← Blog

14 November 2026

Obesity is not just about excess calories. How do hormones regulate hunger, satiety and body weight?

obesity

Obesity is a chronic, relapsing disease whose development depends on the interplay of many biological, environmental and behavioural factors. Although weight gain is linked to a sustained positive energy balance, the mechanisms behind it are far more complex than they might seem. How much we eat, when we feel hungry, how quickly we feel full and how much energy our body uses are all regulated by the nervous system and by hormones. Understanding these mechanisms helps explain why maintaining a healthy body weight can be difficult, why weight is so often regained after losing it, and why treating obesity should not come down to simply advising people to eat less.

What is obesity and why does it develop?

Obesity is defined as a chronic disease characterised by excessive accumulation of body fat that may harm health. In everyday practice we use body mass index (BMI) for an initial assessment of body weight, but it does not show body composition or where fat is distributed. Assessment of a patient should therefore also take into account waist circumference, the presence of metabolic complications and a history of weight changes.

The development of obesity is influenced by, among others:

In most patients no single cause of obesity can be identified. The disease develops gradually as many factors accumulate.

What is energy balance and how does it affect body weight?

Energy balance is the difference between the energy the body receives from food and the energy it expends. If, over a longer period, we take in more energy than we use, the excess may be stored, mainly as body fat. If energy expenditure exceeds intake, the body draws on its stores, which leads to weight loss. This does not mean, however, that energy balance is a fixed value fully controlled by conscious decisions.

What does total energy expenditure consist of?

Total energy expenditure consists of:

Basal metabolic rate usually accounts for the largest part of daily energy expenditure, but its share depends on age, body composition and activity level. In practice, differences in spontaneous physical activity can be particularly important. Two people doing similar workouts may differ considerably in total energy expenditure because of how they spend the rest of the day.

Why does the body start to conserve energy during weight loss?

During weight loss, energy expenditure usually decreases. In part this is because a smaller body needs less energy to function and move. In addition, adaptive mechanisms may appear, referred to as adaptive thermogenesis. This means that energy expenditure may fall by more than would be explained by the change in body mass and composition alone. At the same time, the body may strengthen hunger signals and increase the motivation to eat. This is one reason why maintaining a reduced body weight is often harder than the initial weight loss.

How does the brain control hunger and satiety?

Food intake is regulated mainly in the central nervous system. The hypothalamus is particularly important: it integrates information about energy availability, nutritional status and hormonal signals from other organs. The arcuate nucleus of the hypothalamus contains, among others, two populations of neurons with opposing effects.

NPY/AgRP neurons stimulate food intake and take part in the body's response to energy deficiency.

POMC/CART neurons take part in suppressing appetite and regulating energy expenditure.

Their activity is modified by hormones and metabolic signals that tell the brain about the body's current energy state. Eating, however, does not depend only on physiological hunger. The reward system also plays an important role: food can be a source of pleasure, and the sight, smell or availability of food can stimulate the desire to eat even when the body does not need extra energy.

Which hormones affect food intake?

Leptin, the signal about energy stores

Leptin is a hormone produced mainly by adipose tissue. Its level usually rises with the amount of body fat. Leptin tells the brain about the availability of energy stores. Under normal conditions it helps suppress hunger and regulate energy expenditure. So why can people with obesity, who often have high leptin levels, still feel strong hunger?

One mechanism is reduced sensitivity of the central nervous system to leptin, known as leptin resistance. This means that despite a high level of the hormone, its appetite-regulating effect may be weakened. Importantly, during weight loss leptin levels fall. The body may interpret this change as a signal of decreasing energy availability, which promotes stronger hunger and lower energy expenditure.

Ghrelin, a hormone linked to feeling hungry

Ghrelin is produced mainly in the stomach and takes part in stimulating appetite. Its level often rises before a meal and falls after eating, although this relationship is not the same in everyone. Ghrelin acts, among other things, on NPY/AgRP neurons in the hypothalamus, increasing the motivation to eat. During weight loss, ghrelin levels may rise, which is one of the mechanisms making it harder to maintain results in the long term.

GLP-1, a gut hormone that affects satiety

GLP-1, or glucagon-like peptide 1, is an incretin hormone secreted mainly by L cells of the intestine in response to food intake.

Its effects include:

Natural GLP-1 is rapidly broken down by the enzyme DPP-4, so its action is short-lived. The action of GLP-1 receptor agonists, used among other things in the treatment of obesity and type 2 diabetes, is based on this pathway. These drugs are not identical to the natural hormone, however. They were designed so that their action lasts much longer and produces a stronger and more lasting pharmacological effect.

GIP and its role in metabolism

GIP, or glucose-dependent insulinotropic polypeptide, is the second important incretin hormone. It is secreted by K cells of the small intestine in response to nutrients. Like GLP-1, GIP increases insulin secretion in a glucose-dependent manner. Its action is more complex, however, and also includes effects on glucagon secretion, adipose tissue metabolism and mechanisms regulating food intake. Unlike GLP-1, whose appetite-reducing action is well understood, the physiological role of GIP in regulating body weight remains the subject of research.

Interestingly, drugs that activate both GIP and GLP-1 receptors can lead to very large weight reduction.

An example is tirzepatide, which uses both hormonal pathways. This does not mean, however, that raising the level of natural GIP in the body would by itself produce the same effect as pharmacological treatment.

Other hormones involved in regulating satiety

Food intake is also influenced by other hormones secreted in the digestive tract.

They include, among others:

Appetite regulation therefore does not depend on a single hormone. It is the result of many signals working together, which may reinforce or weaken one another.

Why does insulin also affect body weight regulation?

Insulin is a hormone produced by the beta cells of the pancreas. Its basic role is to regulate carbohydrate metabolism and to help maintain a normal blood glucose level.

Insulin:

Insulin is therefore not only a hormone regulating glucose levels, but also one of the signals involved in the long-term regulation of energy balance. This does not mean, however, that insulin secretion alone is the cause of obesity. Weight gain depends on the long-term relationship between energy intake and expenditure, which is influenced by many mechanisms.

What is insulin resistance and why does it often accompany obesity?

Insulin resistance means a reduced response of tissues to the action of insulin. In this situation the body may need a larger amount of the hormone to achieve a similar metabolic effect. In the early stages the pancreas often compensates for the reduced tissue sensitivity by increasing insulin secretion. As a result, the glucose level may remain normal for a long time.

Insulin resistance is not, however, a separate disease diagnosed solely on the basis of a raised insulin level. It is a metabolic disorder that can occur in various physiological and pathological states.

How does adipose tissue contribute to the development of insulin resistance?

Adipose tissue is not just an energy store. It is also an active endocrine organ that secretes many substances affecting metabolism and immune function. Of particular importance is excessive accumulation of visceral fat and the deposition of lipids in organs that are not adapted to storing them for long periods.

The development of insulin resistance may be promoted by:

As insulin resistance develops, the liver may respond less to the inhibitory action of insulin and so produce excessive amounts of glucose. Skeletal muscles, in turn, may use glucose less efficiently. If the beta cells of the pancreas can no longer compensate for the increased demand for insulin, carbohydrate metabolism disorders progress and, in some patients, type 2 diabetes develops.

Does insulin resistance cause obesity?

The relationship between obesity and insulin resistance is complex and works in both directions. Excessive accumulation of fat tissue, especially visceral and ectopic fat, is one of the main factors promoting insulin resistance. At the same time, metabolic and hormonal disorders may affect how energy is stored and how adipose tissue functions. It cannot be said, however, that insulin resistance is a universal cause of obesity. Not everyone with obesity has significant insulin resistance, and not everyone with insulin resistance has obesity.

Importantly, weight reduction, regular physical activity and better metabolic fitness can increase tissue sensitivity to insulin.

Can hormones be a cause of weight gain?

Some endocrine diseases can indeed promote weight gain or a change in the distribution of body fat.

The most important include:

It is worth remembering, however, that classic hormonal diseases account for only some cases of weight gain. For example, hypothyroidism can lead to moderate weight gain, partly related to water retention. It is rarely the only explanation for significant obesity.

Similarly, a raised insulin level in a person with obesity does not automatically mean that the cause of the disease is a primary hormonal disorder.

Endocrine diagnostics should therefore be based on history, physical examination and symptoms, not on routinely measuring all hormones in every patient.

Why is it so easy to regain weight after losing it?

The human body has extensive mechanisms that protect against energy deficiency. During weight loss, hormonal and metabolic changes occur that may promote eating more again.

Among other things, the following are observed:

Not all of these changes occur to the same degree in every patient. Their intensity depends, among other things, on the amount of weight lost, how long the loss took and individual biological factors. This is precisely why obesity is a relapsing disease, and maintaining the effects of treatment often requires long-term management.

How do modern drugs used to treat obesity work?

Modern pharmacotherapy for obesity makes use of, among others, the hormonal mechanisms involved in regulating appetite and metabolism.

GLP-1 receptor agonists, such as semaglutide, act on the receptors for this hormone, leading among other things to reduced hunger, increased satiety and a smaller amount of food eaten.

Tirzepatide, in turn, is a dual agonist of the GIP and GLP-1 receptors.

By acting on hormonal pathways linked to the regulation of food intake, these drugs can lead to significant weight reduction. It is important, however, to distinguish the action of natural incretins from the pharmacological effect. Natural GLP-1 and GIP are secreted in response to a meal, and their action is relatively short-lived. The drugs, by contrast, were designed so that activation of the relevant receptors lasts much longer.

Pharmacotherapy does not abolish the rules of energy balance. It helps to influence the mechanisms that regulate how much food is eaten, which can make it easier to achieve and maintain a negative energy balance.

Treatment should be chosen individually, taking into account indications, contraindications, possible adverse effects and a long-term treatment plan.

Can the hunger and satiety hormones be influenced without medication?

Everyday habits can affect hunger, satiety and the amount of food eaten. This does not mean, however, that a suitable diet can produce an effect comparable to pharmacological activation of GLP-1 or GIP receptors.

In practice, it is worth paying attention to a few elements.

An adequate amount of protein in the diet

Protein promotes satiety, and an adequate intake also helps limit loss of muscle mass during weight reduction.

Foods rich in fibre

Fibre can increase the volume of a meal, affect the rate of gastric emptying and support the feeling of fullness.

Regular physical activity

Exercise increases energy expenditure, improves tissue sensitivity to insulin and helps maintain metabolic fitness. A combination of aerobic activity and resistance training is particularly valuable.

Enough sleep

Lack of sleep can increase appetite, heighten the response to food cues and promote higher energy intake.

The food environment

Availability of high-energy foods, portion size, frequent snacking and eating in response to external cues can make it harder to regulate how much food is eaten. It is worth remembering that a healthy lifestyle is a fundamental part of obesity treatment, but in some patients it is not enough to achieve and maintain clinically significant weight reduction in the long term.

Why should obesity treatment be long-term?

Obesity is not merely the consequence of individual dietary decisions. It is a disease in which the biological mechanisms regulating appetite, energy expenditure and energy storage are important. Effective treatment should therefore include not only weight reduction but also preventing weight regain and improving metabolic health. Depending on the clinical situation, management may include:

There is no single treatment scheme that suits everyone.

What to remember about obesity and hormones

Energy balance remains the basic mechanism determining changes in body weight. It is not, however, independent of the body's biology. Hormones such as leptin, ghrelin, GLP-1, GIP and insulin take part in regulating hunger, satiety, metabolism and the way energy is used. As obesity develops, metabolic disorders may appear, including insulin resistance, which increase the risk of type 2 diabetes and other complications. During weight loss, in turn, the body activates adaptive mechanisms that may intensify hunger and reduce energy expenditure.

Understanding these relationships makes it possible to see the treatment of obesity not as a short-term diet but as long-term medical management aimed at improving health.

This article is for educational purposes and does not replace an individual medical consultation.

Need a consultation? Book a visit or see the types of visits.