The Science of Appetite Control: How Hormones Regulate Hunger and Satiety

By Vijay Kumar MalesuReviewed by Benedette Cuffari, M.Sc.

Introduction
Hormonal control of appetite
Macronutrient effects on hormones
Fiber and gastric emptying
Human studies
Translational insights
References
Further reading

This article explains how dietary protein, carbohydrates, fats, and different types of fiber influence key appetite-regulating hormones, including GLP-1, PYY, ghrelin, CCK, and leptin. Drawing from controlled human trials and mechanistic research, it clarifies how nutrient composition affects satiety signaling, energy balance, and weight regulation through the gut–brain axis.

Image Credit: Rido / Shutterstock.com

Introduction

Appetite regulation refers to the complex physiological processes that control hunger, satiety, and energy balance through coordinated central and peripheral signals. These processes involve bidirectional communication between the gastrointestinal tract, adipose tissue, and central nervous system, particularly the hypothalamic arcuate nucleus and brainstem nuclei.^1,2,3 Appetite is regulated through both homeostatic mechanisms that maintain energy balance and hedonic pathways that integrate reward, memory, and environmental cues.^1,3  

Hormonal control of appetite

Hormonal control of appetite is regulated by a coordinated gut–brain axis that integrates peripheral hormonal signals with central neural circuits to regulate hunger and satiety.^1,3 Signals from the gastrointestinal tract are relayed via vagal afferents to the brainstem dorsal vagal complex, including the nucleus tractus solitarius, before interacting with hypothalamic nuclei.³

Glucagon-like peptide-1 (GLP-1) and peptide YY (PYY), both of which are secreted from enteroendocrine L-cells located primarily in the distal small intestine and colon, reduce hunger after eating food.³ GLP-1 delays gastric emptying, controls blood sugar levels, and reduces food intake by acting on appetite-regulating centers in the hypothalamus and brainstem.

Similarly, PYY supports satiety by inhibiting orexigenic neuropeptide Y neurons and activating anorexigenic pro-opiomelanocortin pathways.^2,3 In contrast, ghrelin is the primary peripheral hunger hormone that stimulates appetite by activating growth hormone secretagogue receptors in the hypothalamus, particularly within the arcuate nucleus.^2,3 Ghrelin concentrations typically rise preprandially and fall rapidly following food intake.²

Macronutrient effects on hormones

Protein

High-protein meals facilitate the release of GLP-1 and PYY, which reduce hunger; controlled feeding studies demonstrate that protein-rich meals produce higher, more sustained circulating levels of GLP-1 and PYY than isocaloric meals rich in fat or carbohydrates.⁴ However, despite these hormonal differences, ad libitum energy intake at a subsequent meal may not significantly differ when meals are matched for volume and calories.⁴ Simultaneously, increased dietary protein intake has been shown to suppress postprandial ghrelin concentrations in some studies, although total ghrelin suppression may not differ between macronutrients under tightly controlled conditions.⁴

Branched-chain amino acids such as leucine are proposed to contribute to satiety signaling, although much of the direct mechanistic evidence comes from experimental and translational models rather than large-scale human trials.^1,3

Carbohydrates

Foods with a high glycemic index cause a rapid spike in blood glucose and insulin levels, which may be associated with earlier hunger onset in some observational and experimental contexts. However, when carbohydrate-containing foods are consumed with substantial protein, measured meal glycemic index and glycemic load values may decrease due to protein-induced insulin responses and altered glucose kinetics.⁵ Comparatively, foods with a low glycemic index are digested and absorbed slowly, which prolongs satiety.

Dietary fiber, especially soluble or viscous fiber, helps control appetite by slowing digestion. Highly viscous fibers increase gastric distension and delay gastric emptying, thereby enhancing satiation and reducing subsequent intake in both animal and human models.⁷ Variations in results have been observed; however, viscous fiber typically improves fullness by reducing the rate of sugar absorption and metabolic responses.⁵

Fats

Dietary fat affects appetite control by stimulating the release of gut hormones, particularly cholecystokinin (CCK), in response to fat intake. Short-term feeding studies show that postprandial CCK concentrations may decrease during energy-restricted diets, independent of macronutrient distribution. In an eight-week randomized trial comparing low-carbohydrate and low-fat, low-energy diets, postprandial CCK decreased in both groups, suggesting that energy restriction, rather than dietary fat content per se, influenced CCK responses. Overall, the impact of dietary fat on appetite hormones can vary and depends on energy balance, diet composition, and metabolic state.⁶

Fiber and gastric emptying

Dietary fiber influences appetite regulation through both physical effects on digestion and metabolic responses following its fermentation in the large intestine. Viscous fibers increase the thickness of stomach contents, which leads to slower nutrient delivery to the small intestine, prolonged digestion, and increased satiety.⁷ By reducing the rate of glucose absorption and extending gastrointestinal transit time, viscous fibers contribute to earlier meal termination and sustained satiety.⁵

When fibers like resistant starch and beta-glucans are fermented by bacteria, they produce short-chain fatty acids (SCFAs). Fermentable fibers have been shown in animal models to alter GLP-1, PYY, ghrelin, and leptin concentrations; however, effects vary depending on fiber viscosity and fermentability, and findings do not uniformly support SCFA-driven increases in GLP-1 in all contexts.⁷

Human studies

Human studies on appetite regulation typically combine short-term feeding trials to measure hormonal responses, fullness, and weight changes.

In one randomized crossover trial, meals with the same caloric value but different macronutrient composition had different gut hormone responses. For example, high-protein meals increase GLP-1 and PYY levels compared with high-fat or high-carbohydrate meals, but these differences did not significantly reduce subsequent ad libitum energy intake under controlled laboratory conditions.⁴

In an 8-week randomized trial, both low-carbohydrate and low-fat diets led to weight loss. However, the low-carbohydrate diet was more effective, as it led to reduced postprandial ghrelin (total area under the curve) and increased subjective fullness ratings, while fasting ghrelin did not differ between groups.⁶

Translational insights

After food is consumed, GLP-1 and PYY are released, with their concentrations dependent on the calorie and nutrient content of the meal.^1,3 Peripheral adiposity signals such as leptin also interact with hypothalamic circuits to modulate long-term energy balance, although leptin resistance is common in obesity.²

Consuming a balanced diet rich in various nutrients is an effective way to simultaneously regulate multiple satiety hormones to support weight management. Whereas protein intake reduces hunger by increasing the release of GLP-1 and PYY and decreasing ghrelin levels, carbohydrates with high fiber content and a low glycemic index slow the rate of sugar absorption and digestion, enhancing satiety.

Fats stimulate the release of CCK to regulate food intake; however, these effects are determined by each individual’s metabolic rate. Fermentable fibers also control appetite through complex interactions involving viscosity, fermentability, and gut hormone modulation rather than SCFA production alone.⁷

References

1. Hong, S. & Choi, K. M. (2024). Gut hormones and appetite regulation. Current Opinion in Endocrinology & Diabetes and Obesity 31(3); 115-121. DOI: 10.1097/MED.0000000000000859. https://journals.lww.com/co-endocrinology/abstract/2024/06000/gut_hormones_and_appetite_regulation.4.aspx
2. Skoracka, K., Hryhorowicz, S., Schulz, P., et al. (2025). The role of leptin and ghrelin in the regulation of appetite in obesity. Peptides 186. DOI: 10.1016/j.peptides.2025.171367. https://www.sciencedirect.com/science/article/pii/S0196978125000282
3. De Silva, A. & Bloom, S. R. (2012). Gut hormones and appetite control: a focus on PYY and GLP-1 as therapeutic targets in obesity. Gut and Liver 6(1); 10-20. DOI: 10.5009/gnl.2012.6.1.10. https://www.gutnliver.org/journal/view.html?volume=6&number=1&spage=10&year=2012
4. van der Klaauw, A. A., Keogh, J. M., Henning, E., et al. (2013). High protein intake stimulates postprandial GLP1 and PYY release. Obesity 21(8); 1602-1607. DOI: 10.1002/oby.20154. https://onlinelibrary.wiley.com/doi/10.1002/oby.20154
5. Meng, H., Matthan, N. R., Ausman, L. M., & Lichtenstein, A. H. (2017). Effect of macronutrients and fiber on postprandial glycemic responses and meal glycemic index and glycemic load value determinations. The American Journal of Clinical Nutrition 105(4); 842-853. DOI: 10.3945/ajcn.116.144162. https://www.sciencedirect.com/science/article/pii/S0002916522048304
6. Lundanes, J., Storliløkken, G.E., Solem, M.S., et al. (2025). Gastrointestinal hormones and subjective ratings of appetite after low-carbohydrate vs low-fat low-energy diets in females with lipedema–A randomized controlled trial. Clinical Nutrition ESPEN 65; 16-24. DOI: 10.1016/j.clnesp.2024.11.018. https://www.sciencedirect.com/science/article/pii/S2405457724015274
7. Schroeder, N., Marquart, L. F., & Gallaher, D. D. (2013). The Role of Viscosity and Fermentability of Dietary Fibers on Satiety- and Adiposity-Related Hormones in Rats. Nutrients 5(6); 2093-2113. DOI: 10.3390/nu5062093. https://www.mdpi.com/2072-6643/5/6/2093

Further Reading

• All Appetite Content
• How the Menstrual Cycle Affects Appetite, Metabolism, and Nutrition
• Cachexia Management
• Hypothalamus and Food Intake
• Ghrelin and Leptin

Last Updated: Feb 23, 2026