Neuropeptide Y paradoxically increases food intake yet causes conditioned flavor aversions

Sipols, Alfred J.; Brief, Deborah J.; Ginter, Kari L.; Saghafi, Saman; Woods, Stephen C.

doi:10.1016/0031-9384(92)90317-u

Cited by 31 publications

(20 citation statements)

References 20 publications

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“…Importantly, animals in negative energy balance have low levels of adiposity hormones, resulting in elevated NPY mRNA in the ARC. Local replacement of either insulin or leptin in the vicinity of the ARC normalizes the elevated NPY mRNA in the ARC of fasted animals (Schwartz et al, 1992;Sipols et al, 1992). Hence, the activity of these ARC NPY neurons is under the direct influence of at least two adiposity signals.…”

Section: A Anabolic Effector Systemsmentioning

confidence: 98%

Insulin and Leptin as Adiposity Signals

Benoit

Clegg

Seeley

et al. 2004

Recent Progress in Hormone Research

241

163

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There is now considerable consensus that the adipocyte hormone leptin and the pancreatic hormone insulin are important regulators of food intake and energy balance. Leptin and insulin fulfill many of the requirements to be putative adiposity signals to the brain. Plasma leptin and insulin levels are positively correlated with body weight and with adipose mass in particular. Furthermore, both leptin and insulin enter the brain from the plasma. The brain expresses both insulin and leptin receptors in areas important in the control of food intake and energy balance. Consistent with their roles as adiposity signals, exogenous leptin and insulin both reduce food intake when administered locally into the brain in a number of species under different experimental paradigms. Additionally, central administration of insulin antibodies increases food intake and body weight. Recent studies have demonstrated that both insulin and leptin have additive effects when administered simultaneously. Finally, we recently have demonstrated that leptin and insulin share downstream neuropeptide signaling pathways. Hence, insulin and leptin provide important negative feedback signals to the central nervous system, proportional to peripheral energy stores and coupled with catabolic circuits.

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Section: A Anabolic Effector Systemsmentioning

confidence: 98%

Insulin and Leptin as Adiposity Signals

Benoit

Clegg

Seeley

et al. 2004

Recent Progress in Hormone Research

241

163

View full text Add to dashboard Cite

show abstract

“…It has been reported that NPY causes CTA, pica, and suppression of need-induced sodium appetite (Madden et al, 1999;Sipols, Brief, Ginter, Saghafi, & Woods, 1992), but it seems unlikely that the NPY reduction of burst size at 1.0 M sucrose was due to a CTA, for several reasons. First, intake was not suppressed on test days following NPY injection (data not shown).…”

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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“…Although CFA and learned flavour aversion appear to measure the malaise producing potential of a stimulus, this is probably not always true. For example, intracerebroventricular infusions of neuropeptide Y produce robust increases in food intake in the rat, but also generate learned flavour aversions (Sipols et al, 1992), which suggests that the hunger stimulus can also produce conditioned flavour aversion.…”

Section: Conditioned Flavour Avoidance (Cfa)-manymentioning

confidence: 99%

Signals for nausea and emesis: Implications for models of upper gastrointestinal diseases

Andrews

Horn

2006

Autonomic Neuroscience

220

201

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Nausea and vomiting are amongst the most common symptoms encountered in medicine as either symptoms of diseases or side effects of treatments. In a more biological setting they are also important components of an organism's defences against ingested toxins. Identification of treatments for nausea and vomiting and reduction of emetic liability of new therapies has largely relied on the use of animal models, and although such models have proven invaluable in identification of the anti-emetic effects of both 5-hydroxytryptamine3 and neurokinin1 receptor antagonists selection of appropriate models is still a matter of debate. The present paper focuses on a number of controversial issues and gaps in our knowledge in the study of the physiology of nausea and vomiting including: The choice of species for the study of emesis and the underlying behavioural (e.g. neophobia), anatomical (e.g. elongated, narrow abdominal oesophagus with reduced ability to shorten) and physiological (e.g. brainstem circuitry) mechanisms that explain the lack of a vomiting reflex in certain species (e.g. rats); The choice of response to measure (emesis[retching and vomiting], conditioned flavour avoidance or aversion, ingestion of clay [pica], plasma hormone levels[e.g. vasopressin], gastric dysrhythmias) and the relationship of these responses to those observed in humans and especially to the sensation of nausea; The stimulus coding of nausea and emesis by abdominal visceral afferents and especially the vagus-how do the afferents encode information for normal postprandial sensations, nausea and finally vomiting?; Understanding the central processing of signals for nausea and vomiting is particularly problematic in the light of observations that vomiting is more readily amenable to pharmacological treatment than is nausea, despite the assumption that nausea represents "low" intensity activation of pathways that can evoke vomiting when stimulated more intensely.

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Neuropeptide Y paradoxically increases food intake yet causes conditioned flavor aversions

Cited by 31 publications

References 20 publications

Insulin and Leptin as Adiposity Signals

Insulin and Leptin as Adiposity Signals

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

Signals for nausea and emesis: Implications for models of upper gastrointestinal diseases

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