Neuropeptide Y increases food intake in 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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Effect of fourth ventricular neuropeptide Y and peptide YY on ingestive and other behaviors

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1990.259.2.r317 ◽

1990 ◽

Vol 259 (2) ◽

pp. R317-R323 ◽

Cited By ~ 13

Author(s):

E. S. Corp ◽

L. D. Melville ◽

D. Greenberg ◽

J. Gibbs ◽

G. P. Smith

Keyword(s):

Food Intake ◽

Neuropeptide Y ◽

Water Intake ◽

Fourth Ventricle ◽

Peptide Yy ◽

Direct Action ◽

Exploratory Activity ◽

Intracerebroventricular Administration ◽

Neural Substrate ◽

Related Increase

We studied the effect of fourth intracerebroventricular administration of neuropeptide Y (NPY) and peptide YY (PYY) on ingestive and other behaviors in awake nondeprived rats. Injection of NPY or PYY into the fourth ventricle produced a significant dose-related increase in food intake and reduction in the latency to eat. PYY was more potent than NPY in increasing food intake and decreasing latency to eat, suggesting that PYY-preferring receptors sensitive to the orexigenic effects of NPY and PYY exist in the hindbrain. In addition, both peptides increased water intake when food was present but not when food was absent, suggesting that a neural substrate supporting a direct action of NPY and PYY on water intake is not present in the hindbrain. In time sampling of behaviors occurring during a 90-min feeding test, we found that both peptides increased the time spent eating and reduced grooming. In addition PYY, but not NPY, reduced apparent sleep and increased exploratory activity. This suggests that PYY, but not NPY, influences a hindbrain neural substrate involved in sleep and activity.

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A potent neuropeptide Y antagonist, 1229U91, suppressed spontaneous food intake in Zucker fatty rats

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1998.274.5.r1500 ◽

1998 ◽

Vol 274 (5) ◽

pp. R1500-R1504 ◽

Cited By ~ 3

Author(s):

A. Ishihara ◽

T. Tanaka ◽

A. Kanatani ◽

T. Fukami ◽

M. Ihara ◽

...

Keyword(s):

Food Intake ◽

Neuropeptide Y ◽

Feeding Behavior ◽

Physiological Role ◽

Abnormal Behavior ◽

Zucker Rats ◽

Intracerebroventricular Administration ◽

Feeding Suppression ◽

Npy Antagonist

Neuropeptide Y (NPY) is one of the most potent orexigenic substances known. 1229U91 was found to be a potent and selective NPY antagonist. To elucidate a physiological role of NPY in hyperphagia in obese animals, we studied the effect of 1229U91 on spontaneous food intake in obese and lean Zucker rats. The food intake of Zucker rats was suppressed by intracerebroventricular administration of 1229U91 more potently in obese than in lean animals without abnormal behavior (31.7 and 67.3% inhibition at doses of 10 and 30 μg, respectively, in Zucker fatty rats and 22.2% inhibition at 30 μg in lean rats). This compound markedly suppressed NPY-induced food intake at 30 μg but did not affect galanin-induced food intake, suggesting that the feeding suppression seen in Zucker fatty and lean rats is pharmacologically and behaviorally specific. These results suggest that NPY is involved in feeding behavior in Zucker fatty rats and that NPY contributes to feeding to a greater degree in Zucker fatty than in lean rats. The hyperphagia in Zucker fatty rats may be due to the abnormal overactivation of the NPYergic system.

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Adiposity and plane of nutrition influence reproductive neuroendocrine and appetite responses to intracerebroventricular insulin and neuropeptide-Y in sheep

Reproduction Fertility and Development ◽

10.1071/rd10150 ◽

2011 ◽

Vol 23 (2) ◽

pp. 329 ◽

Cited By ~ 6

Author(s):

D. W. Miller ◽

E. J. Bennett ◽

J. L. Harrison ◽

P. A. Findlay ◽

C. L. Adam

Keyword(s):

Food Intake ◽

Nutritional Status ◽

Neuropeptide Y ◽

Intracerebroventricular Administration ◽

Short Term ◽

Neuroendocrine Responses ◽

Acute Changes ◽

Lh Secretion ◽

Voluntary Food Intake

Long-term nutritional background is thought to influence hypothalamic appetite and reproductive neuroendocrine responses to short-term nutritional feedback. In order to investigate this phenomenon, the effects of intracerebroventricular administration of insulin or neuropeptide-Y (NPY) on LH secretion and voluntary food intake (VFI) were examined in sheep that were initially thin and kept on an increasing nutritional plane (INP), or initially fat and kept on a decreasing nutritional plane (DNP), for 10 weeks. Intracerebroventricular insulin stimulated LH secretion and suppressed VFI in INP sheep when initially thin, but not when they became fat, and had no effect on LH in DNP sheep when initially fat, and stimulated LH secretion when they became thin. Intracerebroventricular NPY had no effect on LH or VFI in INP sheep when initially thin, decreased LH secretion and increased VFI when they became fat, and decreased LH secretion in DNP sheep when initially fat but had no effect when they became thin. Therefore, sensitivity to insulin increases with low or decreasing nutritional status and decreases with high or increasing nutritional status, whereas sensitivity to NPY increases with high or increasing nutritional status and decreases with low or decreasing nutritional status. In conclusion, reproductive neuroendocrine and appetite responses to acute changes in nutritional feedback signals depend on the individual’s longer-term nutritional background.

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Postnatal glucocorticoid exposure alters the adult phenotype

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.00349.2003 ◽

2004 ◽

Vol 287 (1) ◽

pp. R198-R208 ◽

Cited By ~ 22

Author(s):

Jing He ◽

Amit Varma ◽

Lisa A. Weissfeld ◽

Sherin U. Devaskar

Keyword(s):

Body Weight ◽

Weight Gain ◽

Food Intake ◽

Neuropeptide Y ◽

Water Intake ◽

Glucose Transporter ◽

Body Weight Gain ◽

Adult Males ◽

Subsequent Increase ◽

Males And Females

We examined the effect of six doses of dexamethasone (Dex) administered daily (2–7 days of age) to postnatal rats on body weight gain, food and water intake, peripheral hormonal/metabolic milieu, and hypothalamic neuropeptides that regulate food intake. We observed a Dex-induced acute (3 days of age) suppression of endogenous corticosterone and an increase in circulating leptin concentrations that were associated with a decrease in body weight in males and females. Followup during the suckling, postsuckling, and adult stages (7–120 days of age) revealed hypoleptinemia in males and females, and hypoinsulinemia, a relative increase in the glucose-to-insulin ratio, and a larger increase in skeletal muscle glucose transporter (GLUT 4) concentrations predominantly in the males, reflective of a catabolic state associated with a persistent decrease in body weight gain. The increase in the glucose-to-insulin ratio and hyperglycemia was associated with an increase in water intake. In addition, the changes in the hormonal/metabolic milieu were associated with an increase in hypothalamic neuropeptide Y content in males and females during the suckling phase, which persisted only in the 120-day-old female with a transient postnatal decline in α-melanocyte-stimulating hormone and corticotropin-releasing factor. This increase in neuropeptide Y (NPY) during the suckling phase in males and females was associated with a subsequent increase in adult food intake that outweighed the demands of body weight gain. In contrast to the adult hypothalamic findings, cerebral ventricular dilatation was more prominent in adult males. We conclude that postnatal Dex treatment causes permanent sex-specific changes in the adult phenotype, setting the stage for future development of diabetes (increased glucose:insulin ratio), obesity (increased NPY and food intake), and neurological impairment (loss of cerebral volume).

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Anti-Diabetic Activity of a Mineraloid Isolate, in vitro and in Genetically Diabetic Mice

International Journal for Vitamin and Nutrition Research ◽

10.1024/0300-9831/a000048 ◽

2011 ◽

Vol 81 (1) ◽

pp. 34-42 ◽

Cited By ~ 1

Author(s):

Joel Deneau ◽

Taufeeq Ahmed ◽

Roger Blotsky ◽

Krzysztof Bojanowski

Keyword(s):

Dna Microarrays ◽

Human Fibroblasts ◽

Diabetic Animal ◽

In Vitro Tests ◽

Diabetic Mice ◽

Fossil Material ◽

Expression Of Genes ◽

Enhanced Expression ◽

Genetically Diabetic Mice

Type II diabetes is a metabolic disease mediated through multiple molecular pathways. Here, we report anti-diabetic effect of a standardized isolate from a fossil material - a mineraloid leonardite - in in vitro tests and in genetically diabetic mice. The mineraloid isolate stimulated mitochondrial metabolism in human fibroblasts and this stimulation correlated with enhanced expression of genes coding for mitochondrial proteins such as ATP synthases and ribosomal protein precursors, as measured by DNA microarrays. In the diabetic animal model, consumption of the Totala isolate resulted in decreased weight gain, blood glucose, and glycated hemoglobin. To our best knowledge, this is the first description ever of a fossil material having anti-diabetic activity in pre-clinical models.

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