Wednesday, May 18, 2022

What Part Of The Brain Controls Hunger And Satiety

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How Satiety Hormones Affect Appetite

What is Hunger?

Satiety is the sense of food satisfaction and fullness experienced after eating. Hunger and satiety both depend on a complex feedback loop involving many hormones and other substances secreted by the gut that interact with control centers in the brain The gut participates in the hunger-satiety circuit by secreting two important hormones, cholecystokinin and glucagon-like peptide-1 , among others.

Cholecystokinin is recognized to suppress appetite in humans. When a partially digested meal rich in fats or proteins leaves the stomach to enter the duodenum , the duodenal mucosa cells secrete CCK. In turn, CCK stimulates the pancreas to secrete numerous enzymes to help digest food. CCK also acts on the gallbladder to stimulate the release of bile into the small intestine, which helps to emulsify and break down fats. Most important to appetite control, CCK acts to slow gastric emptying and to promote a feeling of fullness, thus suppressing further food intake.19

Glucagon-like peptide-1 is another hormone that is intimately connected with fullness and satiety. Produced in the small intestine in response to fat and carbohydrates, GLP-1 works in part by activating the “ileal brake” mechanism. This slows down the absorption of food in the gut, promoting feelings of fullness and satiety, and therefore limits the desire for further food intake.20

Insight Into The Brain’s Control Of Hunger And Satiety

by Beth Israel Deaconess Medical Center

Beth Israel Deaconess Medical Center researchers have identified previously unknown neural circuitry that plays a role in promoting satiety, the feeling of having had enough to eat. The discovery revises the current models for homeostatic controlthe mechanisms by which the brain maintains the body’s status quoof feeding behavior. Published online today in Nature Neuroscience, the findings offer new insight into the regulation of hunger and satiety and could help researchers find solutions to the ongoing obesity epidemic.

“Current models lack a rapidly-acting satiety mechanism analogous to the hunger-promoting neurons,” said corresponding author Bradford B. Lowell, MD, PhD, a professor of medicine in the Division of Endocrinology, Diabetes and Metabolism at BIDMC. “This component we identified provides the full ‘yang’ to the hunger-promoting neurons’ ‘yin.'”

Researchers have long known that hunger is regulated by two kinds of neurons: Agouti-related protein neurons and pro-opiomelanocortin neurons. AgRP neurons drive hunger; stimulating these nerves triggers eating within minutes. The opposing group of neurons, POMC, has been shown to promote satiety. Lab mice engineered to lack POMC neurons eat large quantities of food and become massively obese.

To follow up, the scientists will further investigate the interactions among the three types of neurons and the role they play in obesity.

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What Are Two Emotions That Influence Eating When Someone Isn’t Hungry

Hungereathungertwo emotionstwo emotions that influence eating when someone isn’t hungryThe Factors That Influence Our Food Choices

  • Biological determinants such as hunger, appetite, and taste.
  • Economic determinants such as cost, income, availability.
  • Physical determinants such as access, education, skills and time.
  • Social determinants such as culture, family, peers and meal patterns.

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From The Mouth To The Brain

Perceptions of the food on our plate start with the senses and the first chemical signals are released during mastication. For example, fatty acids are detected in the mouth and a message is sent to the brain, explains Christophe Magnan, a university professor and head of the research team focusing on blood sugar regulation by the central nervous system at the Functional and Adaptive Biology Unit .1 Taste buds on the tongue thus recognise the presence of fatty acids via the CD36 receptor. Within seconds, the central nervous system is alerted to the ingestion of fat. The rapid detection of fat in mammals could be explained from an evolutionary point of view, because weight-for-weight, lipids supply twice as much energy as carbohydrates. A craving for fat is therefore vital. ;

As soon as digestion starts, changes to the blood levels of fatty acids are detected by specialised neurons in the hypothalamus. In rodents, it has been shown in the laboratory that an increase in fatty acids such as oleic acid is identified by hypothalamic neurons which, in return, alter dietary consumption. Experiments have demonstrated that increasing the oleic acid content in the diet of rats reduced their food intake, says Christophe Magnan. Inversely, by suppressing the action of CD36, the appetite suppressant effect of fatty acids is lost and the rats rapidly become obese.;;;

Consumption From Within: How The Brain Controls Our Appetite

What part of the brain controls hunger?
Researchers show how our brain activates self-destruct mechanisms when it is low on energy to regulate appetite. The scientists have uncovered the mechanisms behind the enzyme that controls our appetite in response to low glucose availability in the brain.

Korean researchers show how our brain activates self-destruct mechanisms when it is low on energy to regulate appetite.

Researchers from Daegu Gyeongbuk Institute of Science and Technology in Korea have uncovered the mechanisms behind the enzyme that controls our appetite in response to low glucose availability in the brain.

Understanding how our appetite is controlled and influenced by our body and brain is important for countering the worldwide obesity epidemic. To maintain a healthy energy balance, our appetite needs to increase or decrease, depending on our caloric intake through food and energy use in our daily lives. Previous research has shown that a region of the brain, known as the hypothalamus, senses levels of sugar and hormones in the blood, and uses these signals to regulate food intake. However, many questions remain about the mechanisms by which the hypothalamus does this.

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Research Shows How Brain Can Override Hunger In Eating Disorders

Those individuals with anorexia and bulimia have brains that function differently in order to restrict eating from their non-eating disordered peers. Dr Guido Frank from the University of Colorado Denver, was the lead author on a study which indicated that the brains of those with eating disorders show significant alterations, suggesting that the brain overrides hunger signals .This study tested brain structure and function, using brain activation data, with those with and without eating disorders.

The participants tasted certain sugars meant to activate hunger cues in the brain, and the sugar consumption showed a reverse effect for those participants identified as having anorexia and bulimia. In a non-disordered brain, typically the hypothalamus motivates an individual to eat. In those with an eating disorder, signals from other regions of the brain override the signal in the hypothalamus. This indicates that the brain can reject signals, including taste-reward and hunger .

Are Your Eyes Bigger Than Your Stomach

It remains that in human beings, starting or stopping to eat is not just a question of satiety and metabolic regulation. The human diet is based also, and above all, on pleasure. This is a so-called hedonic control that will condition the choice and frequency of our meals, as well as our food preferences.;

Depending on our senses sight, taste and smell we will stop eating or not. Although we may start a meal with pleasure, this epicurean sensation will not last. We then lay down our cutlery, or we move from the starter to the main dish, explains Moustafa Bensafi, research professor at the Lyon Neuroscience Recherche Centre .3 This balance between pleasure and lack of pleasure will govern how we eat. ;

This change to the hedonic value of a food is reflected in the brain. If what you are eating is pleasant, it is the median orbitofrontal cortex that is stimulated. Its activity then declines as does our pleasure, Moustafa Bensafi adds. The lateral orbitofrontal cortex then takes over and induces restrictive behaviours. In other words, after a few pieces of chocolate, the sensory pleasure is no longer the same, and this generally drives us to put the rest of the bar back in the cupboard. This is an essential function because it allows us to have the most varied and balanced diet possible; without it, we would be eating all the time and always the same thing!

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Other Benefits Of Pinolenic Acid

In another study, Japanese researchers fed pinolenic acid to animals bred to develop high blood pressure, a known risk factor for cardiovascular diseases like stroke and heart attack. After five weeks of feeding, the animals’ blood pressure readings were substantially lowered. Decreased cholesterol levels also were noted in the pinolenic acid-fed animals.33

Scientists have investigated the mechanism by which pinolenic acid lowers cholesterol. They found that after adding concentrated pinolenic acid extracted from pine nuts, enhanced uptake of detrimental LDL by liver cells was observed. The scientists suggest that the pinolenic acid concentrate may have LDL-lowering properties by enhancing liver LDL uptake.34

Reprinted with exclusive permission of Life Extension.

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Hormonal Effects Of Pinolenic Acid

The Brain’s Hunger/Satiety Pathways and Obesity, Animation

Among the pinolenic acid subjects, levels of GLP-1 initially climbed in both the placebo and pinolic acid subjects. In the placebo group, however, GLP-1 values began to drop after 30 minutes and continued to decline steadily for the remainder of the four-hour test period. In the women supplemented with pinolenic acid, GLP-1 levels continued to rise, peaking at one hour and reaching a level well above that achieved by placebo subjects. GLP-1 levels remained comfortably above those of placebo subjects throughout the trial, peaking again at three hours post-dose, and this time achieving an even greater increase in levels of this satiety-enhancing hormone over placebo subjects. In total, over four hours, GLP-1 increased 25% more in subjects who took pinolenic acid than in those who took the placebo.7

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The Hypothalamus And Weight Loss

When someone wants to lose weight, they could have a hard time due to problems in the hypothalamus and pituitary gland. ;Its important to see a doctor before trying to influence the chemicals in the body in any way. ;You dont want to make a bad situation worse if theres a chemical imbalance due to a problem in the body.

What Controls Our Hunger

The hypothalamus houses the hunger and satiety centers. Several neural centers in the hypothalamus are involved in the control of food intake. The lateral nuclei of the hypothalamus act as the feeding center, because when stimulated they excite a voracious appetite .

In contrast, the destruction of the lateral hypothalamus cancels the desire for food and leads to progressive starvation, a state characterized by noticeable weight loss, muscle weakness, and reduced metabolism.

The lateral hypothalamic feeding center emits motor impulses for foraging. Rather, the ventromedial nuclei of the hypothalamus serve as an important satiety center and are believed to confer a sense of nutritional pleasure that inhibits the eating center.

Electrical stimulation of this region can induce complete satiety and, in fact, when very appetizing foods are offered, the animal rejects them .

On the contrary, the destruction of the ventromedial nuclei motivates a voracious and continuous feeding until the animal reaches extreme obesity, sometimes quadrupling its weight.

The paraventricular, dorsomedial, and arcuate nuclei of the hypothalamus are also believed to be instrumental in regulating food intake.

For example, lesions of the paraventricular nuclei usually lead to overeating, while those of the dorsomedial nuclei generally reduce eating behavior.

The hypothalamus receives:

  • Signals from hormones released by adipose tissue,
  • Signals from the cerebral cortex that modify eating behavior.

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A Wave Of Information From The Gut To The Brain

Under normal circumstances, we are not hungry all the time, a state that is referred to as satiety. It can last for hours and results from a flow of information from the digestive tract to the brain. Satiety should not be confused with being satisfied, explains Gilles Mithieux, research professor at the INSERM and head of the nutrition, diabetes and brain laboratory at the Université Claude Bernard in Lyon . Being satisfied means no longer being hungry, a feeling triggered by signals from the digestive tract to the brain, which indicate that the stomach is full. Satiety, on the other hand, is the absence of hunger that follows a meal and will last until the next one. Its duration can vary, based on the content of the previous meal.

But what are these indicators? Depending on the presence or not of food in the stomach, the brain will release signals that are orexigenic if they stimulate appetite or anorexigenic if they suppress hunger. Thus the central nervous system and brain conduct a dialogue via numerous chemical mediators such as cholecystokinine. This peptide, which notably serves to release bile, also has the effect of reducing hunger by communicating with the brain, explains Gilles Mithieux. However, the appetite suppressant effects of cholecystokinine vary according to individuals and their age. For example, while this mediator induces a drastic reduction in hunger in young male rats, it will have a much weaker anorectic effect in elderly or obese animals. ;

Excessive Sugar Consumption Affects The Brain In The Long Term

Why You

The fact remains that in the long term, chronic and excessive sugar consumption can affect the functioning of the brain from a neurobiological point of view, having an impact on cognitive, motivational and emotional processes, stresses Martine Cador, research professor and leader of the AddicTeam at the Aquitaine Institute for Cognitive and Integrative Neuroscience .5 This is the case in particular when such consumption occurs during adolescence, at a time when neurons are maturing. Mice that overconsume sugar in that period of life, at levels similar to those found in fizzy drinks, develop impaired motivation to find sugar in adulthood, a condition called anhedonia. It is as if the sweet sensation had become less pleasant, suggests Martine Cador. Consumption at that age also increases the risks of depressive syndrome and reduces neurogenesis, or the formation of new neurons.;

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The Ventral Tegmental Area

The VTA and substantia nigra pars compacta are immediately caudal to the posterior hypothalamus, brace the third ventricle, and contain the major source of dopaminergic outflow to the rest of the brain. The SNc is best known for its role in the nigrostriatal pathway regulating the dorsal striatum in movement, and the VTA for mediating salience, motivation, and reward and aversion-related learning . Salience refers to the attention paid to the stimulus; an increase in salience means the stimulus, if identified, will be more likely to draw the organisms attention. The value of the stimulus, whether it is rewarding or aversive, refers to whether a stimulus induces behavior to acquire it or avoid it, respectively . Rewarding stimuli produce a positive valence when acquired and a negative valence when unable to be acquired; the converse is true with aversive stimuli .

Satiety Neurocircuits Decrease The Activity Of The Reward System

The neurocircuitry of satiety is not as well-known as that of hunger. The general paradigm appears to be as follows: peripheral signals of positive energy balance, primarily hormonal, travel to the brain to inhibit the activity of hunger-producing neurocircuits. However, three populations of neurons within the CNS, defined by their neuropeptide content, are activated by these signals and directly influence the reward system. These are the POMC neurons of the Arc, the POMC neurons of the nucleus tractus solitarius , and the preproglucagon neurons of the NTS. The NTS neurons integrate peripheral satiety signals, such as leptin, cholecystokinin , glucagon-like peptide 1 , and gut distention, to induce rapid satiety. The role of POMC neurons is more complex, but appears to reduce the immediate value of the food reward while maintaining future responsiveness to that same reward.

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The Paradox Of Fatty Acids

This satietogenic potential will depend on the type of fatty acid released, notes Christophe Magnan, who has studied the action of these molecules on the brain. During a meal, any fat ingested is burned or stored in the form of triglycerides in the adipose tissue. During the night or fasting, this stored fat is released into the bloodstream in the form of fatty acids. But if the latter have a considerable satietogenic potential, why are we hungry when we wake up in the morning? Specialists have been addressing this apparent nutritional paradox for many years. The high levels of fatty acids measured when waking up in the morning should indeed suppress the desire to eat! the researcher insists.;

In fact, it has been shown that fatty acids arising from the melting of adipose tissue and those produced from triglycerides are not processed in the same way by the brain. The hypothesis which has now been confirmed is that after a meal, circulating triglycerides are hydrolysed directly at the level of the brain.;

Can Intestinal Glucose Prevent Obesity

Hunger and Satiety and the roles of Hormones and Peptides in Regulation

Around ten years ago, Gilles Mithieux and Christophe Magnan discovered another important mechanism regulating dietary behaviour: intestinal neoglucogenesis. The intestine does not just absorb glucose, it can also produce it, explains Gilles Mithieux. It was observed that two types of nutrients, proteins and dietary fibre, can trigger this synthesis of intestinal glucose. The intestinal glucose from these foods acts as a messenger to inform the brain of the presence of fibre or protein in the gut, which in turn leads to a reduction in hunger and an improved regulation of blood sugar levels, summarises the scientist.

This glucose protects against diabetes and obesity, as shown in mice that have been mutated to overexpress the enzyme that enables the production of intestinal glucose. The result is that they put on half as much weight, even with a very fatty diet, points out Gilles Mithieux. Until a molecule is found that can stimulate this glucose production, eating fibre and proteins appears to be a good way to prevent obesity and diabetes. ;;

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