Glucagon-Like Peptide-1 and Hypothalamic Regulation of Satiation: Cognitive and Neural Insights from Human and Animal Studies

Glucagon-like peptide-1 receptor agonists (GLP-1RAs) have emerged as blockbuster drugs for treating metabolic diseases. Glucagon-like peptide-1 (GLP-1) plays a pivotal role in glucose homeostasis by enhancing insulin secretion, suppressing glucagon release, delaying gastric emptying, and acting on t...

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Main Authors: Joon Seok Park, Kyu Sik Kim, Hyung Jin Choi
Format: Article
Language:English
Published: Korean Diabetes Association 2025-05-01
Series:Diabetes & Metabolism Journal
Subjects:
Online Access:http://e-dmj.org/upload/pdf/dmj-2025-0106.pdf
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author Joon Seok Park
Kyu Sik Kim
Hyung Jin Choi
author_facet Joon Seok Park
Kyu Sik Kim
Hyung Jin Choi
author_sort Joon Seok Park
collection DOAJ
description Glucagon-like peptide-1 receptor agonists (GLP-1RAs) have emerged as blockbuster drugs for treating metabolic diseases. Glucagon-like peptide-1 (GLP-1) plays a pivotal role in glucose homeostasis by enhancing insulin secretion, suppressing glucagon release, delaying gastric emptying, and acting on the central nervous system to regulate satiation and satiety. This review summarizes the discovery of GLP-1 and the development of GLP-1RAs, with a particular focus on their central mechanisms of action. Human neuroimaging studies demonstrate that GLP-1RAs influence brain activity during food cognition, supporting a role in pre-ingestive satiation. Animal studies on hypothalamic feed-forward regulation of hunger suggest that cognitive hypothalamic mechanisms may also contribute to satiation control. We highlight the brain mechanisms of GLP-1RA-induced satiation and satiety, including cognitive impacts, with an emphasis on animal studies of hypothalamic glucagon-like peptide-1 receptor (GLP-1R) and GLP-1R-expressing neurons. Actions in non-hypothalamic regions are also discussed. Additionally, we review emerging combination drugs and oral GLP-1RA formulations aimed at improving efficacy and patient adherence. In conclusion, the dorsomedial hypothalamus (DMH)—a key GLP-1RA target—mediates pre-ingestive cognitive satiation, while other hypothalamic GLP-1R neurons regulate diverse aspects of feeding behavior, offering potential therapeutic targets for obesity treatment.
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series Diabetes & Metabolism Journal
spelling doaj-art-2c1cdd8562c6408d8cf4056f4e7eacc02025-08-20T03:49:42ZengKorean Diabetes AssociationDiabetes & Metabolism Journal2233-60792233-60872025-05-0149333334710.4093/dmj.2025.01062947Glucagon-Like Peptide-1 and Hypothalamic Regulation of Satiation: Cognitive and Neural Insights from Human and Animal StudiesJoon Seok Park0Kyu Sik Kim1Hyung Jin Choi2 Department of Medicine, Seoul National University College of Medicine, Seoul, Korea Department of Biomedical Sciences, Seoul National University College of Medicine, Seoul, Korea Department of Medicine, Seoul National University College of Medicine, Seoul, KoreaGlucagon-like peptide-1 receptor agonists (GLP-1RAs) have emerged as blockbuster drugs for treating metabolic diseases. Glucagon-like peptide-1 (GLP-1) plays a pivotal role in glucose homeostasis by enhancing insulin secretion, suppressing glucagon release, delaying gastric emptying, and acting on the central nervous system to regulate satiation and satiety. This review summarizes the discovery of GLP-1 and the development of GLP-1RAs, with a particular focus on their central mechanisms of action. Human neuroimaging studies demonstrate that GLP-1RAs influence brain activity during food cognition, supporting a role in pre-ingestive satiation. Animal studies on hypothalamic feed-forward regulation of hunger suggest that cognitive hypothalamic mechanisms may also contribute to satiation control. We highlight the brain mechanisms of GLP-1RA-induced satiation and satiety, including cognitive impacts, with an emphasis on animal studies of hypothalamic glucagon-like peptide-1 receptor (GLP-1R) and GLP-1R-expressing neurons. Actions in non-hypothalamic regions are also discussed. Additionally, we review emerging combination drugs and oral GLP-1RA formulations aimed at improving efficacy and patient adherence. In conclusion, the dorsomedial hypothalamus (DMH)—a key GLP-1RA target—mediates pre-ingestive cognitive satiation, while other hypothalamic GLP-1R neurons regulate diverse aspects of feeding behavior, offering potential therapeutic targets for obesity treatment.http://e-dmj.org/upload/pdf/dmj-2025-0106.pdfcentral nervous systemdiabetes mellitus, type 2glucagon-like peptide 1glucagon-like peptide-1 receptorglucagon-like peptide-1 receptor agonistshypothalamusincretinsobesitysatiation
spellingShingle Joon Seok Park
Kyu Sik Kim
Hyung Jin Choi
Glucagon-Like Peptide-1 and Hypothalamic Regulation of Satiation: Cognitive and Neural Insights from Human and Animal Studies
Diabetes & Metabolism Journal
central nervous system
diabetes mellitus, type 2
glucagon-like peptide 1
glucagon-like peptide-1 receptor
glucagon-like peptide-1 receptor agonists
hypothalamus
incretins
obesity
satiation
title Glucagon-Like Peptide-1 and Hypothalamic Regulation of Satiation: Cognitive and Neural Insights from Human and Animal Studies
title_full Glucagon-Like Peptide-1 and Hypothalamic Regulation of Satiation: Cognitive and Neural Insights from Human and Animal Studies
title_fullStr Glucagon-Like Peptide-1 and Hypothalamic Regulation of Satiation: Cognitive and Neural Insights from Human and Animal Studies
title_full_unstemmed Glucagon-Like Peptide-1 and Hypothalamic Regulation of Satiation: Cognitive and Neural Insights from Human and Animal Studies
title_short Glucagon-Like Peptide-1 and Hypothalamic Regulation of Satiation: Cognitive and Neural Insights from Human and Animal Studies
title_sort glucagon like peptide 1 and hypothalamic regulation of satiation cognitive and neural insights from human and animal studies
topic central nervous system
diabetes mellitus, type 2
glucagon-like peptide 1
glucagon-like peptide-1 receptor
glucagon-like peptide-1 receptor agonists
hypothalamus
incretins
obesity
satiation
url http://e-dmj.org/upload/pdf/dmj-2025-0106.pdf
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