You’ve come to the right place if you want to understand why you sometimes still feel hungry after eating.
This article will look deeper into our bodies to see which hormones can trigger sensations of hunger and satiety.
Armed with essential knowledge about hunger and satiety hormones, we’ll further derive natural ways to control appetite.
What are Hunger and Satiety Hormones?
Hormones are chemical messengers that provide authoritative signals to regulate hunger, satiety, thirst, body temperature, or even bodyweight (Starka et al. 20201).
With the help of a control center in the brain, the hypothalamus, the hormone system is significantly involved in regulating bodily functions to remain in a healthy balance.
Eating behavior is also coordinated with the help of the hypothalamus, which acts as a control center for appetite (Austin et al. 20092).
Hunger and satiety hormones sometimes tell the brain how much energy you have already consumed and how much you still need.
The goal is energy homeostasis: the balance between energy production (metabolism) and energy consumption by cells (Vergara et al. 20193).
This article reviews the major hormones involved in balancing hunger and satiety.
In addition to the chemical messengers on this list, other hormones and neurotransmitters exist that can influence appetite regulation.
However, the following hormones are the best researched to understand how they affect our food intake.
In addition, sufficient research exists regarding these six hunger and satiety hormones to infer the influence of modern lifestyle factors on hormone balance.
For this reason, we can also derive how we can naturally regulate these hormones.
First among them is the essential initiator of appetite.
Hunger Hormone Ghrelin
Ghrelin is better known as the hunger hormone. And for a good reason. Ultimately, ghrelin is the only neurotransmitter outside the central nervous system that triggers appetite (Austin et al. 20094).
The body releases ghrelin in response to an empty stomach to tell you to eat again shortly (Klok et al. 20075).
Additionally, the reward center in your brain is stimulated to make food more interesting to you (Müller et al. 20156).
After a meal, on the other hand, ghrelin levels are low. When the stomach is full, there is no longer a need for food intake.
A healthy ghrelin level correlates negatively with body fat, i.e., it is higher in lean individuals and lower in obese individuals (Austin et al. 20097).
However, in obese people, ghrelin levels do not always decrease as they should after a meal. Because they continue to feel hungry, these people risk overeating (Klok et al. 20078).
Consequently, an imbalance in ghrelin secretion can lead to weight gain. Conversely, ghrelin balance must function properly to lose weight successfully.
Satiety Hormone Leptin
Leptin is the counterpart of the hunger hormone ghrelin. Accordingly, it is also known as the satiety hormone.
Unlike ghrelin, leptin has to do directly with body fat. It is the fat cells themselves that produce the hormone.
When you eat, and your fat cells determine that you’ve put in enough energy, they release leptin, which signals the brain to stop eating.
If your leptin levels are low, on the other hand, your brain receives the message that fat stores are empty, which in turn triggers hunger (Friedman et al. 19989).
Consequently, leptin is responsible for regulating the total amount of stored energy in the body. Hence, leptin levels correlate positively with your body fat (Austin et al. 200910).
When the signaling to regulate body fat stops working correctly, it is called leptin resistance.
When the body is constantly flooded with high amounts of leptin, it becomes less responsive to the hormonal signal over time. Therefore, leptin sensitivity decreases.
In short, with leptin resistance, your brain takes longer to recognize that you’re already full.
The result can be overeating, weight gain, obesity, and other metabolic disorders (Myers et al. 201011).
Leptin resistance is associated with chronic inflammation, obesity, cardiovascular disease, insulin resistance, and type 2 diabetes (Martin et al. 200812).
Researchers hypothesize that excessive levels of the storage hormone insulin, which is also instrumental in weight gain, cause leptin resistance (Lustig et al. 200413).
The more you eat those foods that stimulate insulin secretion, the worse leptin or insulin resistance can become.
Other Satiety and Hunger Hormones
In addition to the well-known satiety hormone leptin, three other well-researched hormones inhibit appetite. And these are all mainly produced in your intestine.
In addition, researchers revealed a fascinating hormone that initiates hunger in your brain. Since it interacts closely with the primary hunger and satiety hormones, let’s look at the neurotransmitter in detail.
With neuropeptide Y (NPY), we move into the central nervous system. There it is the most abundant peptide.
NPY is primarily found in the hypothalamus and is both a hormone and a neurotransmitter. Moreover, NPY is considered the most potent appetite-stimulating compound in the human body.
Every other hunger or satiety hormone regulates food intake by acting on NPY in the hypothalamus. While leptin suppresses NPY activity, ghrelin stimulates it (Austin et al. 200914).
Accordingly, elevated NPY increases food cravings, predominantly carbohydrates (Beck 200615).
For this reason, like ghrelin, we can refer to it as a hunger hormone.
In addition to hunger, NPY stimulates fat storage and weight gain via the central nervous system while decreasing sex drive, locomotion, energy expenditure, and body temperature (Minor et al. 200916).
Moreover, stress increases NPY levels in fat cells, contributing to abdominal fat storage (Kuo et al. 200717).
However, elevated NPY levels make sense as a stress response because NPY has stress-reducing, anxiety-relieving, and neuroprotective properties, according to researchers at the University of Graz, Austria (Reichmann et al. 201618).
You may have also heard that researchers have found that many living things can live at least 33% longer if they eat less (McDonald et al. 201019).
Because NPY acts as the primary hunger signal in this context, researchers suspect it plays an essential role in extending lifespan (Minor et al. 200920).
Like NPY, peptide YY (PYY) is a crucial brain-gut peptide. Therefore, the actions of both peptides are closely related to appetite regulation and the development of obesity (Wu et al. 201921).
PYY is produced in the intestine after eating. Here, the amount secreted is proportional to the fat ingested with food (Pironi et al. 199322).
It enters the hypothalamus in the brain via the bloodstream, reducing appetite (Wu et al. 201923).
Hence, it is a satiety hormone.
According to studies, individuals with obesity exhibited attenuated peptide YY responses after eating, leading to uncontrolled overeating (Zwirska-Korczala et al. 200724).
Therefore, adequate PYY levels are essential in reducing increased food intake, especially after extensive exercise (Zouhal et al. 201925).
In addition, researchers at Oxford have found that obese individuals do not already have high fasting PYY levels, but chronic overeating elevates them.
According to the researchers, this suggests a protective mechanism against excessive food intake and other satiety hormones (Cahill et al. 201126).
The next satiety hormone, glucagon-like peptide-1 (GLP-1), is secreted along with PYY in the gut in response to nutrient intake.
Its main functions are to keep blood glucose levels stable and produce a feeling of satiety (Müller et al. 201927).
This hormone could also help weight loss and reduce body mass index (BMI) or waist circumference in overweight adults (Zhang et al. 201528).
Moreover, researchers explain the reduced hunger and increased satiety after gastric bypass surgery by an increased GLP-1 response to food intake (Morinigo et al. 200629).
The beneficial effects of GLP-1 make this hormone an exciting candidate for the treatment of obesity, diabetes, and neurodegenerative diseases (Müller et al. 201930).
Research suggests that people with obesity may experience problems with GLP-1 signaling (Anandhakrishnan et al. 201631).
As with the other appetite hormones, this suggests a possible type of GLP-1 resistance. This decreasing GLP-1 sensitivity may also explain the elevated fasted plasma GLP-1 levels in obese children and adults (Stinson et al. 202132).
The last in our series of satiety hormones is cholecystokinin (CCK). Also, cells in the gut produce CCK in response to a meal.
CCK is the first gut hormone known to affect appetite (Gibbs et al. 197333). It is closely related to the primary satiety hormone leptin in this context.
An elevated CCK level can be detected in the human body approximately 15 minutes after eating (Liddle et al. 198536).
In addition to satiety, cholecystokinin also plays an essential role in the following processes in the body (Okonkwo et al. 202137):
- Inhibition of gastric acid secretion and release of digestive enzymes
- Contraction of the gallbladder and regulation of bile acid
- Regulation of gastric emptying
- Energy production, protein synthesis, and cell growth
Our bodies produce CCK when we consume protein or fat (Dockray et al. 201238). As a result, food intake and, in particular, our cravings for sugar and carbohydrates are reduced (Lieverse et al. 199539).
Recent research suggests that obese people develop a type of CCK resistance. Reduced sensitivity to the hormone makes them more likely to overeat, which may contribute to the progression of CCK resistance (Cawthon et al. 202140).
How to Regulate Appetite Naturally
Even though science is still far from being able to fully explain all the hormones surrounding hunger and their complex interplay, tips can be derived for sustainable satiety.
We cannot completely control our appetite, but we can bring our modern lifestyle and thus our hormone balance back into the equilibrium that nature originally intended.
How to Control Hunger Hormones
Ghrelin is the essential circulating hunger hormone in the body, closely related to NPY, the primary hunger hormone in the central nervous system.
Together they initiate hunger while being influenced by other peripheral hormones.
Although ghrelin stimulates appetite, you should by no means consider taking ghrelin blockers. Ghrelin is also vital for learning, memory, gastric acid secretion, sleep-wake cycles, and reward behavior and should not be artificially unbalanced (Müller et al. 201541).
Instead, studies show that the eating behavior itself can curb the release of hunger hormones.
1. Focus Protein-Rich Foods
According to an Oxford study that compared the consumption of a high-protein meal with a high-carbohydrate meal, protein consumption can significantly lower ghrelin levels in the body (Blom et al. 200642).
Similarly, in Oxford, researchers found that reducing protein in the diet caused a more significant release of NPY and more body fat (White et al. 199443).
2. Increase Intake of Healthy Fats
High levels of NPY fuel carbohydrate cravings. In contrast, fat consumption inhibits NPY activity more than other macronutrients, which may reduce cravings (Beck 200644).
To summarize, natural foods high in fat and protein are excellent choices to curb appetite.
In addition to fattier cuts of meat, fatty fish, such as salmon or mackerel, is ideal, as its omega-3 fatty acids can further support satiety (Parra et al. 200845).
3 Avoid Fructose
The supposed fruit sugar is often marketed as healthy, which it is not. Fructose is the sweet molecule besides glucose in conventional table sugar. Therefore, a piece of dextrose (glucose) is not distinctively sweet because it lacks fructose.
Metabolic researchers have found that diets high in fructose can increase ghrelin levels, causing obesity (Teff et al. 200446).
Accordingly, the sweet molecule fuels cravings and promotes changes in the brain’s reward system, leading to overconsumption.
In addition, fructose causes the development of new fat and insulin resistance in the liver, leading to chronic metabolic diseases such as fatty liver and type 2 diabetes.
These effects on the liver become easier to understand when we realize that fructose is closely related to alcohol and can cause the same diseases.
The fermentation of fructose produces ethanol – alcohol. The main difference is that fructose is 100% metabolized in the liver and not in the brain, sparing sensations of intoxication and hangovers (Lustig 201347).
In addition, fructose significantly affects the satiety hormone leptin, as we will see shortly.
How to Increase Satiety Hormones
Sustained satiety goes far beyond a short-term feeling of fullness due to stomach distension. Since the essential satiety hormones have been more adequately researched, we can draw meaningful conclusions about which meals make us feel full in the long term and which do not.
Interesting starting points also already exist regarding the influences of other lifestyle factors such as exercise and sleep on our satiety hormones. According to science, here are the best tips to increase those hormones that cause satiety.
1. Reduce Carbs
This first point may sound like old news, yet it cannot be repeated often enough. The industrialization of food production has creepily, yet significantly, increased carbohydrate consumption over the decades.
Refined carbohydrates like sugar can turn off the leptin receptors in the brain, so you need longer or higher levels of leptin to get full (Shapiro et al. 200848).
To summarize, added sugar in foods makes you hungry for more.
In this regard, the fructose in sugar is more dangerous than other carbohydrates when it comes to developing leptin resistance and obesity (Shapiro et al. 200849).
Therefore, it is advisable to avoid high fructose concentrations such as in high-fructose corn syrup, agave syrup, candy, and other processed foods.
Moreover, carbohydrate-rich meals not only stimulate the satiety hormone PYY the least, but their level also decreases rapidly afterward. In contrast, PYY continues to rise for hours after high-fat and high-protein meals (Lomenick et al. 200950).
For this reason, processed carbohydrates such as those in cookies or other baking goods do not keep you full for long. Moreover, they promote inflammation in the body (Buyken et al. 201451).
And inflammation is not only often associated with obesity, but it inhibits the release of GLP-1, thereby inhibiting satiety (Gagnon et al. 201552).
2. Prefer Natural Fats to Seed Oils
Refined seed oils, such as soybean, sunflower, or canola oil, are just as pro-inflammatory as refined carbohydrates (Marchix et al. 201553).
And like sugars, they are found in a wide variety of highly processed foods today.
In contrast, extra virgin olive oil could increase GLP-1 levels (Bodnaruc et al. 201654).
Furthermore, consumption of natural fats in extra virgin olive oil, grass-fed butter, or grass-fed beef supports CCK production, thereby maintaining satiety longer (Dockray et al. 201255).
Although fat is more nutritious than carbohydrates, excessive fat consumption does not lead to leptin resistance (Dirlewanger et al. 200056).
Moreover, the secretion of the satiety hormone PYY increases proportionally to the amount of fat consumed via diet (Pironi et al. 199357).
In short, a high-fat, low-carbohydrate diet such as the keto diet is ideal for increasing satiety and avoiding cravings.
3. Eat Enough Protein
Like healthy fats, protein increases the release of satiety hormones in the gut.
Accordingly, one study found that a high-protein diet, as opposed to a high-carbohydrate diet, can help increase CCK levels and thus feelings of satiety (Chungchunlam et al. 201558).
Similarly, protein-rich foods can increase GLP-1 levels (Gillespie et al. 201559). In particular, collagen, the essential protein for skin, hair, bone, and joints, promotes satiety via GLP-1 (Rubio et al. 200860).
In terms of PYY, high-protein meals satiate even more effectively than high-fat meals (Lomenick et al. 200961).
4. Get Regular, Quality Sleep
Here is the evidence if you’ve ever heard that sleep is vital for weight loss.
Among many other essential tasks, sleep helps you use leptin properly. Researchers have found that shorter sleep results in lower levels of the satiety hormone leptin in the body (Spiegel et al. 200462).
A brand new study even states that sleep deprivation can lead to obesity and subsequently type 2 diabetes by impairing leptin regulation, as it increases appetite and food intake (Mosavat et al. 202163).
Furthermore, studies consistently show that sleep deprivation leads to increased ghrelin levels and decreased leptin (Cooper et al. 201864).
A recent review of 21 studies involving 2,250 individuals concluded that reduced sleep duration is associated with increased ghrelin levels, whereas sleep disturbance affects leptin and ghrelin levels (Lin et al. 202065).
Consequently, sleep hygiene significantly affects the regulation of appetite. To avoid the risk of increasing your body mass index, you should regularly get more than 7 hours of quality net sleep per night (Cooper et al. 201866).
5. Don’t Rely on Exercise Alone
It is true that exercise helps increase leptin sensitivity, increasing the hormone’s perception and, therefore, satiety (Kang et al. 201367).
However, overall, study results are mixed regarding the effects of exercise on hunger and satiety hormones.
While individuals of average weight can increase their PYY levels with exercise, overweight individuals achieved this result only with long-term training for at least 32 weeks (Jones et al. 200968).
In contrast, there is evidence that high-intensity interval training (HIIT) or the combination of aerobic and strength training could increase CCK levels (Zouhal et al. 201969).
However, do not forget that exercise promotes hunger. And for some people, this compensatory effect of food intake is even more significant than it should be (Melanson et al. 201372).
Accordingly, exercise is not the tool of choice for regulating appetite. If the necessary dietary intervention is not provided, athletic ambitions can backfire by craving foods that reduce satiety, promoting overeating in the long run.
Do You Regulate Appetite, or Do Hormones Control You?
Hunger is not a bad feeling per se. Instead, hunger and satiety are standard physiological signals that keep us alive and contribute to the body’s optimal functioning.
Our lifestyle, marked by psychological stress and changes in food production, affects the natural balance of hunger and satiety hormones.
Although appetite and the hormones involved in it represent a complex interplay that we do not yet understand precisely, research has yielded revealing results in recent years.
Highly processed foods with refined carbohydrates and added sugars contribute to our feeling more hungry in the long term.
In particular, the fructose in sugar inhibits satiety signals and fuels cravings (Shapiro et al. 200873).
In contrast to these processed carbohydrates, natural fatty acids and proteins can contribute to lasting satiety and lower inflammation levels.
As a result, we get a low-carbohydrate, high-fat diet that relies on natural protein sources such as fatty fish.
Accordingly, brand-new studies highlight that such ketogenic diets prevent an increase in the hunger hormone ghrelin, which is otherwise seen after weight loss, and instead reduce feelings of hunger (Deemer et al. 202074).
In a direct comparison with a low-fat, high-carbohydrate (LFHC) diet, a low-carb, high-fat (LCHF) diet significantly increased satiety after it released 55% more PYY in the gut (Essah et al. 200775).
In addition to diet, sleep is the second major factor that can help curb appetite via healthy hormone balance. Therefore, you should always prioritize regular, quality sleep.
According to science, intermittent fasting is an effective way to increase sleep quality, REM sleep, and balance in as little as two weeks (Michalsen et al. 200376).
Learn how to successfully integrate fasting into your daily routine in my new book: Intermittent Fasting 101: The Science-Backed Beginner’s Guide to Lose Weight Without Dieting and Working Out.
Hunger and Satiety Hormones FAQ
Which hormones are involved in hunger and satiety?
The hormones ghrelin, leptin, neuropeptide Y, peptide YY, GLP-1, and CCK are involved in hunger and satiety.
Which hormones increase hunger?
The hormones ghrelin and neuropeptide Y increase hunger.
What is the satiety hormone called?
The satiety hormone is called leptin.
How can I control my hunger hormones?
You can control your hunger hormones by reducing carbohydrates and sugar while increasing protein and fat intake.
Studies click to expand!
2Austin J, Marks D. Hormonal regulators of appetite. Int J Pediatr Endocrinol. 2009;2009:141753. doi: 10.1155/2009/141753. Epub 2008 Dec 3. PubMed PMID: 19946401; PubMed Central PMCID: PMC2777281.
3Vergara RC, Jaramillo-Riveri S, Luarte A, Moënne-Loccoz C, Fuentes R, Couve A, Maldonado PE. The Energy Homeostasis Principle: Neuronal Energy Regulation Drives Local Network Dynamics Generating Behavior. Front Comput Neurosci. 2019;13:49. doi: 10.3389/fncom.2019.00049. eCollection 2019. PubMed PMID: 31396067; PubMed Central PMCID: PMC6664078.
4Austin J, Marks D. Hormonal regulators of appetite. Int J Pediatr Endocrinol. 2009;2009:141753. doi: 10.1155/2009/141753. Epub 2008 Dec 3. PubMed PMID: 19946401; PubMed Central PMCID: PMC2777281.
5Klok MD, Jakobsdottir S, Drent ML. The role of leptin and ghrelin in the regulation of food intake and body weight in humans: a review. Obes Rev. 2007 Jan;8(1):21-34. doi: 10.1111/j.1467-789X.2006.00270.x. Review. PubMed PMID: 17212793.
6Müller TD, Nogueiras R, Andermann ML, Andrews ZB, Anker SD, Argente J, Batterham RL, Benoit SC, Bowers CY, Broglio F, Casanueva FF, D’Alessio D, Depoortere I, Geliebter A, Ghigo E, Cole PA, Cowley M, Cummings DE, Dagher A, Diano S, Dickson SL, Diéguez C, Granata R, Grill HJ, Grove K, Habegger KM, Heppner K, Heiman ML, Holsen L, Holst B, Inui A, Jansson JO, Kirchner H, Korbonits M, Laferrère B, LeRoux CW, Lopez M, Morin S, Nakazato M, Nass R, Perez-Tilve D, Pfluger PT, Schwartz TW, Seeley RJ, Sleeman M, Sun Y, Sussel L, Tong J, Thorner MO, van der Lely AJ, van der Ploeg LH, Zigman JM, Kojima M, Kangawa K, Smith RG, Horvath T, Tschöp MH. Ghrelin. Mol Metab. 2015 Jun;4(6):437-60. doi: 10.1016/j.molmet.2015.03.005. eCollection 2015 Jun. Review. PubMed PMID: 26042199; PubMed Central PMCID: PMC4443295.
7Austin J, Marks D. Hormonal regulators of appetite. Int J Pediatr Endocrinol. 2009;2009:141753. doi: 10.1155/2009/141753. Epub 2008 Dec 3. PubMed PMID: 19946401; PubMed Central PMCID: PMC2777281.
8Klok MD, Jakobsdottir S, Drent ML. The role of leptin and ghrelin in the regulation of food intake and body weight in humans: a review. Obes Rev. 2007 Jan;8(1):21-34. doi: 10.1111/j.1467-789X.2006.00270.x. Review. PubMed PMID: 17212793.
9Friedman JM, Halaas JL. Leptin and the regulation of body weight in mammals. Nature. 1998 Oct 22;395(6704):763-70. doi: 10.1038/27376. Review. PubMed PMID: 9796811.
10Austin J, Marks D. Hormonal regulators of appetite. Int J Pediatr Endocrinol. 2009;2009:141753. doi: 10.1155/2009/141753. Epub 2008 Dec 3. PubMed PMID: 19946401; PubMed Central PMCID: PMC2777281.
11Myers MG Jr, Leibel RL, Seeley RJ, Schwartz MW. Obesity and leptin resistance: distinguishing cause from effect. Trends Endocrinol Metab. 2010 Nov;21(11):643-51. doi: 10.1016/j.tem.2010.08.002. Epub 2010 Sep 16. Review. PubMed PMID: 20846876; PubMed Central PMCID: PMC2967652.
12Martin SS, Qasim A, Reilly MP. Leptin resistance: a possible interface of inflammation and metabolism in obesity-related cardiovascular disease. J Am Coll Cardiol. 2008 Oct 7;52(15):1201-10. doi: 10.1016/j.jacc.2008.05.060. Review. PubMed PMID: 18926322; PubMed Central PMCID: PMC4556270.
13Lustig RH, Sen S, Soberman JE, Velasquez-Mieyer PA. Obesity, leptin resistance, and the effects of insulin reduction. Int J Obes Relat Metab Disord. 2004 Oct;28(10):1344-8. doi: 10.1038/sj.ijo.0802753. PubMed PMID: 15314628.
14Austin J, Marks D. Hormonal regulators of appetite. Int J Pediatr Endocrinol. 2009;2009:141753. doi: 10.1155/2009/141753. Epub 2008 Dec 3. PubMed PMID: 19946401; PubMed Central PMCID: PMC2777281.
15Beck B. Neuropeptide Y in normal eating and in genetic and dietary-induced obesity. Philos Trans R Soc Lond B Biol Sci. 2006 Jul 29;361(1471):1159-85. doi: 10.1098/rstb.2006.1855. Review. PubMed PMID: 16874931; PubMed Central PMCID: PMC1642692.
16Minor RK, Chang JW, de Cabo R. Hungry for life: How the arcuate nucleus and neuropeptide Y may play a critical role in mediating the benefits of calorie restriction. Mol Cell Endocrinol. 2009 Feb 5;299(1):79-88. doi: 10.1016/j.mce.2008.10.044. Epub 2008 Nov 11. Review. PubMed PMID: 19041366; PubMed Central PMCID: PMC2668104.
17Kuo LE, Kitlinska JB, Tilan JU, Li L, Baker SB, Johnson MD, Lee EW, Burnett MS, Fricke ST, Kvetnansky R, Herzog H, Zukowska Z. Neuropeptide Y acts directly in the periphery on fat tissue and mediates stress-induced obesity and metabolic syndrome. Nat Med. 2007 Jul;13(7):803-11. doi: 10.1038/nm1611. Epub 2007 Jul 1. PubMed PMID: 17603492.
18Reichmann F, Holzer P. Neuropeptide Y: A stressful review. Neuropeptides. 2016 Feb;55:99-109. doi: 10.1016/j.npep.2015.09.008. Epub 2015 Sep 30. Review. PubMed PMID: 26441327; PubMed Central PMCID: PMC4830398.
19McDonald RB, Ramsey JJ. Honoring Clive McCay and 75 years of calorie restriction research. J Nutr. 2010 Jul;140(7):1205-10. doi: 10.3945/jn.110.122804. Epub 2010 May 19. PubMed PMID: 20484554; PubMed Central PMCID: PMC2884327.
20Minor RK, Chang JW, de Cabo R. Hungry for life: How the arcuate nucleus and neuropeptide Y may play a critical role in mediating the benefits of calorie restriction. Mol Cell Endocrinol. 2009 Feb 5;299(1):79-88. doi: 10.1016/j.mce.2008.10.044. Epub 2008 Nov 11. Review. PubMed PMID: 19041366; PubMed Central PMCID: PMC2668104.
21Wu Y, He H, Cheng Z, Bai Y, Ma X. The Role of Neuropeptide Y and Peptide YY in the Development of Obesity via Gut-brain Axis. Curr Protein Pept Sci. 2019;20(7):750-758. doi: 10.2174/1389203720666190125105401. Review. PubMed PMID: 30678628.
22Pironi L, Stanghellini V, Miglioli M, Corinaldesi R, De Giorgio R, Ruggeri E, Tosetti C, Poggioli G, Morselli Labate AM, Monetti N. Fat-induced ileal brake in humans: a dose-dependent phenomenon correlated to the plasma levels of peptide YY. Gastroenterology. 1993 Sep;105(3):733-9. doi: 10.1016/0016-5085(93)90890-o. PubMed PMID: 8359644.
23Wu Y, He H, Cheng Z, Bai Y, Ma X. The Role of Neuropeptide Y and Peptide YY in the Development of Obesity via Gut-brain Axis. Curr Protein Pept Sci. 2019;20(7):750-758. doi: 10.2174/1389203720666190125105401. Review. PubMed PMID: 30678628.
24Zwirska-Korczala K, Konturek SJ, Sodowski M, Wylezol M, Kuka D, Sowa P, Adamczyk-Sowa M, Kukla M, Berdowska A, Rehfeld JF, Bielanski W, Brzozowski T. Basal and postprandial plasma levels of PYY, ghrelin, cholecystokinin, gastrin and insulin in women with moderate and morbid obesity and metabolic syndrome. J Physiol Pharmacol. 2007 Mar;58 Suppl 1:13-35. PubMed PMID: 17443025.
25Zouhal H, Sellami M, Saeidi A, Slimani M, Abbassi-Daloii A, Khodamoradi A, El Hage R, Hackney AC, Ben Abderrahman A. Effect of physical exercise and training on gastrointestinal hormones in populations with different weight statuses. Nutr Rev. 2019 Jul 1;77(7):455-477. doi: 10.1093/nutrit/nuz005. Review. PubMed PMID: 31125091.
26Cahill F, Shea JL, Randell E, Vasdev S, Sun G. Serum peptide YY in response to short-term overfeeding in young men. Am J Clin Nutr. 2011 Apr;93(4):741-7. doi: 10.3945/ajcn.110.003624. Epub 2011 Feb 2. PubMed PMID: 21289220.
27Müller TD, Finan B, Bloom SR, D’Alessio D, Drucker DJ, Flatt PR, Fritsche A, Gribble F, Grill HJ, Habener JF, Holst JJ, Langhans W, Meier JJ, Nauck MA, Perez-Tilve D, Pocai A, Reimann F, Sandoval DA, Schwartz TW, Seeley RJ, Stemmer K, Tang-Christensen M, Woods SC, DiMarchi RD, Tschöp MH. Glucagon-like peptide 1 (GLP-1). Mol Metab. 2019 Dec;30:72-130. doi: 10.1016/j.molmet.2019.09.010. Epub 2019 Sep 30. Review. PubMed PMID: 31767182; PubMed Central PMCID: PMC6812410.
28Zhang F, Tong Y, Su N, Li Y, Tang L, Huang L, Tong N. Weight loss effect of glucagon-like peptide-1 mimetics on obese/overweight adults without diabetes: A systematic review and meta-analysis of randomized controlled trials. J Diabetes. 2015 May;7(3):329-39. doi: 10.1111/1753-0407.12198. Epub 2014 Sep 10. Review. PubMed PMID: 25043423.
29Morínigo R, Moizé V, Musri M, Lacy AM, Navarro S, Marín JL, Delgado S, Casamitjana R, Vidal J. Glucagon-like peptide-1, peptide YY, hunger, and satiety after gastric bypass surgery in morbidly obese subjects. J Clin Endocrinol Metab. 2006 May;91(5):1735-40. doi: 10.1210/jc.2005-0904. Epub 2006 Feb 14. PubMed PMID: 16478824.
30Müller TD, Finan B, Bloom SR, D’Alessio D, Drucker DJ, Flatt PR, Fritsche A, Gribble F, Grill HJ, Habener JF, Holst JJ, Langhans W, Meier JJ, Nauck MA, Perez-Tilve D, Pocai A, Reimann F, Sandoval DA, Schwartz TW, Seeley RJ, Stemmer K, Tang-Christensen M, Woods SC, DiMarchi RD, Tschöp MH. Glucagon-like peptide 1 (GLP-1). Mol Metab. 2019 Dec;30:72-130. doi: 10.1016/j.molmet.2019.09.010. Epub 2019 Sep 30. Review. PubMed PMID: 31767182; PubMed Central PMCID: PMC6812410.
31Anandhakrishnan A, Korbonits M. Glucagon-like peptide 1 in the pathophysiology and pharmacotherapy of clinical obesity. World J Diabetes. 2016 Dec 15;7(20):572-598. doi: 10.4239/wjd.v7.i20.572. Review. PubMed PMID: 28031776; PubMed Central PMCID: PMC5155232.
32Stinson SE, Jonsson AE, Lund MAV, Frithioff-Bøjsøe C, Aas Holm L, Pedersen O, Ängquist L, Sørensen TIA, Holst JJ, Christiansen M, Holm JC, Hartmann B, Hansen T. Fasting Plasma GLP-1 Is Associated With Overweight/Obesity and Cardiometabolic Risk Factors in Children and Adolescents. J Clin Endocrinol Metab. 2021 May 13;106(6):1718-1727. doi: 10.1210/clinem/dgab098. PubMed PMID: 33596309; PubMed Central PMCID: PMC8118577.
33Gibbs J, Young RC, Smith GP. Cholecystokinin elicits satiety in rats with open gastric fistulas. Nature. 1973 Oct 12;245(5424):323-5. doi: 10.1038/245323a0. PubMed PMID: 4586439.
34Konturek JW, Konturek SJ, Kwiecień N, Bielański W, Pawlik T, Rembiasz K, Domschke W. Leptin in the control of gastric secretion and gut hormones in humans infected with Helicobacter pylori. Scand J Gastroenterol. 2001 Nov;36(11):1148-54. doi: 10.1080/00365520152584761. PubMed PMID: 11686213.
35Peters JH, Simasko SM, Ritter RC. Modulation of vagal afferent excitation and reduction of food intake by leptin and cholecystokinin. Physiol Behav. 2006 Nov 30;89(4):477-85. doi: 10.1016/j.physbeh.2006.06.017. Epub 2006 Jul 26. Review. PubMed PMID: 16872644.
36Liddle RA, Goldfine ID, Rosen MS, Taplitz RA, Williams JA. Cholecystokinin bioactivity in human plasma. Molecular forms, responses to feeding, and relationship to gallbladder contraction. J Clin Invest. 1985 Apr;75(4):1144-52. doi: 10.1172/JCI111809. PubMed PMID: 2580857; PubMed Central PMCID: PMC425438.
37Okonkwo O, Zezoff D, Adeyinka A. Biochemistry, Cholecystokinin. [Updated 2021 May 9]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2022 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK534204/
38Dockray GJ. Cholecystokinin. Curr Opin Endocrinol Diabetes Obes. 2012 Feb;19(1):8-12. doi: 10.1097/MED.0b013e32834eb77d. Review. PubMed PMID: 22157397.
39Lieverse RJ, Jansen JB, Masclee AA, Lamers CB. Satiety effects of a physiological dose of cholecystokinin in humans. Gut. 1995 Feb;36(2):176-9. doi: 10.1136/gut.36.2.176. PubMed PMID: 7883212; PubMed Central PMCID: PMC1382399.
40Cawthon CR, de La Serre CB. The critical role of CCK in the regulation of food intake and diet-induced obesity. Peptides. 2021 Apr;138:170492. doi: 10.1016/j.peptides.2020.170492. Epub 2021 Jan 8. Review. PubMed PMID: 33422646.
41Müller TD, Nogueiras R, Andermann ML, Andrews ZB, Anker SD, Argente J, Batterham RL, Benoit SC, Bowers CY, Broglio F, Casanueva FF, D’Alessio D, Depoortere I, Geliebter A, Ghigo E, Cole PA, Cowley M, Cummings DE, Dagher A, Diano S, Dickson SL, Diéguez C, Granata R, Grill HJ, Grove K, Habegger KM, Heppner K, Heiman ML, Holsen L, Holst B, Inui A, Jansson JO, Kirchner H, Korbonits M, Laferrère B, LeRoux CW, Lopez M, Morin S, Nakazato M, Nass R, Perez-Tilve D, Pfluger PT, Schwartz TW, Seeley RJ, Sleeman M, Sun Y, Sussel L, Tong J, Thorner MO, van der Lely AJ, van der Ploeg LH, Zigman JM, Kojima M, Kangawa K, Smith RG, Horvath T, Tschöp MH. Ghrelin. Mol Metab. 2015 Jun;4(6):437-60. doi: 10.1016/j.molmet.2015.03.005. eCollection 2015 Jun. Review. PubMed PMID: 26042199; PubMed Central PMCID: PMC4443295.
42Blom WA, Lluch A, Stafleu A, Vinoy S, Holst JJ, Schaafsma G, Hendriks HF. Effect of a high-protein breakfast on the postprandial ghrelin response. Am J Clin Nutr. 2006 Feb;83(2):211-20. doi: 10.1093/ajcn/83.2.211. PubMed PMID: 16469977.
43White BD, He B, Dean RG, Martin RJ. Low protein diets increase neuropeptide Y gene expression in the basomedial hypothalamus of rats. J Nutr. 1994 Aug;124(8):1152-60. doi: 10.1093/jn/124.8.1152. PubMed PMID: 8064364.
44Beck B. Neuropeptide Y in normal eating and in genetic and dietary-induced obesity. Philos Trans R Soc Lond B Biol Sci. 2006 Jul 29;361(1471):1159-85. doi: 10.1098/rstb.2006.1855. Review. PubMed PMID: 16874931; PubMed Central PMCID: PMC1642692.
45Parra D, Ramel A, Bandarra N, Kiely M, Martínez JA, Thorsdottir I. A diet rich in long chain omega-3 fatty acids modulates satiety in overweight and obese volunteers during weight loss. Appetite. 2008 Nov;51(3):676-80. doi: 10.1016/j.appet.2008.06.003. Epub 2008 Jun 14. PubMed PMID: 18602429.
46Teff KL, Elliott SS, Tschöp M, Kieffer TJ, Rader D, Heiman M, Townsend RR, Keim NL, D’Alessio D, Havel PJ. Dietary fructose reduces circulating insulin and leptin, attenuates postprandial suppression of ghrelin, and increases triglycerides in women. J Clin Endocrinol Metab. 2004 Jun;89(6):2963-72. doi: 10.1210/jc.2003-031855. PubMed PMID: 15181085.
47Lustig RH. Fructose: it’s “alcohol without the buzz”. Adv Nutr. 2013 Mar 1;4(2):226-35. doi: 10.3945/an.112.002998. PubMed PMID: 23493539; PubMed Central PMCID: PMC3649103.
48Shapiro A, Mu W, Roncal C, Cheng KY, Johnson RJ, Scarpace PJ. Fructose-induced leptin resistance exacerbates weight gain in response to subsequent high-fat feeding. Am J Physiol Regul Integr Comp Physiol. 2008 Nov;295(5):R1370-5. doi: 10.1152/ajpregu.00195.2008. Epub 2008 Aug 13. PubMed PMID: 18703413; PubMed Central PMCID: PMC2584858.
49Shapiro A, Mu W, Roncal C, Cheng KY, Johnson RJ, Scarpace PJ. Fructose-induced leptin resistance exacerbates weight gain in response to subsequent high-fat feeding. Am J Physiol Regul Integr Comp Physiol. 2008 Nov;295(5):R1370-5. doi: 10.1152/ajpregu.00195.2008. Epub 2008 Aug 13. PubMed PMID: 18703413; PubMed Central PMCID: PMC2584858.
50Lomenick JP, Melguizo MS, Mitchell SL, Summar ML, Anderson JW. Effects of meals high in carbohydrate, protein, and fat on ghrelin and peptide YY secretion in prepubertal children. J Clin Endocrinol Metab. 2009 Nov;94(11):4463-71. doi: 10.1210/jc.2009-0949. Epub 2009 Oct 9. PubMed PMID: 19820013; PubMed Central PMCID: PMC2775646.
51Buyken AE, Goletzke J, Joslowski G, Felbick A, Cheng G, Herder C, Brand-Miller JC. Association between carbohydrate quality and inflammatory markers: systematic review of observational and interventional studies. Am J Clin Nutr. 2014 Apr;99(4):813-33. doi: 10.3945/ajcn.113.074252. Epub 2014 Feb 19. Review. PubMed PMID: 24552752.
52Gagnon J, Sauvé M, Zhao W, Stacey HM, Wiber SC, Bolz SS, Brubaker PL. Chronic Exposure to TNFα Impairs Secretion of Glucagon-Like Peptide-1. Endocrinology. 2015 Nov;156(11):3950-60. doi: 10.1210/en.2015-1361. Epub 2015 Aug 13. PubMed PMID: 26270730.
53Marchix J, Choque B, Kouba M, Fautrel A, Catheline D, Legrand P. Excessive dietary linoleic acid induces proinflammatory markers in rats. J Nutr Biochem. 2015 Dec;26(12):1434-41. doi: 10.1016/j.jnutbio.2015.07.010. Epub 2015 Jul 30. PubMed PMID: 26337666.
54Bodnaruc AM, Prud’homme D, Blanchet R, Giroux I. Nutritional modulation of endogenous glucagon-like peptide-1 secretion: a review. Nutr Metab (Lond). 2016;13:92. doi: 10.1186/s12986-016-0153-3. eCollection 2016. Review. PubMed PMID: 27990172; PubMed Central PMCID: PMC5148911.
55Dockray GJ. Cholecystokinin. Curr Opin Endocrinol Diabetes Obes. 2012 Feb;19(1):8-12. doi: 10.1097/MED.0b013e32834eb77d. Review. PubMed PMID: 22157397.
56Dirlewanger M, di Vetta V, Guenat E, Battilana P, Seematter G, Schneiter P, Jéquier E, Tappy L. Effects of short-term carbohydrate or fat overfeeding on energy expenditure and plasma leptin concentrations in healthy female subjects. Int J Obes Relat Metab Disord. 2000 Nov;24(11):1413-8. doi: 10.1038/sj.ijo.0801395. PubMed PMID: 11126336.
57Pironi L, Stanghellini V, Miglioli M, Corinaldesi R, De Giorgio R, Ruggeri E, Tosetti C, Poggioli G, Morselli Labate AM, Monetti N. Fat-induced ileal brake in humans: a dose-dependent phenomenon correlated to the plasma levels of peptide YY. Gastroenterology. 1993 Sep;105(3):733-9. doi: 10.1016/0016-5085(93)90890-o. PubMed PMID: 8359644.
58Chungchunlam SM, Henare SJ, Ganesh S, Moughan PJ. Dietary whey protein influences plasma satiety-related hormones and plasma amino acids in normal-weight adult women. Eur J Clin Nutr. 2015 Feb;69(2):179-86. doi: 10.1038/ejcn.2014.266. Epub 2015 Jan 7. PubMed PMID: 25563737.
59Gillespie AL, Calderwood D, Hobson L, Green BD. Whey proteins have beneficial effects on intestinal enteroendocrine cells stimulating cell growth and increasing the production and secretion of incretin hormones. Food Chem. 2015 Dec 15;189:120-8. doi: 10.1016/j.foodchem.2015.02.022. Epub 2015 Feb 18. PubMed PMID: 26190610.
60Rubio IG, Castro G, Zanini AC, Medeiros-Neto G. Oral ingestion of a hydrolyzed gelatin meal in subjects with normal weight and in obese patients: Postprandial effect on circulating gut peptides, glucose and insulin. Eat Weight Disord. 2008 Mar;13(1):48-53. doi: 10.1007/BF03327784. PubMed PMID: 18319637.
61Lomenick JP, Melguizo MS, Mitchell SL, Summar ML, Anderson JW. Effects of meals high in carbohydrate, protein, and fat on ghrelin and peptide YY secretion in prepubertal children. J Clin Endocrinol Metab. 2009 Nov;94(11):4463-71. doi: 10.1210/jc.2009-0949. Epub 2009 Oct 9. PubMed PMID: 19820013; PubMed Central PMCID: PMC2775646.
62Spiegel K, Leproult R, L’hermite-Balériaux M, Copinschi G, Penev PD, Van Cauter E. Leptin levels are dependent on sleep duration: relationships with sympathovagal balance, carbohydrate regulation, cortisol, and thyrotropin. J Clin Endocrinol Metab. 2004 Nov;89(11):5762-71. doi: 10.1210/jc.2004-1003. PubMed PMID: 15531540.
63Mosavat M, Mirsanjari M, Arabiat D, Smyth A, Whitehead L. The Role of Sleep Curtailment on Leptin Levels in Obesity and Diabetes Mellitus. Obes Facts. 2021;14(2):214-221. doi: 10.1159/000514095. Epub 2021 Mar 23. Review. PubMed PMID: 33756469; PubMed Central PMCID: PMC8138234.
64Cooper CB, Neufeld EV, Dolezal BA, Martin JL. Sleep deprivation and obesity in adults: a brief narrative review. BMJ Open Sport Exerc Med. 2018;4(1):e000392. doi: 10.1136/bmjsem-2018-000392. eCollection 2018. PubMed PMID: 30364557; PubMed Central PMCID: PMC6196958.
65Lin J, Jiang Y, Wang G, Meng M, Zhu Q, Mei H, Liu S, Jiang F. Associations of short sleep duration with appetite-regulating hormones and adipokines: A systematic review and meta-analysis. Obes Rev. 2020 Nov;21(11):e13051. doi: 10.1111/obr.13051. Epub 2020 Jun 15. Review. PubMed PMID: 32537891.
66Cooper CB, Neufeld EV, Dolezal BA, Martin JL. Sleep deprivation and obesity in adults: a brief narrative review. BMJ Open Sport Exerc Med. 2018;4(1):e000392. doi: 10.1136/bmjsem-2018-000392. eCollection 2018. PubMed PMID: 30364557; PubMed Central PMCID: PMC6196958.
67Kang S, Kim KB, Shin KO. Exercise training improves leptin sensitivity in peripheral tissue of obese rats. Biochem Biophys Res Commun. 2013 Jun 7;435(3):454-9. doi: 10.1016/j.bbrc.2013.05.007. Epub 2013 May 11. PubMed PMID: 23669042.
68Jones TE, Basilio JL, Brophy PM, McCammon MR, Hickner RC. Long-term exercise training in overweight adolescents improves plasma peptide YY and resistin. Obesity (Silver Spring). 2009 Jun;17(6):1189-95. doi: 10.1038/oby.2009.11. Epub 2009 Feb 26. PubMed PMID: 19247279; PubMed Central PMCID: PMC3845441.
69Zouhal H, Sellami M, Saeidi A, Slimani M, Abbassi-Daloii A, Khodamoradi A, El Hage R, Hackney AC, Ben Abderrahman A. Effect of physical exercise and training on gastrointestinal hormones in populations with different weight statuses. Nutr Rev. 2019 Jul 1;77(7):455-477. doi: 10.1093/nutrit/nuz005. Review. PubMed PMID: 31125091.
70Khajehnasiri N, Khazali H, Sheikhzadeh F, Ghowsi M. One-month of high-intensity exercise did not change the food intake and the hypothalamic arcuate nucleus proopiomelanocortin and neuropeptide Y expression levels in male Wistar rats. Endocr Regul. 2019 Jan 1;53(1):8-13. doi: 10.2478/enr-2019-0002. PubMed PMID: 31517616.
71Benite-Ribeiro SA, Putt DA, Santos JM. The effect of physical exercise on orexigenic and anorexigenic peptides and its role on long-term feeding control. Med Hypotheses. 2016 Aug;93:30-3. doi: 10.1016/j.mehy.2016.05.005. Epub 2016 May 11. PubMed PMID: 27372853.
72Melanson EL, Keadle SK, Donnelly JE, Braun B, King NA. Resistance to exercise-induced weight loss: compensatory behavioral adaptations. Med Sci Sports Exerc. 2013 Aug;45(8):1600-9. doi: 10.1249/MSS.0b013e31828ba942. Review. PubMed PMID: 23470300; PubMed Central PMCID: PMC3696411.
73Shapiro A, Mu W, Roncal C, Cheng KY, Johnson RJ, Scarpace PJ. Fructose-induced leptin resistance exacerbates weight gain in response to subsequent high-fat feeding. Am J Physiol Regul Integr Comp Physiol. 2008 Nov;295(5):R1370-5. doi: 10.1152/ajpregu.00195.2008. Epub 2008 Aug 13. PubMed PMID: 18703413; PubMed Central PMCID: PMC2584858.
74Deemer SE, Plaisance EP, Martins C. Impact of ketosis on appetite regulation-a review. Nutr Res. 2020 May;77:1-11. doi: 10.1016/j.nutres.2020.02.010. Epub 2020 Feb 20. Review. PubMed PMID: 32193016.
75Essah PA, Levy JR, Sistrun SN, Kelly SM, Nestler JE. Effect of macronutrient composition on postprandial peptide YY levels. J Clin Endocrinol Metab. 2007 Oct;92(10):4052-5. doi: 10.1210/jc.2006-2273. Epub 2007 Aug 28. PubMed PMID: 17726080.
76Michalsen A, Schlegel F, Rodenbeck A, Lüdtke R, Huether G, Teschler H, Dobos GJ. Effects of short-term modified fasting on sleep patterns and daytime vigilance in non-obese subjects: results of a pilot study. Ann Nutr Metab. 2003;47(5):194-200. doi: 10.1159/000070485. PubMed PMID: 12748412.