GLP-1 Weight Loss Medication Restores Cognitive Function in Obese Individuals
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Obesity Damages the Brain: GLP-1 Weight Loss Medication Restores Cognitive Function in Obese Individuals
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Obesity Damages the Brain: GLP-1 Weight Loss Medication Restores Cognitive Function in Obese Individuals.
In order to regulate our behavior, our brains must be capable of forming associations.
For example, connecting a neutral external stimulus with the subsequent outcome, such as seeing a red light on a stove and associating it with the potential for a burn. In this way, the brain understands what external stimuli mean.
Associative learning forms the foundation for neural connections and is driven by an area of the brain known as the dopaminergic midbrain.
This region contains receptors that receive signals from molecules in the body, like insulin, enabling our behavior to adapt to physiological needs.
But what happens when our insulin sensitivity decreases due to obesity? Does this alter our brain activity and our ability to engage in associative learning, thereby changing our behavior?
On August 17, 2023, researchers from the University of Cologne in Germany published a study titled “Liraglutide restores impaired associative learning in individuals with obesity” in the journal Nature Metabolism.
The study measured associative learning in normal-weight participants (30 volunteers with high insulin sensitivity) and obese participants (24 volunteers with low insulin sensitivity).
The results indicated that obese individuals had poorer associative learning abilities, with reduced brain activity in the regions responsible for encoding this type of learning.
However, administering a dose of GLP-1 receptor agonist Liraglutide restored the brain activity of obese individuals to that of normal-weight individuals, thereby improving their associative learning.
Liraglutide is a GLP-1 receptor agonist developed by Novo Nordisk. It activates GLP-1 receptors in the body, stimulating insulin secretion and promoting a feeling of fullness. It is commonly used to treat obesity and type 2 diabetes, administered as a once-daily injection.
Low insulin sensitivity impairs the brain’s ability to associate sensory stimuli. In this study, participants were injected with Liraglutide or a placebo in the evening, and the following morning, they were assigned a learning task to measure the effectiveness of their associative learning.
The results showed that obese participants had less pronounced abilities to associate sensory stimuli compared to normal-weight participants, along with reduced brain activity in the regions responsible for encoding this learning.
However, after a single Liraglutide injection, obese participants no longer exhibited these brain impairments, and there was no difference in brain activity between normal-weight and obese participants. In other words, Liraglutide restored the brain activity of obese individuals to that of normal-weight individuals.
Marc Tittgemeyer, the corresponding author of the study, emphasized the significance of this research, highlighting that it demonstrates that fundamental behaviors like associative learning depend not only on external environmental conditions but also on the body’s metabolic state.
Therefore, whether a person is overweight or obese also determines how the brain learns to associate sensory signals and what motivations it generates.
The use of drugs like Liraglutide can normalize these processes in obese patients, aligning with their role in restoring a normal sense of fullness, which helps people eat less and lose weight.
Ruth Hanssen, the first author of the paper, noted that while existing medications have a positive impact on the brain activity of obese patients, it is concerning that even in young, uncomplicated cases of obesity, the brain shows changes. Therefore, obesity prevention should play a larger role in future healthcare systems because lifelong medication for weight loss is unlikely to be widely embraced compared to preventing obesity in the first place.
In summary, this study suggests that GLP-1 receptor activation can restore associative learning in obese individuals. This finding provides evidence of how metabolic signals serve as neural regulators that adapt our behavior to our internal bodily states, and how GLP-1 receptor agonists function in a clinical setting.
Link to the paper: [Nature Metabolism Article](https://www.nature.com/articles/s42255-023-00859-y)
Obesity Damages the Brain: GLP-1 Weight Loss Medication Restores Cognitive Function in Obese Individuals
(source:internet, reference only)
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