Research
Hormonal
The orexigenic effects of Neuropeptide Y are mediated primarily through Y1 and Y5 receptors, with Y1 playing a dominant role in appetitive behavior and Y5 in consummatory behavior.
The brain uses specific receptors (Y1 and Y5) to process hunger signals from Neuropeptide Y. Blocking these receptors can inhibit the hunger-stimulating effects of NPY.
GoodSupportsHIGH confidence
The effects on feeding are mediated through at least two receptors, the Y1 and Y5 receptors... The effects of selective receptor agonists suggest that the Y5 receptor might mediate the consummatory behaviour, whereas the appetitive behaviour might be more related to the Y1 receptor
Why this rating
Supported by multiple studies using agonists, antagonists, and knockout mice, though some conflicting data on Y5 knockout exists.
Source
Neuropeptide Y in normal eating and in genetic and dietary-induced obesity
Bernard Beck · Philosophical Transactions of the Royal Society B Biological Sciences · 2006
DOI 10.1098/rstb.2006.1855
narrative_reviewCited 278×
Read the paper DOI resolved against Crossref · corpus check 2026-06-10
More from this paper
- Central administration of Neuropeptide Y (NPY) acts as a potent orexigenic signal that stimulates food intake, specifically increasing carbohydrate preference, reducing the latency to eat, and delaying satiety to augment meal size.Strong
- Fasting and energy restriction upregulate the NPY system (increasing mRNA and peptide content in the arcuate nucleus), while refeeding and high-fat/high-energy diets tend to downregulate or decrease NPY expression as a counter-regulatory mechanism.Strong
- Genetic obesity models with leptin signaling failure (e.g., Zucker rats, ob/ob mice) exhibit increased NPY mRNA and peptide levels, whereas other genetic obesity models (e.g., agouti, tubby mice) show decreased NPY in the arcuate nucleus but increased expression in the dorsomedial nucleus.Good
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