◽  
Rebekah I. Webster ◽  
Elizabeth Gilbert ◽  
Paul B. Siegel ◽  
...  
Keyword(s):  
Food Intake ◽  
Neuropeptide Y ◽  
Hypothalamic Nuclei

scholarly journals Hypothalamic Expression of Neuropeptide Y (NPY) and Pro-OpioMelanoCortin (POMC) in Adult Male Mice Is Affected by Chronic Exposure to Endocrine Disruptors

Metabolites ◽  
2021 ◽  
Vol 11 (6) ◽  
pp. 368
Author(s):  
Marilena Marraudino ◽  
Elisabetta Bo ◽  
Elisabetta Carlini ◽  
Alice Farinetti ◽  
Giovanna Ponti ◽  
...  
Keyword(s):  
Food Intake ◽  
Energy Expenditure ◽  
Neuropeptide Y ◽  
Adult Male ◽  
Endocrine Disrupting Chemicals ◽  
Endocrine System ◽  
Male Mice ◽  
Hypothalamic Nuclei ◽  
Short Term Exposure ◽  
Control Food Intake

In the arcuate nucleus, neuropeptide Y (NPY) neurons, increase food intake and decrease energy expenditure, and control the activity of pro-opiomelanocortin (POMC) neurons, that decrease food intake and increase energy expenditure. Both systems project to other hypothalamic nuclei such as the paraventricular and dorsomedial hypothalamic nuclei. Endocrine disrupting chemicals (EDCs) are environmental contaminants that alter the endocrine system causing adverse health effects in an intact organism or its progeny. We investigated the effects of long-term exposure to some EDCs on the hypothalamic NPY and POMC systems of adult male mice that had been previously demonstrated to be a target of some of these EDCs after short-term exposure. Animals were chronically fed for four months with a phytoestrogen-free diet containing two different concentrations of bisphenol A, diethylstilbestrol, tributyltin, or E2. At the end, brains were processed for NPY and POMC immunohistochemistry and quantitatively analyzed. In the arcuate and dorsomedial nuclei, both NPY and POMC immunoreactivity showed a statistically significant decrease. In the paraventricular nucleus, only the NPY system was affected, while the POMC system was not affected. Finally, in the VMH the NPY system was affected whereas no POMC immunoreactive material was observed. These results indicate that adult exposure to different EDCs may alter the hypothalamic circuits that control food intake and energy metabolism.

Neuropeptide Y fails to increase intraoral intake in rats

1995 ◽  
Vol 268 (2) ◽  
pp. R423-R427 ◽  
Author(s):  
R. J. Seeley ◽  
C. J. Payne ◽  
S. C. Woods
Keyword(s):  
Food Intake ◽  
Oral Cavity ◽  
Neuropeptide Y ◽  
Food Deprivation ◽  
Sucrose Solution ◽  
Third Ventricle ◽  
Saline Control ◽  
The Third ◽  
Hypothalamic Nuclei ◽  
Control Food

Neuropeptide Y (NPY) has a potent orexigenic effect when administered either into the third ventricle or directly into hypothalamic nuclei, but the mechanism by which NPY increases intakes is poorly understood. The present study tested the ability of NPY to increase intake of the rat in the intraoral intake test, which focuses on the highly stereotyped consummatory phase of ingestion by introducing a 0.1 M sucrose solution directly into the oral cavity of rats via indwelling intraoral cannulas. Doses of 3, 9.5, and 30 micrograms of NPY, when administered into the third ventricle, all failed to change intraoral intake compared with a saline control. Food deprivation (24 h), however, nearly doubled intraoral intake. Additionally, in separate experiments, 9.5 micrograms of NPY significantly increased both 1-h food intake and 1-h bottle intake of 0.1 M sucrose. These results are consistent with two conclusions. 1) NPY does not affect the consummatory phase of ingestion. 2) NPY administration does not completely mimic the stimulus state associated with food deprivation, since food deprivation but not NPY administration increases intake in the intraoral intake test.

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

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

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

Endocrinology ◽  
2002 ◽  
Vol 143 (12) ◽  
pp. 4513-4519 ◽  
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.

Regulation of food intake by neuropeptide Y in goldfish

2000 ◽  
Vol 279 (3) ◽  
pp. R1025-R1034 ◽  
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.

Neuropeptide Y increases food intake in mice

1987 ◽  
Vol 253 (3) ◽  
pp. R516-R522 ◽  
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.

scholarly journals Adiponectin receptors are expressed in hypothalamus and colocalized with proopiomelanocortin and neuropeptide Y in rodent arcuate neurons

2008 ◽  
Vol 200 (1) ◽  
pp. 93-105 ◽  
Author(s):  
E Guillod-Maximin ◽  
A F Roy ◽  
C M Vacher ◽  
A Aubourg ◽  
V Bailleux ◽  
...  
Keyword(s):  
Neuropeptide Y ◽  
Energy Homeostasis ◽  
Fluorescent Protein ◽  
Peripheral Tissues ◽  
Rat Hypothalamus ◽  
Ampk Phosphorylation ◽  
Hypothalamic Nuclei ◽  
Green Fluorescent ◽  
Amp Activated Protein Kinase

Adiponectin is involved in the control of energy homeostasis in peripheral tissues through Adipor1 and Adipor2 receptors. An increasing amount of evidence suggests that this adipocyte-secreted hormone may also act at the hypothalamic level to control energy homeostasis. In the present study, we observed the gene and protein expressions of Adipor1 and Adipor2 in rat hypothalamus using different approaches. By immunohistochemistry, Adipor1 expression was ubiquitous in the rat brain. By contrast, Adipor2 expression was more limited to specific brain areas such as hypothalamus, cortex, and hippocampus. In arcuate and paraventricular hypothalamic nuclei, Adipor1, and Adipor2 were expressed by neurons and astrocytes. Furthermore, using transgenic green fluorescent protein mice, we showed that Adipor1 and Adipor2 were present in pro–opiomelanocortin (POMC) and neuropeptide Y (NPY) neurons in the arcuate nucleus. Finally, adiponectin treatment by intracerebroventricular injection induced AMP-activated protein kinase (AMPK) phosphorylation in the rat hypothalamus. This was confirmed byin vitrostudies using hypothalamic membrane fractions. In conclusion, Adipor1 and Adipor2 are both expressed by neurons (including POMC and NPY neurons) and astrocytes in the rat hypothalamic nuclei. Adiponectin is able to increase AMPK phosphorylation in the rat hypothalamus. These data reinforced a potential role of adiponectin and its hypothalamic receptors in the control of energy homeostasis.

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

1997 ◽  
Vol 34 (1) ◽  
pp. 58-62
Author(s):  
Y.-H. CHOI ◽  
N. OHNO ◽  
J. OKUMURA ◽  
D. M. DENBOW ◽  
M. FURUSE
Keyword(s):  
Food Intake ◽  
Neuropeptide Y ◽  
Intracerebroventricular Injection
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