Effects of neuropeptide Y on ingestion of flavored solutions in nondeprived rats

Lynch, Wesley C.; Grace, Martha K.; Billington, Charles J.; Levine, Allen S.

doi:10.1016/0031-9384(93)90295-q

Cited by 42 publications

(32 citation statements)

References 9 publications

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“…The bases for these discrepancies are unclear; however, it is worth noting that studies reporting a CTA after ICV NPY used a larger dose (9.5 g) and a bitter taste stimulus (unsweetened Kool-Aid; Sipols et al, 1992). Indeed, when sweetened Kool-Aid was used as a conditioned stimulus, rats formed a conditioned preference for it after exposure to NPY (Lynch et al, 1993). Overall, it is clear that NPY affected burst initiation processes (engaging the spout), as the number of bursts in sucrose meals was roughly quadrupled by NPY.…”

Section: Measures Of Gustatory Evaluationmentioning

confidence: 99%

Effects of neuropeptide Y on feeding microstructure: Dissociation of appetitive and consummatory actions.

Baird

Gray

Fischer

2006

Behavioral Neuroscience

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The effects of intracerebroventricular application of Neuropeptide Y (NPY) on licking microstructure for sucrose, saccharin, and water solutions were evaluated. In Experiment 1, NPY increased meal size for three sucrose concentrations (0.03 M, 0.3 M, and 1.0 M) by increasing licking burst number but not size and by extending meals more than four-fold in duration with a slow, sustained rate of ingestion in late phases of the meal. Results are consistent with the interpretation that NPY suppressed inhibitory postingestive feedback. Experiment 2 supported this conclusion. NPY significantly increased the number of meals initiated for water, 0.1% saccharin, and 1.0 M sucrose solutions, but meal size was only increased for 1.0 M sucrose. Therefore, NPY also increased appetitive feeding behaviors, but its consummatory effects were limited to caloric solutions. The results are discussed with regard to their potential to explain current discrepancies in the literature.

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Section: Measures Of Gustatory Evaluationmentioning

confidence: 99%

Effects of neuropeptide Y on feeding microstructure: Dissociation of appetitive and consummatory actions.

Baird

Gray

Fischer

2006

Behavioral Neuroscience

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“…This is supported by an experiment where different solutions either sweetened with sucrose or saccharin were tested in fully sated rats. NPY increased the intake of the different sucrose solutions (2-10%) as well as the preferred saccharin solution (Lynch et al 1993). Orosensory mechanisms might therefore play a role on the stimulatory effects of NPY on carbohydrate intake.…”

Section: Npy and Normal Feeding Behaviourmentioning

confidence: 99%

Neuropeptide Y in normal eating and in genetic and dietary-induced obesity

Beck

2006

Phil. Trans. R. Soc. B

208

129

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Neuropeptide Y (NPY) is one the most potent orexigenic peptides found in the brain. It stimulates food intake with a preferential effect on carbohydrate intake. It decreases latency to eat, increases motivation to eat and delays satiety by augmenting meal size. The effects on feeding are mediated through at least two receptors, the Y1 and Y5 receptors. The NPY system for feeding regulation is mostly located in the hypothalamus. It is formed of the arcuate nucleus (ARC), where the peptide is synthesized, and the paraventricular (PVN), dorsomedial (DMN) and ventromedial (VMN) nuclei and perifornical area where it is active. This activity is modulated by the hindbrain and limbic structures. It is dependent on energy availability, e.g. upregulation with food deprivation or restriction, and return to baseline with refeeding. It is also sensitive to diet composition with variable effects of carbohydrates and fats. Leptin signalling and glucose sensing which are directly linked to diet type are the most important factors involved in its regulation. Absence of leptin signalling in obesity models due to gene mutation either at the receptor level, as in the Zucker rat, the Koletsky rat or the db/db mouse, or at the peptide level, as in ob/ob mouse, is associated with increased mRNA abundance, peptide content and/or release in the ARC or PVN. Other genetic obesity models, such as the Otsuka-Long-Evans-Tokushima Fatty rat, the agouti mouse or the tubby mouse, are characterized by a diminution in NPY expression in the ARC nucleus and by a significant increase in the DMN. Further studies are necessary to determine the exact role of NPY in these latter models. Long-term exposure to high-fat or high-energy palatable diets leads to the development of adiposity and is associated with a decrease in hypothalamic NPY content or expression, consistent with the existence of a counter-regulatory mechanism to diminish energy intake and limit obesity development. On the other hand, an overactive NPY system (increased mRNA expression in the ARC associated with an upregulation of the receptors) is characteristic of rats or rodent strains sensitive to dietary-induced obesity. Finally, NPY appears to play an important role in body weight and feeding regulation, and while it does not constitute the only target for drug treatment of obesity, it may nevertheless provide a useful target in conjunction with others.

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“…1A) or consumption of caloric, but less preferred, corn starch (35). Furthermore, NPY produces a conditioned preference for sweetened, but not for unsweetened, Kool-Aid solutions (49,70). Interestingly, neither forebrain nor hind-brain ICV NPY treatments increased meal size for the noncaloric tastant saccharin, although an increase in saccharin intake over 2-to 4-h periods in which multiple meals could be expressed has been reported (7,33,49).…”

Section: Effects Of Npy On Licking Microstructurementioning

confidence: 96%

“…Furthermore, NPY produces a conditioned preference for sweetened, but not for unsweetened, Kool-Aid solutions (49,70). Interestingly, neither forebrain nor hind-brain ICV NPY treatments increased meal size for the noncaloric tastant saccharin, although an increase in saccharin intake over 2-to 4-h periods in which multiple meals could be expressed has been reported (7,33,49). Saccharin was preferred over water in this study and in our laboratory's previous study, over 0.03 M sucrose, suggesting that the effects of NPY on meal size also covary with the postingestive cues provided by ingesta (Ref.…”

Section: Effects Of Npy On Licking Microstructurementioning

confidence: 97%

Effects of hindbrain melanin-concentrating hormone and neuropeptide Y administration on licking for water, saccharin, and sucrose solutions.

et al. 2007

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Effects of neuropeptide Y on ingestion of flavored solutions in nondeprived rats

Cited by 42 publications

References 9 publications

Effects of neuropeptide Y on feeding microstructure: Dissociation of appetitive and consummatory actions.

Effects of neuropeptide Y on feeding microstructure: Dissociation of appetitive and consummatory actions.

Neuropeptide Y in normal eating and in genetic and dietary-induced obesity

Effects of hindbrain melanin-concentrating hormone and neuropeptide Y administration on licking for water, saccharin, and sucrose solutions.

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