Home Medizin Neue Forschungsergebnisse geben Aufschluss darüber, wie GLP-1-Adipositas-Medikamente das Verlangen nach Essen verändern können

Neue Forschungsergebnisse geben Aufschluss darüber, wie GLP-1-Adipositas-Medikamente das Verlangen nach Essen verändern können

von NFI Redaktion

In a recent review published in the International Journal of Obesity, researchers examined the potential of glucagon-like peptide-1 (GLP-1) analog treatments to alter food preferences and consumption and reduce obesity.

They concluded that while the results show that GLP-1 reduces appetite and consumption in the short term, they rely on self-reports of intake. Further studies are needed to assess weight maintenance using objective intake measurements.

Study: Changes in food preferences and intake behavior after treatment with glucagon-like peptide-1 analogs: Techniques and possibilities. Photo credit: SHISANUPONG1986 / ShutterstockStudy: Changes in food preferences and intake behavior after treatment with glucagon-like peptide-1 analogs: Techniques and possibilities. Photo credit: SHISANUPONG1986 / Shutterstock

Background

Of the three primary interventions against obesity, namely surgical procedures, lifestyle changes, and medications, pharmacology has proven to be minimally invasive, promisingly effective in weight loss, and long-term sustainable.

GLP-1 analog medications such as Semaglutide and Liraglutide are commonly prescribed for the treatment of obesity. Current studies have focused on the mechanisms underlying their weight loss effects, particularly how they alter food preferences and consumption.

About the Study

This review focused on GLP-1 analog medications, assessing how they have been studied and synthesizing what is currently known about their effects. The authors found relevant research results in the medical literature database PubMed by using search terms such as „obesity,“ „Semaglutide,“ „Liraglutide,“ and „GLP-1 analog.“

The results were filtered to ensure they pertained to studies involving human and rodent participants and published within a 25-year period. The results focused on taste preference, food intake, weight loss, and maintenance. Information on publication year, location, methods, results, and study type was noted.

Results

Researchers have examined eating behavior using food and beverage monitors and often rely on verbal reports and visual analog scales to assess satiety. Self-reported data are used to assess food preferences and eating control.

Functional magnetic resonance imaging (fMRI) studies have shown that individuals taking GLP-1 analog medications exhibit reduced responses to food images, particularly in brain regions associated with reward and appetite, such as the amygdala, insula, orbitofrontal cortex, and putamen.

Semaglutide appears to target circumventricular organs, binding to GLP-1 receptors and altering food preferences through interaction with amphetamine- and cocaine-regulated transcripts and proopiomelanocortin neurons.

After treatment with Semaglutide, patients experience weight loss for 12-18 months before stabilizing their weight during the maintenance phase. Individuals taking Semaglutide reported reduced cravings for salty, spicy, fatty, sweet, and savory foods, less desire for starches and dairy, and less difficulty resisting binge eating and controlling food intake. However, animal studies suggest that Semaglutide treatment may also increase sucrose consumption in the lower and middle ranges.

During the weight loss phase, patients consumed smaller meals and showed a decreased preference for high-energy foods, leading to reduced energy intake. No eating behavior during the maintenance phase was reported in studies. Therefore, it is unknown whether patients revert to their original eating habits.

Some gastrointestinal effects of Semaglutide, such as diarrhea, constipation, nausea, and vomiting, have been reported, but it has been found that treatment with lower drug doses can address this issue.

Another GLP-1 analog, Liraglutide, reduces hunger and increases feelings of fullness in the initial phase by binding to GLP-1 receptors in the arcuate nucleus and subcortical brain regions, stimulating proopiomelanocortin neurons. It may slow gastric emptying, but how this occurs is not clear.

Conclusions

Evidence suggests that GLP-1 analog medications alter food preferences and reduce cravings and food intake, which could lead to long-term weight loss and maintenance. However, animal studies also suggest that these medications may increase sucrose consumption, which should be investigated in humans.

Less attention has been given to intake, appetite, and consumption behavior during the weight maintenance phase. Instead, most studies have focused on the weight loss phase and many have asked participants to report on their own cravings, portion control, and appetite.

While such data are easier to collect, they can lead to biases regarding memory and social desirability. Objective measurements are required to understand the impact of obesity medications.

The authors note that the weight-reducing effect of GLP-1 analogs is well established and new medications are in development.

Understanding the behavioral mechanisms through which these medications work, using studies in humans and rodents, can allow researchers and physicians to refine treatments and tailor interventions to the needs of individual patients, thereby improving overall outcomes.

Furthermore, focusing on the weight maintenance phase of treatment can reduce unrealistic expectations from patients and their doctors and decrease misinformation about the long-term effects of the medications, which could jeopardize people’s willingness to use these medications for obesity treatment in the future.

Journal Reference:

  • Changes in food preferences and intake behavior after treatment with glucagon-like peptide-1 analogs: Techniques and possibilities. Bettadapura, S., Dowling, K., Jablon, K., Al-Humadi, AW, le Roux, CW International Journal of Obesity(2024). DOI: 10.1038/s41366-024-01500-y, https://www.nature.com/articles/s41366-024-01500-y

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