Appetite Regulation: How Hunger & Satiety Arise
Hunger and satiety are not a matter of willpower. They are a finely tuned hormone system. Ghrelin drives hunger, while leptin, insulin and the gut hormones GLP-1, PYY and CCK signal fullness. The hypothalamus conducts. How this works, why sleep loss and stress override these signals, and how you can support your body's own regulation.
The most common story I hear about weight goes like this: „I just have no discipline." I rarely believe it. Because hunger is not a character flaw. Hunger is a hormone signal, as real as thirst or tiredness. Your body has a precise system of messengers that decides when you feel appetite and when you become full. When this system falls out of rhythm, pulling yourself together does not move you forward, understanding does. In this text we look at which hormones control hunger and satiety, where the control center sits, and what modern nutrition, sleep loss and stress do to these signals. Not to replace willpower, but to make it less necessary.
This spoke is the foundation of the weight cluster. We first clarify why weight is a hormonal signal and not a pure calculation. Then we go through the hunger hormone ghrelin, the satiety hormones from gut and fat tissue, the control center in the hypothalamus, the difference between real and reward-driven hunger, and the factors that override this system, above all sleep. At the end there are concrete directions with which you can support your body's own regulation.
Why weight is a signal, not a pure calculation
Many people know the feeling of fighting against their own body. Eat less, move more, and hunger still speaks up louder than ever. That is not failure. The calorie balance is physically correct, energy does not disappear. But it does not explain what controls hunger, satiety and storage. And that is exactly what matters.
The proof that nutrition is finely tuned by hormones lies at the very start of every life. A breastfed baby counts no calories. It drinks until a satiety signal arrives, then stops. Growth and food intake run via messengers, not via conscious calculation. We do not lose this basic principle as adults, but we overlay it with cues, stress and sleep loss. The body can regulate hunger and satiety itself. The question is whether we help it or get in its way.
„Eat less, move more" is not wrong, but it is half the sentence. The other half reads: make sure your body gets a clean satiety signal at all. Anyone who only turns the dial on quantity but ignores the hormonal effect of food fights against their own physiology. The quality and hormonal effect of food come before mere quantity.
Ghrelin: the hunger hormone that calls before eating
Let us start with hunger. The only known hormone in the body that actively creates appetite is called ghrelin. It is produced mainly in the stomach lining and acts on the appetite center in the brain. Picture ghrelin like a doorbell that rings before visitors arrive. Before a meal it rises, after eating it falls.
Ghrelin rises before eating, even without a clock or food cue
Human study, experimental David Cummings and colleagues measured ghrelin and hunger in 2004 in the American Journal of Physiology in people who moved on to the next meal spontaneously, without any time information and without food cues. In almost all of them ghrelin rose before the self-chosen meal, across very different time windows of 320 to 425 minutes. Remarkably, the ghrelin curve and the subjective hunger curve ran almost identically. This argues that ghrelin is not merely a reaction to the expectation of food but a genuine trigger of the meal.
Cummings DE, Frayo RS, Marmonier C, Aubert R, Chapelot D. Am J Physiol Endocrinol Metab. 2004;287(2):E297-304. doi:10.1152/ajpendo.00582.2003 · PMID: 15039149
So ghrelin is the body's own „time to eat" call. In a world where we used to have real pauses between meals, this was a sensible system. Today, with constantly available food and many small cues, this call can come more often and louder than the body needs in energy. Ghrelin also lowers energy expenditure and promotes fat storage, a sensible protection in times of food scarcity that can become a problem in today's environment.
Ghrelin in the energy balance
Review Laura Mihalache and colleagues summarized the role of ghrelin in 2016 in the journal Hormones. Ghrelin is the only peripheral hormone that activates the appetite receptors in the hypothalamus. In humans there is a rise before and a fall after the meal, which argues for a role in meal initiation and may co-determine how much and what is eaten. The authors note that these originally protective mechanisms can turn into a disadvantage in today's food abundance.
Mihalache L, Gherasim A, Niţă O, et al. Hormones (Athens). 2016;15(2):186-196. doi:10.14310/horm.2002.1672 · PMID: 27376422
The satiety signals: what tells you that enough is enough
Now to the other side. Satiety is not a single signal but a chorus of several hormones. They come from the gut, the pancreas and fat tissue and work in different time windows.
During and after eating, the gut releases three important satiety hormones: CCK, GLP-1 and PYY. CCK comes from cells of the small intestine, responds mainly to fat and protein, and slows gastric emptying and appetite via the vagus nerve. GLP-1 dampens hunger, among other things by slowing gastric emptying. PYY is released after eating, and the more calorie-rich the meal, the more of it.
Ghrelin
From the stomach. Rises before eating, creates appetite. The only peripheral hunger hormone.
Leptin
From fat tissue. Signals how full the energy stores are, dampens appetite over the long term.
GLP-1
From the gut. Slows gastric emptying, lowers energy intake. The principle of weight-loss injections.
PYY
From the gut. Released after eating in proportion to the calorie amount.
CCK
From the small intestine. Responds to fat and protein, slows gastric emptying and appetite via the vagus.
Insulin
From the pancreas. Controls energy storage and serves in the brain as a co-satiety signal.
PYY lowers food intake by a third
Human study, experimental Rachel Batterham and colleagues showed in 2002 in Nature that PYY is released after eating in proportion to the calorie amount. When they infused healthy people with normal, post-meal amounts of PYY, food intake over 24 hours fell by 33 percent. The hormone acts at a specific receptor in the nucleus arcuatus, a core region of the hypothalamus. This established that the gut sends a strong stop signal directly to the appetite center.
Batterham RL, Cowley MA, Small CJ, et al. Nature. 2002;418(6898):650-4. doi:10.1038/nature00887 · PMID: 12167864
GLP-1 lowers energy intake dose-dependently
Meta-analysis Corinne Verdich and colleagues analyzed in 2001 in the Journal of Clinical Endocrinology and Metabolism the individual data of 115 people from GLP-1 infusion studies. Result: under GLP-1, energy intake fell on average by 727 kilojoules, that is around 11.7 percent, and dose-dependently. The effect appeared in lean and overweight people alike. Part of the effect was due to slowed gastric emptying. This is exactly the body's own principle used by the modern GLP-1 medications, the so-called weight-loss injections.
Verdich C, Flint A, Gutzwiller JP, et al. J Clin Endocrinol Metab. 2001;86(9):4382-9. doi:10.1210/jcem.86.9.7877 · PMID: 11549680
An important point from clinical practice, well supported by science: these satiety signals need time and the right building blocks. Protein, fat and fiber trigger them more strongly than fast, highly processed calories. And they act with a delay. Anyone who eats very fast often already has the next portion in their mouth before the first stop signal has even reached the brain.
CCK, the early satiety signal from the gut
Review Graham Dockray summarized the role of CCK in 2012 in Current Opinion in Endocrinology, Diabetes and Obesity. CCK from the I-cells of the small intestine responds to fat and protein and inhibits food intake and gastric emptying via the vagus nerve. Interestingly, leptin strengthens the CCK effect while ghrelin weakens it. In obesity the response to CCK is often reduced. This shows how closely the individual hormones are wired together rather than acting in isolation.
Dockray GJ. Curr Opin Endocrinol Diabetes Obes. 2012;19(1):8-12. doi:10.1097/MED.0b013e32834eb77d · PMID: 22157397
Leptin: the long-term signal and why it can fail
While ghrelin, GLP-1, PYY and CCK work from meal to meal, there is one hormone for the big picture: leptin. It is produced in fat tissue and tells the brain how full the energy stores are. Lots of fat tissue, lots of leptin, and that dampens appetite over the long term. So much for the theory.
The problem: in many people with overweight the leptin level is high, but the signal arrives less well. This is called leptin resistance. The body has full stores yet still signals hunger. Picture a smoke detector whose battery is full but which no longer reliably beeps. The fat is there, the message „I have enough" does not get through.
How leptin acts in the brain and why it can be blocked
Review Obin Kwon and colleagues described in 2016 in Cellular and Molecular Life Sciences the leptin signaling pathways in the hypothalamic neurons. Leptin binds to receptors and triggers several signaling cascades that regulate food intake and energy balance. In leptin resistance, molecules such as SOCS3 and PTP1B as well as inflammatory signaling pathways and cellular stress inhibit these cascades. Simply put: inflammation and stress in the control neurons can brake the satiety signal. This is well described mechanistically but not clarified in every detail in humans.
Kwon O, Kim KW, Kim MS. Cell Mol Life Sci. 2016;73(7):1457-77. doi:10.1007/s00018-016-2133-1 · PMID: 26786898
Leptin resistance is why „just eat less" is so agonizing for some people. The brain believes it is in scarcity even though the stores are full. That is not an excuse, it is biology. So the question is not only „how do I eat less" but „how do I get my satiety signal to come through again". You will find the deep dive on leptin, insulin and weight regulation in its own spoke.
The control center: the hypothalamus as conductor
All these signals, ghrelin, leptin, insulin, GLP-1, PYY and CCK, converge in one place: the hypothalamus, deep in the brain. There sits the nucleus arcuatus, and within it two neuron groups work against each other. One group creates appetite, the other creates fullness. You can picture it like a mixing desk where the balance between „eat more" and „stop" is constantly adjusted.
The neuroendocrine control of food intake
Review Elena Valassi and colleagues described in 2007 in Nutrition, Metabolism and Cardiovascular Diseases how the system works together. The satiety signals from the gut, that is CCK, GLP-1 and PYY, run via the vagus nerve to the brainstem and from there to the nucleus arcuatus in the hypothalamus. There they meet the appetite-stimulating neurons with the messengers NPY and AgRP and the satiating neurons with POMC. Leptin and insulin provide, as adiposity signals, the information about the long-term stores. From this integration the individual response to a meal arises.
Valassi E, Scacchi M, Cavagnini F. Nutr Metab Cardiovasc Dis. 2007;18(2):158-68. doi:10.1016/j.numecd.2007.06.004 · PMID: 18061414
The gut hormones talk directly to the appetite regions
Systematic review Davide Zanchi and colleagues analyzed 40 imaging studies in 2017 in Neuroscience and Biobehavioral Reviews. The result paints a clear picture: a high ghrelin level, the hunger hormone, was linked with stronger activation of reward and evaluation regions such as prefrontal cortex, amygdala and insula, and with dampened activity in the hypothalamus. The satiety signals glucose, insulin, leptin, PYY and GLP-1 acted in the opposite direction in the same regions. In short: your gut hormones are in constant conversation with the appetite regions of your brain.
Zanchi D, Depoorter A, Egloff L, et al. Neurosci Biobehav Rev. 2017;80:457-475. doi:10.1016/j.neubiorev.2017.06.013 · PMID: 28669754
Two kinds of hunger: real need and reward
There is a second strand that everyone knows from daily life. You have just eaten, you are actually full, and still the wish for the chocolate next to the couch speaks up. That is not real energy hunger. That is hedonic, reward-driven hunger. It arises not in the hypothalamus but in the brain's reward system, the mesolimbic dopamine system.
Liking and wanting: two sides of food craving
Review Ileana Morales and Kent Berridge summarized the brain mechanisms of reward eating in 2020 in Physiology and Behavior. They distinguish liking, that is the actual enjoyment, from wanting, that is the motivation to obtain something. Both arise in partly separate circuits. With strong cue over-reactivity, wanting can decouple from liking: one strongly craves a food that one no longer even enjoys much when eating it. The authors see in this a possible mechanism in some forms of overweight and binge eating.
Morales I, Berridge KC. Physiol Behav. 2020;227:113152. doi:10.1016/j.physbeh.2020.113152 · PMID: 32846152
The good news: homeostatic and hedonic hunger are interwoven. When real satiety works cleanly, that also dampens the reward response. Highly processed, energy-dense products are a problem because they strongly stimulate the reward system and at the same time trigger the real satiety signal more weakly. They deliver a lot of reward and little brake.
„Anyone who cannot resist sweets has no discipline." From a KPNI view that falls short. Part of this craving comes from the reward system and can decouple from real need. That is no free pass, but it shifts the question: away from „pull yourself together" toward „how do I reduce the cues and strengthen real satiety". That is more honest and usually more effective.
What overrides the regulation: sleep, stress, modern food
Now to perhaps the most important practical point. This finely balanced system can be shifted from the outside. The best-documented factor is sleep. Too little sleep shifts the appetite hormones measurably toward more hunger, and independently of willpower.
Two nights of short sleep shift ghrelin and leptin
RCT, n=12 Karine Spiegel and colleagues studied 12 healthy young men in 2004 in the Annals of Internal Medicine under controlled conditions, with the same calorie intake and activity. After two nights of shortened sleep, the satiety hormone leptin fell by 18 percent and the hunger hormone ghrelin rose by 28 percent. At the same time, hunger increased by 24 percent and appetite by 23 percent, especially for calorie- and carbohydrate-rich food, there even by 33 to 45 percent. Short sleep thus shifts the hormonal balance directly toward more appetite.
Spiegel K, Tasali E, Penev P, Van Cauter E. Ann Intern Med. 2004;141(11):846-50. doi:10.7326/0003-4819-141-11-200412070-00008 · PMID: 15583226
In the population too: short sleep, more hunger hormone
Cohort study, n=1024 Shahrad Taheri and colleagues studied 1024 people of the Wisconsin Sleep Cohort in 2004 in PLoS Medicine with sleep measurement in the laboratory and fasting blood values. Those who slept less had on average lower leptin and higher ghrelin, independently of body weight. For five instead of eight hours of sleep, the models predicted around 15.5 percent less leptin and 14.9 percent more ghrelin. The connection between sleep and body weight was U-shaped. The laboratory finding of Spiegel thus also appears in the broad population.
Taheri S, Lin L, Austin D, Young T, Mignot E. PLoS Med. 2004;1(3):e62. doi:10.1371/journal.pmed.0010062 · PMID: 15602591
Short sleep raises snack calories above all
RCT, n=11 Arlet Nedeltcheva and colleagues had 11 volunteers spend 14 days each with 5.5 or 8.5 hours in bed in the sleep laboratory in 2008 in the American Journal of Clinical Nutrition, with free access to palatable food. The calories from the main meals stayed the same. But the calories from snacks rose clearly with short sleep, from around 866 to 1087 kilocalories per day, with a higher carbohydrate share, especially in the evening and night hours. Too little sleep thus hits evening snacking in particular.
Nedeltcheva AV, Kilkus JM, Imperial J, Kasza K, Schoeller DA, Penev PD. Am J Clin Nutr. 2008;89(1):126-33. doi:10.3945/ajcn.2008.26574 · PMID: 19056602
Beyond sleep, other factors play in. Chronic stress and the stress hormone cortisol can influence appetite and belly fat. Highly processed food delivers many fast calories with a weak satiety signal. And silent inflammation, for example from the gut or from visceral fat, can disturb the leptin signaling chain. These are the dials that the modern environment turns, often without our noticing.
Four lenses on appetite regulation
Nervous system
The gut satiety signals run via the vagus nerve to the brainstem and on to the hypothalamus (Valassi 2007). Ghrelin and the satiety hormones change the activity in reward and control regions of the brain (Zanchi 2017). Appetite is thus also a question of the nerve pathways, not only of the stomach.
Immune system and inflammation
Silent inflammation can brake the leptin effect in the hypothalamic neurons via pathways such as SOCS3, PTP1B and inflammatory cascades (Kwon 2016). From a KPNI view, low-grade inflammation, for example from gut or visceral fat, is an often invisible brake on satiety.
Metabolism
Insulin controls energy storage and serves in the brain as a co-satiety signal (Valassi 2007). Strongly fluctuating blood sugar can favor cravings. The composition of the meal, that is protein, fat and fiber, co-determines how strongly the satiety hormones respond (Dockray 2012).
Hormone system
Ghrelin, leptin, GLP-1, PYY, CCK and insulin form a network in which the hormones strengthen or inhibit each other (Dockray 2012). Sleep too intervenes hormonally and shifts ghrelin and leptin (Spiegel 2004). Appetite is a hormonal overall picture, not a single value.
What does not work (and why it is everywhere anyway)
An honest look at common advice that often promises more than it delivers.
- Pure willpower against hunger. When ghrelin rises and leptin comes through poorly, you are fighting against a hormone signal. You can keep that up for a while, but it is grinding and rarely lasting. It makes more sense to change the signals themselves.
- Counting calories only. The amount is not irrelevant, but it ignores how strongly a meal fills you. 500 calories from protein and fiber trigger different satiety signals than 500 liquid, fast calories (Dockray 2012, Batterham 2002).
- Eating very fast. The satiety hormones act with a delay. Anyone who eats in a few minutes already has the next portion inside before the stop signal arrives.
- Treating sleep as a side issue. Too little sleep shifts ghrelin and leptin measurably toward hunger (Spiegel 2004, Taheri 2004). Anyone who wants to lose weight and sleeps poorly is working against their own hormone situation.
Hunger is not a willpower problem, it is a signal
Your body has a precise system that controls hunger and satiety. It can be shifted, by sleep loss, stress and modern food, and it can be supported. When you understand the system, you stop fighting against yourself and start working with your physiology.
Three directions with which you support your regulation
Prioritize your sleep
Too little sleep lowers the satiety signal leptin and raises the hunger hormone ghrelin (Spiegel 2004, Taheri 2004), especially noticeable in evening snacking (Nedeltcheva 2008). Sufficient, regular sleep is one of the most effective levers for a calmer appetite. It is not a side issue but part of weight regulation.
Build meals that fill you
Protein, fat and fiber trigger the gut satiety hormones more strongly than fast, highly processed calories (Dockray 2012, Batterham 2002). Eat more slowly so the signals have time to reach the brain. This does not aim at eating less through going without, but at more satiety per bite.
Reduce the constant cues
Reward-driven hunger responds to cues (Morales and Berridge 2020). Constantly visible, highly processed food keeps the reward system busy. Fewer of these cues within reach can dampen the wanting, entirely without constant self-discipline. Environment beats willpower.
Persistent, unusually strong hunger, suddenly increasing appetite, unintended weight loss or weight gain, strong thirst, palpitations or other new symptoms should be examined medically. Possible causes range from thyroid and blood sugar disorders to side effects of medications. Regarding the GLP-1 medications, the so-called weight-loss injections: they are prescription-only and belong in medical supervision, this is not a self-experiment. This text serves for information and does not replace a medical examination, diagnosis or treatment.
Frequently asked questions about appetite regulation
Which hormones control hunger and satiety?
The only known peripheral hunger hormone is ghrelin, produced mainly in the stomach. It rises before meals and falls afterward (Mihalache 2016, Cummings 2004). On the satiety side there are several signals: from the gut GLP-1, PYY and CCK, from the pancreas insulin, and from fat tissue as a long-term storage signal leptin. GLP-1 lowers energy intake in human studies by around 12 percent on average (Verdich 2001). PYY reduced food intake over 24 hours by about a third (Batterham 2002). All signals converge in the hypothalamus. No single hormone decides alone, it is an interplay.
What is ghrelin and why do I get hungry before eating?
Ghrelin is the hunger hormone. It is produced mainly in the stomach lining and acts on the appetite center in the hypothalamus. Its concentration rises before a meal and falls after eating. Cummings 2004 showed something remarkable: the ghrelin rise occurs even when people begin eating spontaneously without a clock and without food cues. Ghrelin curve and hunger curve ran almost identically. So your feeling of hunger before eating is a real hormone signal, not imagination and not a sign of weakness.
Why do I lack a feeling of fullness?
A missing or weak feeling of fullness can have many causes. The gut satiety hormones GLP-1, PYY and CCK are triggered mainly by protein, fat and fiber (Dockray 2012, Batterham 2002). Very quickly eaten, highly processed and liquid calories often trigger this signal more weakly. Sleep loss also shifts the balance: it lowers leptin and raises ghrelin (Spiegel 2004). With overweight, leptin resistance can add to this, where the satiety signal reaches the brain less well (Kwon 2016). And reward-driven hunger can override real satiety (Morales and Berridge 2020).
What does leptin resistance mean?
Leptin is a hormone from fat tissue. It tells the brain how full the energy stores are and dampens appetite over the long term (Kwon 2016). With overweight the leptin level is often high but works less well. This is called leptin resistance. Mechanistically, inflammatory signals, cellular stress and braking molecules such as SOCS3 and PTP1B can block the leptin signaling chain in the neurons (Kwon 2016). The result: the body signals hunger even though the stores are full. This is not yet clarified in every detail scientifically, but it explains why losing weight is not a pure question of willpower for many people.
How are sleep and appetite connected?
Too little sleep shifts the appetite hormones measurably toward more hunger. Spiegel 2004 showed in a controlled crossover with 12 healthy young men that two nights of sleep restriction lowered leptin by 18 percent, raised ghrelin by 28 percent, and clearly increased hunger and appetite, especially for calorie- and carbohydrate-rich food. Taheri 2004 found the same connection in the Wisconsin cohort with over 1000 people: short sleep, low leptin, high ghrelin, higher BMI. Nedeltcheva 2008 showed that shortened sleep raises snack calories in the evening in particular.
What is the difference between homeostatic and hedonic hunger?
Homeostatic hunger is real energy hunger. It arises when the body lacks energy and is controlled through ghrelin, leptin and the gut hormones. Hedonic hunger is reward-driven appetite. It arises in the mesolimbic dopamine system and can occur independently of actual energy need, such as the wish for something sweet despite a full meal. Morales and Berridge 2020 distinguish liking from wanting. With strong cue over-reactivity, wanting can decouple from liking and drive excessive food craving. Both systems are interwoven in the brain.
Can I curb my appetite naturally?
Instead of suppressing appetite with willpower, it makes more sense to support the body's own satiety signals. Protein and fiber trigger the gut satiety hormones more strongly (Dockray 2012). Enough and regular sleep keeps the ratio of ghrelin and leptin more favorable (Spiegel 2004, Taheri 2004). Eating more slowly gives the satiety signals time to reach the brain, since GLP-1, PYY and CCK only act with a delay. Stable blood sugar patterns can cushion craving spikes. These are directions, not guarantees, and they do not replace individual medical assessment, but they work with your physiology rather than against it.
How do the gut hormones GLP-1, PYY and CCK work?
These three hormones are produced in the gut and are satiety signals. CCK comes from the I-cells of the small intestine, responds to fat and protein, and slows gastric emptying and appetite via the vagus nerve (Dockray 2012). GLP-1 lowers energy intake dose-dependently, among other things through slowed gastric emptying (Verdich 2001). PYY is released after eating in proportion to the calorie amount and acts via the Y2 receptor in the hypothalamus (Batterham 2002). All three reach the appetite center in the brain via the vagus nerve and brainstem (Zanchi 2017, Valassi 2007). The principle of GLP-1 is the same one used by modern weight-loss injections.
Do highly processed foods make you less full?
This is mechanistically plausible and fits clinical observation, even though the study evidence is nuanced. The gut satiety hormones CCK, GLP-1 and PYY are triggered mainly by protein, fat and fiber and need time and digestive work (Dockray 2012, Batterham 2002). Highly processed products are often energy dense, low in fiber, quickly eaten and partly liquid. They deliver many calories before the satiety signals fully take hold. In addition, they strongly stimulate the reward system (Morales and Berridge 2020). The combination can lead to eating more than the body needs in energy.
Is constant hunger a sign of illness?
Not necessarily, but persistent, unusually strong hunger should be checked medically. Common and mostly harmless causes are sleep loss, stress, very fast eating, protein- and fiber-poor food, and strongly fluctuating blood sugar. But there are also medical reasons, such as an overactive thyroid, a blood sugar metabolism out of balance, or certain medications. If hunger suddenly increases sharply, comes with weight loss, strong thirst, palpitations or other symptoms, you should not put it down to willpower but have it checked medically. This text does not replace a medical examination.
Related topics in the weight cluster
- Appetite regulation: hunger and satiety (you are here)
- Leptin, insulin and weight regulation
- Cravings: causes and counter-strategies
- Boosting GLP-1 naturally
- Weight-loss injection: how GLP-1 works
- Sleep and weight loss
Connections to other topics
How leptin and insulin control storage and appetite over the long term and what leptin and insulin resistance mean for weight.
Why cravings arise, the role of blood sugar, ghrelin and the reward system, and in which direction you can steer against them.
GLP-1 is one of the body's own satiety hormones. Which nutrition and lifestyle approaches may favor it.
How the GLP-1 medications act via the body's own satiety mechanism, what they can do and where their limits lie.
Why too little sleep shifts the appetite hormones toward hunger and how better sleep can support weight regulation.
Sources and further reading
- Cummings DE, Frayo RS, Marmonier C, Aubert R, Chapelot D. Plasma ghrelin levels and hunger scores in humans initiating meals voluntarily without time- and food-related cues. Am J Physiol Endocrinol Metab. 2004;287(2):E297-304. doi:10.1152/ajpendo.00582.2003 · PMID: 15039149 [Human study]
- Mihalache L, Gherasim A, Niţă O, Ungureanu MC, Pădureanu SS, Gavril RS, Arhire LI. Effects of ghrelin in energy balance and body weight homeostasis. Hormones (Athens). 2016;15(2):186-196. doi:10.14310/horm.2002.1672 · PMID: 27376422 [Review]
- Batterham RL, Cowley MA, Small CJ, et al. Gut hormone PYY(3-36) physiologically inhibits food intake. Nature. 2002;418(6898):650-4. doi:10.1038/nature00887 · PMID: 12167864 [Human study]
- Batterham RL, Cohen MA, Ellis SM, et al. Inhibition of food intake in obese subjects by peptide YY3-36. N Engl J Med. 2003;349(10):941-8. doi:10.1056/NEJMoa030204 · PMID: 12954742 [RCT]
- Verdich C, Flint A, Gutzwiller JP, et al. A meta-analysis of the effect of glucagon-like peptide-1 (7-36) amide on ad libitum energy intake in humans. J Clin Endocrinol Metab. 2001;86(9):4382-9. doi:10.1210/jcem.86.9.7877 · PMID: 11549680 [Meta-analysis]
- Dockray GJ. Cholecystokinin. Curr Opin Endocrinol Diabetes Obes. 2012;19(1):8-12. doi:10.1097/MED.0b013e32834eb77d · PMID: 22157397 [Review]
- Kwon O, Kim KW, Kim MS. Leptin signalling pathways in hypothalamic neurons. Cell Mol Life Sci. 2016;73(7):1457-77. doi:10.1007/s00018-016-2133-1 · PMID: 26786898 [Review]
- Valassi E, Scacchi M, Cavagnini F. Neuroendocrine control of food intake. Nutr Metab Cardiovasc Dis. 2007;18(2):158-68. doi:10.1016/j.numecd.2007.06.004 · PMID: 18061414 [Review]
- Zanchi D, Depoorter A, Egloff L, et al. The impact of gut hormones on the neural circuit of appetite and satiety: A systematic review. Neurosci Biobehav Rev. 2017;80:457-475. doi:10.1016/j.neubiorev.2017.06.013 · PMID: 28669754 [Systematic review]
- Morales I, Berridge KC. 'Liking' and 'wanting' in eating and food reward: Brain mechanisms and clinical implications. Physiol Behav. 2020;227:113152. doi:10.1016/j.physbeh.2020.113152 · PMID: 32846152 [Review]
- Spiegel K, Tasali E, Penev P, Van Cauter E. Brief communication: Sleep curtailment in healthy young men is associated with decreased leptin levels, elevated ghrelin levels, and increased hunger and appetite. Ann Intern Med. 2004;141(11):846-50. doi:10.7326/0003-4819-141-11-200412070-00008 · PMID: 15583226 [RCT]
- Taheri S, Lin L, Austin D, Young T, Mignot E. Short sleep duration is associated with reduced leptin, elevated ghrelin, and increased body mass index. PLoS Med. 2004;1(3):e62. doi:10.1371/journal.pmed.0010062 · PMID: 15602591 [Cohort study]
- Nedeltcheva AV, Kilkus JM, Imperial J, Kasza K, Schoeller DA, Penev PD. Sleep curtailment is accompanied by increased intake of calories from snacks. Am J Clin Nutr. 2008;89(1):126-33. doi:10.3945/ajcn.2008.26574 · PMID: 19056602 [RCT]