When most people think of GLP-1 (glucagon-like peptide-1), they picture it as a hormone made in the gut—a key player in regulating blood sugar and appetite. And that’s true: GLP-1 is primarily produced by L-cells in the small intestine in response to food.

But here’s what’s less well-known: GLP-1 is also made in your brain.

Where in the brain is GLP-1 made?

Specialized neurons in the nucleus tractus solitarius (NTS) of the brainstem produce GLP-1. In this setting, it functions more like a neurotransmitter than a digestive hormone, sending signals to different parts of the brain that influence appetite, energy use, and more.

What does brain-produced GLP-1 do?

1. Regulates appetite and satiety: Brain-derived GLP-1 communicates with the hypothalamus to help you feel full and to regulate food intake—similar to gut-derived GLP-1, but through direct neural pathways.

2. Influences reward pathways: GLP-1 can reduce the brain’s reward response to highly palatable foods, making it easier to choose balanced meals over calorie-dense, nutrient-poor options.

3. Supports cardiovascular and metabolic control: The brain’s GLP-1 signaling can help regulate heart rate, blood pressure, and glucose metabolism.

4. May protect the brain: Early research suggests neuroprotective effects, potentially reducing oxidative stress and inflammation, and supporting brain cell survival. This has sparked interest in its potential for conditions like Alzheimer’s, Parkinson’s, and stroke recovery.

Why this matters for GLP-1 medications

GLP-1 medications (like semaglutide and tirzepatide) mimic the effects of natural GLP-1. Because GLP-1 acts both in the gut and brain, these medications can:

• Slow digestion and promote fullness through gut pathways
  
  
• Directly influence appetite, cravings, and energy balance via brain pathways

This dual action is a big reason why GLP-1 therapies are so effective—not only for blood sugar control but also for weight regulation and possibly even brain health.

The future: Beyond weight loss

As researchers explore GLP-1’s brain-based benefits, there’s growing interest in its role in longevity, cognitive resilience, and neurodegenerative disease prevention. This broader view shifts the conversation from short-term weight loss to long-term health optimization.

Key takeaway: GLP-1 isn’t just a gut hormone—it’s also a brain-made neurotransmitter with wide-reaching effects on appetite, metabolism, heart health, and potentially even brain aging. Understanding both sides of its production may help unlock its full therapeutic potential.

FAQs

Where in the brain is GLP-1 produced?

GLP-1 is made by specialized neurons in the nucleus tractus solitarius (NTS) of the brainstem. From there, it sends signals to areas like the hypothalamus to influence hunger, satiety, metabolism, and cardiovascular function.

How does brain-derived GLP-1 affect appetite?

Brain-produced GLP-1 helps you feel full by signaling satiety to the hypothalamus. It also dampens the brain’s reward response to high-calorie, ultra-processed foods, making it easier to choose healthier options.

Can GLP-1 protect brain health?

Early studies suggest that GLP-1 has neuroprotective effects. It may reduce inflammation, oxidative stress, and cell damage in the brain. Researchers are investigating its potential role in conditions like Alzheimer’s disease, Parkinson’s disease, and stroke recovery.

How do GLP-1 medications work in the body and brain?

GLP-1 medications, such as semaglutide and tirzepatide, mimic the natural GLP-1 hormone. They slow digestion and promote fullness through gut pathways while also acting on the brain to curb cravings, regulate appetite, and improve metabolic balance.

Are GLP-1 drugs only for weight loss?

No. While GLP-1 medications are well-known for weight loss and blood sugar control, ongoing
research suggests they may also benefit cardiovascular health, cognitive resilience, and even longevity.

References 

Daniels, D., Mietlicki, E. (2018).  doi: 10.2337/dbi18-0045

Lopez, L et al., (2023). https://www.frontiersin.org/journals/neuroscience/articles/10.3389/fnins.2023.1265080/full

Baggio, L., & Drucker, D. (2014). doi: 10.1172/JCI78371