Peptide YY (PYY) is a gut hormone that plays a key role in regulating appetite and digestion, particularly in promoting satiety (the feeling of fullness) after eating.
Overview of Peptide YY (PYY)
1. Origin:
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Secreted primarily by L-cells in the ileum and colon (distal small intestine and large intestine).
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Released in response to food intake, especially fat and protein.
2. Forms:
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Exists mainly in two forms: PYY1-36 and PYY3-36.
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PYY3-36 is the major circulating form and is the one most involved in appetite suppression.
Key Functions
| Function | Description |
|---|---|
| Appetite suppression | PYY3-36 acts on the hypothalamus (especially the Y2 receptor in the arcuate nucleus) to reduce hunger. |
| Slows gastric emptying | Helps prolong digestion and nutrient absorption. |
| Reduces intestinal motility | Allows more time for nutrient absorption in the intestines. |
Clinical Relevance
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Obesity: People with obesity often have lower PYY responses after meals, which may contribute to impaired satiety and overeating.
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Post-bariatric surgery: Procedures like gastric bypass increase PYY secretion, which contributes to reduced appetite and sustained weight loss.
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Therapeutic interest: PYY analogs have been explored as potential treatments for obesity, but so far, no approved drugs are on the market.
Interaction with Other Hormones
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Works synergistically with GLP-1 and cholecystokinin (CCK) to suppress appetite.
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Released later in a meal, contributing to longer-lasting satiety compared to fast-acting hormones like ghrelin (which increases hunger before meals).
A Comparison Of PYY To Other Gut Hormones Like Ghrelin or GLP-1 In Appetite Regulation
Comparison Table: Appetite-Regulating Gut Hormones
| Feature | Ghrelin 🟠 (Hunger Hormone) | GLP-1 🟢 (Satiety Hormone) | PYY 🔵 (Satiety Hormone) |
|---|---|---|---|
| Produced By | Stomach (fundus) | L-cells in ileum/colon | L-cells in ileum/colon |
| Secretion Trigger | Fasting / empty stomach | Nutrient intake (especially carbs & fats) | Nutrient intake (especially fats & proteins) |
| Peak Timing | Before meals | Shortly after eating | ~15–30 min after eating |
| Effect on Appetite | Increases hunger | Reduces hunger, slows gastric emptying | Reduces appetite, slows gut motility |
| Brain Target | Hypothalamus (activates NPY/AgRP neurons) | Hypothalamus (activates POMC neurons) | Hypothalamus (Y2 receptor on NPY neurons) |
| Duration of Effect | Short (drops quickly after eating) | Moderate (~several hours) | Moderate to long-lasting |
| Drug Target? | No approved ghrelin blockers | Yes – GLP-1 receptor agonists | Under study – PYY analogs in development |
| Obesity Link | Often elevated in weight loss (drives regain) | Often blunted response in obesity | Often lower PYY levels in obesity |
🔸 Key Insights:
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Ghrelin is the only orexigenic (hunger-promoting) hormone among the three — it rises before meals and drops sharply afterward.
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GLP-1 and PYY are both anorexigenic (appetite-suppressing), released after eating, and promote satiety.
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GLP-1 acts more immediately post-meal and also helps with insulin secretion and glucose control, making it a major drug target.
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PYY acts a bit later and seems to play a stronger role in sustained satiety, especially after high-fat or high-protein meals.
Graphical Summary (Description)
If you imagine a timeline of a meal:
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Ghrelin spikes before you eat and crashes once you start eating.
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GLP-1 rises shortly after eating, giving an early satiety signal.
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PYY rises a bit later, helping sustain the feeling of fullness and reducing subsequent intake.
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