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How CCK Activates GLP-1 Brain Neurons: Through Noradrenergic and Glutamate Signaling

evidence
The takeaway

CCK stimulated hypothalamic GLP-1 neurons through alpha-1 adrenoceptor-mediated glutamatergic synaptic input, revealing how two gut satiety signals converge in the brain for integrated appetite control.

Key finding

CCK stimulated hypothalamic GLP-1 neurons through alpha-1 adrenoceptor-mediated glutamatergic synaptic input, revealing how two gut satiety signals co

What the researchers found

CCK stimulated hypothalamic GLP-1 neurons through alpha-1 adrenoceptor-mediated glutamatergic synaptic input, revealing how two gut satiety signals converge in the brain for integrated appetite control.

Why it matters

Relevant for peptide research.

How the study worked

research study.

What this study cannot tell us

See abstract.

How to read the evidence

emerging evidence.

When this study was published

Published in 2011.

The bigger picture

Advances peptide research.

Questions still open

  • Further research needed.

Common questions

What was studied?
How CCK Activates GLP-1 Brain Neurons: Through Noradrenergic and Glutamate Signaling
What was found?
CCK stimulated hypothalamic GLP-1 neurons through alpha-1 adrenoceptor-mediated glutamatergic synaptic input, revealing how two gut satiety signals converge in the brain for integrated appetite control.

Read the original research

CCK stimulation of GLP-1 neurons involves α1-adrenoceptor-mediated increase in glutamatergic synaptic inputs.

Diabetes, 60(11), 2701-9

Citation

Hisadome, Kazunari; Reimann, Frank; Gribble, Fiona M; Trapp, Stefan. (2011). CCK stimulation of GLP-1 neurons involves α1-adrenoceptor-mediated increase in glutamatergic synaptic inputs.. Diabetes, 60(11), 2701-9. https://doi.org/10.2337/db11-0489