Deceiving the brain? Semaglutide regulates appetite in the central nervous system

Semaglutide is a glucagon like peptide-1 receptor agonist (GLP-1 RA), whose role in the central nervous system is mainly reflected in reducing food intake by regulating appetite, thereby achieving weight loss.Semaglutide can act on the hypothalamus and hindbrain regions of the brain, which are important centers for appetite regulation. Specifically, it stimulates the activity of appetite regulating neurons in these regions, causing depolarization of POMC/ART neurons, while hyperpolarizing and inactivating NPY/AgRP neurons, thereby reducing appetite. In addition, semaglutide can directly activate the brain regions responsible for regulating appetite, food intake, food preference, and food termination, reducing food cravings and suppressing the appetite of obese individuals.
Semaglutide acts on GLP-1 receptors in the central nervous system, sending a “full” signal to the brain, causing a lack of hunger and suppressing appetite. This effect not only reduces food intake, but also increases satiety and slows down gastric emptying.
Clinical studies have also confirmed the effectiveness of semaglutide in appetite regulation. For example, in a 20 week study, obese patients treated with semaglutide had significantly reduced hunger, higher satiety, significantly decreased food cravings, reduced energy intake by 35%, and an average weight loss of 9.9% compared to the placebo group.
The main function of semaglutide in the central nervous system is to regulate the activity of appetite related neurons, reduce food intake, and increase satiety, thereby effectively controlling weight and lowering blood sugar
What is the specific mechanism of action of semaglutide in the central nervous system?
The specific mechanism of action of semaglutide in the central nervous system is mainly achieved by simulating the function of glucagon like peptide-1 (GLP-1) in vivo. GLP-1 is a hormone that efficiently enters the central nervous system through the blood-brain barrier and is locally synthesized in the brain. Semaglutide, as a GLP-1 receptor agonist, exerts its effects by binding to and activating the GLP-1 receptor.
Appetite suppression: Semaglutide acts on areas of the brain related to appetite regulation, increasing satiety and reducing desire to eat, thereby helping to lose weight.
Increasing satiety: By enhancing insulin signaling in the brain, satiety is increased and appetite is further suppressed.
Delaying gastric emptying: Semaglutide can also delay gastric emptying and reduce energy intake.

What are the differences in the effects of semaglutide on appetite regulation in different types of obese patients (such as type 1 diabetes patients)?
Semaglutide, as a long-acting glucagon like peptide-1 (GLP-1) receptor agonist, achieves weight loss effects through various mechanisms, including slowing gastric emptying, increasing satiety, reducing appetite and energy intake. However, the existing data do not provide clear information about the difference in the effect of semaglutide on appetite regulation in different types of obese patients (such as type 1 diabetes patients).
The current evidence mainly focuses on the application of smeglutide in adult overweight/obese people, especially for obese patients with body mass index (BMI) ≥ 30kg/m ² or overweight patients with BMI between 27-30kg/m ² and at least one weight related complication (such as hypertension, type 2 diabetes or dyslipidemia). These studies indicate that semaglutide can significantly reduce weight and assist in weight management by increasing satiety and reducing appetite.
Although Semaglutide performs well in controlling blood sugar and weight loss, the existing data do not specifically discuss its effect on appetite regulation in patients with type 1 diabetes. Therefore, it is impossible to determine whether the effect of semaglutide on appetite regulation in different types of obese patients (such as type 1 diabetes patients) is significantly different.

What are the comparative research results of semaglutide and other GLP-1 receptor agonists (such as evercept) in appetite regulation?
As a GLP-1 receptor agonist, the mechanism of action of semaglutide in appetite regulation is mainly through simulating the hormone glucagon like peptide-1 (GLP-1) related to appetite regulation, thereby inhibiting appetite and reducing food intake. Specifically, semaglutide can achieve this effect by delaying gastric emptying, increasing satiety, and changing food preferences.
However, the research results on the appetite regulation of ezetimibe (another GLP-1 receptor agonist) were not explicitly mentioned in the materials I searched. Therefore, it is not possible to directly compare the effects of semaglutide and other GLP-1 receptor agonists (such as ezetimibe) in appetite regulation.

What are the safety and side effect reports of semaglutide in clinical trials?
The safety and side effect reports of semaglutide in clinical trials mainly focus on gastrointestinal reactions. According to multiple studies and clinical trials, the most common adverse reactions include nausea, diarrhea, and vomiting. In addition, there are constipation, abdominal pain, headache, fatigue, indigestion, dizziness, bloating, bloating, gastroenteritis, and gastroesophageal reflux disease.
Specifically, in 8 Phase IIIa trials, a total of 4792 patients were exposed to semaglutide, and the most commonly reported adverse reactions were gastrointestinal disorders, including nausea (very common), diarrhea (very common), and vomiting (common). Another study showed that the probability of gastrointestinal side effects in the group treated with semaglutide was as high as 84.1%.
In addition to gastrointestinal reactions, semaglutide may also cause some rare and serious side effects. However, overall, clinical studies have shown that semaglutide has good safety, but it does not mean that it has no side effects.

What are the potential risks or tolerance issues of semaglutide after long-term use?
Semaglutide, as a new glucagon like peptide-1 (GLP-1) receptor agonist, has significant effects on weight loss and diabetes treatment, but there are some potential risks and tolerance problems after long-term use.
Malnutrition and metabolic abnormalities: Long term injection of semaglutide may lead to appetite suppression and reduced food intake, thereby increasing the risk of malnutrition and metabolic abnormalities, including hyperlipidemia and fatty liver.
Gastrointestinal reactions: This is the most common adverse reaction after using semaglutide, including bloating, nausea, vomiting, diarrhea, etc. Especially in non diabetes patients, the probability of gastrointestinal side effects is as high as 84.1%.
Hypoglycemia: Although semaglutide has a lower risk of hypoglycemia compared to other oral hypoglycemic drugs, hypoglycemia may still occur in certain situations, especially when used in combination with insulin or other hypoglycemic drugs, or in cases of irregular diet, excessive exercise, or excessive alcohol intake.
Muscle and bone loss: Rapid weight loss can lead to significant risks associated with long-term use of semaglutide for weight loss, especially for non obese individuals and those aged 65 and above. Therefore, caution should be exercised when using this medication for rapid weight loss.
Eye diseases: Studies have shown that the use of semaglutide greatly increases the risk of eye diseases, and in severe cases, may lead to permanent blindness.
Gallbladder and biliary diseases: The use of semaglutide can increase the incidence of gallbladder or biliary diseases, especially during high-dose, long-term weight loss procedures.
Emotional fluctuations: Some patients may experience emotional fluctuations after using semaglutide, including reduced depression and insomnia anxiety.