Research suggesting GLP1 is a brain drug
Why has modern scientific opinion shifted to GLP1 being a brain drug rather than a gut drug? We dive into the critical research paper supporting the shift.
As research is done and continues, GLP1 Receptor Agonists continue to be great at two things:
- Type 2 Diabetes treatment (improving glucose tolerance)
- Body weight management (weight loss)
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Originally, the theories surrounding why GLP1s were so effective in both of these metrics were related to delayed gastric emptying, or other effects GLP1 drugs had on the gut of the patient.
We've covered this subject before:
Here, we dive into the most compelling piece of research that justifies this stance in the scientific literature.
Progress, driven by mice without GLP1 receptors
The study that started to move the discourse on this was published in the Journal of Clinical Investigation ("JCI"):
In a nutshell, this study checked to see if mice who had GLP1 receptors removed from their brains were able to partake in the benefits provided by GLP1s.
The researchers found that the mice were able to reduce their blood glucose but were not seeing reductions in amounts of food eaten.
While the findings in mouse models do not always translate to human models, this is strong evidence towards the idea that GLP1s are primarily brain drugs in terms of weight loss – when the mice had no GLP1 receptors in the brain, they did not lose weight.
Scientists are still unsure of how GLP1 gets across the blood brain barrier, since GLP1 Receptor Agonists are usually large molecules, but there are theories on how it may possibly be making the jump.
For obvious reasons, it's unlikely to be able to repeat this study in humans, so until scientists can find a way to replicate these findings in humans, this is the most reliable related evidence to use for conjecture.