Understanding Hunger and Fullness Cues

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Gastrointestinal regulation of food intake
Adiponectin acts in the brain to decrease body weight. Acute effects of leptin require PI3K signaling in hypothalamic proopiomelanocortin neurons in mice. Glucose-sensing in glucagon-like peptidesecreting cells. Therefore, gut-hindbrain communication is sufficient for satiation, although this normally interacts with higher cognitive centers to regulate feeding. They produce two different proteins that inhibit hunger: The ability of adiponectin to decrease food intake was dependent on AdipoR1 [ 64 ].

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Hunger (motivational state)

Genetic variations that cause increased appetite or reduced satiety are the major contributors to overeating. In an environment of food surplus, people carrying these genetic variants are at a much greater risk for overweight and obesity. Appetite and satiety are regulated by signals at three levels in the human body: Cellular sensors detect energy levels inside the cell and initiate various processes in response. This protein complex has three subunits and detects the intracellular AMP: It carries and transfers energy to other molecules to fuel all physiological processes.

ATP ratio indicates a lower energy supply, which activates the AMPK cascade, thereby mobilizing carbohydrate and lipid oxidation pathways to generate more energy while suppressing many synthesis pathways to conserve energy at the same time. Peripheral signals are generated by peripheral systems such as the gut, fat tissue, the liver and the pancreas in response to food ingestion as well as the energy status of the body.

There are two types of peripheral signals: Episodic signals are mainly involved in short-term meal to meal while tonic signals are mainly involved in long-term days and weeks regulation of appetite and satiety.

Episodic signals are mainly triggered by glucose levels inside cells. When you begin to eat, ingested food moves into the gastrointestinal tract where the volume and nutritive content are sensed by mechanical and chemosensory mechanisms.

Depending on the type of foods you eat, different hormones or signal molecules are produced in the gastrointestinal tract. For example, CCK cholescystokinin is mainly produced in response to protein and fat ingestion while GLP-1 and PYY are produced in response to carbohydrate and fat ingestion. Tonic signals are mediated by the amount of energy stored as fat in your body. The major tonic signal is leptin, a hormone that is produced in fat tissue, which travels through the bloodstream and functions in the hypothalamus of the brain.

Leptin also regulates the genes involved in basal metabolism. Higher leptin levels are associated with increased basal metabolism and lower levels are associated with decreased basal metabolism. Ultimately, appetite and the desire to eat is determined by the integration of all signals in two neuronal systems in the CNS: It is mainly controlled by two types of neurons in the hypothalamus of the human brain. The hedonic system is controlled by neurons in the limbic regions and the cerebral cortex.

This system controls food choice based on the appearance, smell and taste of foods known from past experience.

Because of this, the hedonic system controls not only food choice but also many other emotional and cognitive aspects in relation to happiness. An impaired hedonic control system often leads to overconsumption of more palatable foods which are often very energy-dense and consequently overconsumption and weight gain.

Genetic mutations in the appetite and satiety signaling systems have also been reported to cause extreme obesity due to an abnormally large appetite. For example, mutations in the LEP gene which makes the tonic satiety signal leptin, often lead to infants constantly feeling hungry and demanding food.

These children often become morbidly obese before their teens and require clinical attention. However, these kinds of mutations are relatively rare in the general population. In comparison, many overweight and obesity risk genes are widely distributed in the human population Table 2. These risk genes predispose their carriers to overweight and obesity if they live in an obesogenic environment with easy access to food and limited physical activity.

Many of them are associated with overeating behavior due to their effect on satiety. People who carry the risk gene variants often overeat without being aware of it. For example, people carrying one or two risk alleles of the FTO gene are less sensitive to satiety signals and may not sense fullness even when they have already eaten more than enough.

However, in our current state of constant food surplus, there is less opportunity to expend excess stored energy and these variants become a health hazard. There are also risk variants, unrelated to satiety, that affect the hedonic system and cause increased energy intake. For example, the DRD2 gene codes for a dopamine receptor that leads to food cravings while the OPRM1 gene codes for a receptor of opioids that causes food preferences.

Obesity risk genes involved in processes other than energy intake have also been reported. For example, certain ADIPOQ gene variant carriers have a reduced basal metabolic rate which results in lower total energy expenditure compared to non-carriers. However, the number and effects of the risk genes involved in energy expenditure are generally less than those involved in energy intake. AMPK is a key sensor and regulator of energy balance at the cellular level.

Its activity is regulated by the ratio of AMP: ATP inside a cell. ATP ratio indicates a lower energy supply and vice versa. AMPK is a heterotrimer comprised of a catalytic alpha-subunit and regulatory beta- and gamma-subunits.

AMPK signaling in energy balance regulation. During times of energy shortage, AMPK is activated in peripheral tissues to favor local ATP production, and in the brain, to stimulate neuroendocrine pathways that increase food intake.

AMPK is also regulated by exercise, metabolic stressors and hormones, and cytokines that affect whole-body energy balance such as leptin, adiponectin, resistin, ghrelin and cannabinoids. Agonists of AMPK have been under development by pharmaceutical companies as potential treatments for obesity Hardie, Peripheral signals are generated in response to food ingestion. They are classified as either episodic or tonic signals.

Episodic signals are short-term and produced between meals eating episodes. They impact our decisions about when and how much to eat. Tonic signals are generated by the body's response to nutrition status in the long term days or weeks.

They potentiate the magnitude of episodic signals and cause us to subconsciously adjust meal frequency and size Fig. Variations of the genes involved in these signaling processes, such as LEP and LEPR, are normally rare but are associated with severe obesity symptoms when they occur.

The main energy balance control signals in human body adopted from Blundell et al, When blood glucose levels drop below a threshold comparable to hypoglycemia level, about 1mM , the expression of ghrelin is activated. It is released into the bloodstream and eventually reaches the arcuate nucleus of the hypothalamus ARC where it activates the expression of agouti-related protein AgRP and neuropeptide Y NPY.

For example, hormones such as epinephrine and norepinephrine stimulate ghrelin release while insulin and somatostatin a peptide hormone produced in the hypothalamus inhibit release Fig 3. Ghrelin is encoded by the GHRL gene. Obestatin is involved in satiety and decreased food intake in rats Zhang et al, , but its function in the human body is less understood. The 28 amino acid ghrelin peptide is inactive until it is acetylated on Ser3 by a medium-chain C8—C10 fatty acid.

It is believed that the acetylation and secretion of ghrelin are regulated differently. Several mutations and polymorphisms of the GHRL gene have been associated with various degrees of obesity, but reports in literature are inconclusive and inconsistent. However, increased ghrelin levels have been reported in individuals with anorexia, which suggests ghrelin resistance may play a role in this condition. Cholecystokinin CCK is an incretin.

Incretin is a group of gastrointestinal hormones that increase insulin in response to intestinal nutrients. CCK is released in the small intestine where it acts in the vagal nervous system to increase satiety. Aromatic amino acids phenylalanine, tryptophan, histidine and tyrosine from dietary protein digestion stimulate CCK release through the extracellular calcium-sensing receptor CaSR. The signal is then transmitted from the vagus nerve to the brain stem where it is relayed to the hypothalamic region and is integrated with other signals to determine whether to stop or continue eating.

Several drugs target the CCK pathway for weight control. Glucagon-like peptide-1 GLP-1 is another incretin hormone. It is synthesized in the gut and released into the bloodstream. GLP-1 also delays gastric emptying transfer of the partially digested food mixture from the stomach to the small intestine and prolongs the feeling of fullness.

The effect of GLP 2 is localized in the gastrointestinal tract. Its main functions include increasing small and large intestinal weight, crypt-villus height and mucosal surface area, and nutrient absorption.

Oxyntomodulin is believed to have the same function as GLP-1, acting via the same receptors. Carbohydrates and fats are the main nutrients that stimulate the release of these hormones. Other signals, such as neurotransmitter acetylcholine and hormones insulin and leptin, also regulate their production Fig. Through the vagal nerve neurons, it delays gastric emptying and stimulates the anorexigenic neurons in the hypothalamus to suppress appetite.

At their highest physiological concentration after a meal , PYY also stimulates the hedonic system in the cortex, generating the sensation of satiation Batterham et al The natural plasma levels of PYY are generally lower in obese people.

Pharmaceutical companies have developed synthetic PYY in the form of a nasal spray for weight control. The stomach feels comfortable, and satisfied — not stuffed. We soon begin to feel calmer, more alert and energized. It takes approximately 20 minutes for fullness signals to transmit from the stomach back to the brain.

When you are eating at a calm, relaxed pace and paying attention to your body, you will notice the following when you have eaten more than physically needed:. If this is the case for you, it will take some time to rediscover hunger and fullness cues, which may require professional guidance. Outside help is especially crucial if: Sometimes, there are emotional reasons for a person being unable to access their hunger and fullness signals.

Getting in touch with body sensations stirs up painful memories for some people, while others feel undeserving of meeting their own needs. If you are one of these people, it is important to work through these issues with a therapist who specializes in eating disorders.

Lastly, in some cases, there are medical explanations for problems with hunger and fullness. For instance, certain medications, specific diseases, depression, stress and pain can clearly increase or decrease the appetite. Research is currently underway to try to better understand the complex mechanisms, and to figure out why some people struggle more than others.

Sometimes, we mistake other signals in our bodies for physical hunger. They are legitimate sensations, but not true stomach hunger. Here are some examples:. Our bodies are not calling for food, but we put it in our mouths as an attempt to relieve anxiety.

We see or smell something that looks so delicious that our mouths start to water. Sometimes just thinking about a food brings on a craving for it. Sometimes we confuse the sluggishness of dehydration with actual hunger. The body is calling for fluids, not food. Rather than acknowledge our feelings and work through our issues, we try to fill the void with food. As you can see, the simple design of physical hunger and fullness is often overshadowed by other body signals, habits, needs and emotions.

Identifying and dealing with them appropriately is a huge step in the process of discerning true stomach hunger. Content may not be distributed without permission. What is stomach hunger?

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