Cited by 484Barrier Structure and Function StudiesDiabetes Treatment and ManagementRegulation of Appetite and Obesity

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Interactions of Glucagon-Like Peptide-1 (GLP-1) with the Blood-Brain Barrier

Kastin, Abba J., Akerstrom, Victoria, Pan, Weihong·2002·Journal of Molecular Neuroscience

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Abstract

Glucagon-like peptide-1 (GLP-1) reduces insulin requirement in diabetes mellitus and promotes satiety. GLP-1 in the periphery (outside the CNS) has been shown to act on the brain to reduce food ingestion. As GLP-1 is readily degraded in blood, we focused on the interactions of [Ser8]GLP-1, an analog with similar biological effects and greater stability, with the blood-brain barrier (BBB). The influx of radiolabeled [Ser8]GLP-1 into brain has several distinctive characteristics: 1. A rapid influx rate of 8.867 +/- 0.798 x 10(4) mL/g-min as measured by multiple-time regression analysis after iv injection in mice. 2. Lack of self-inhibition by excess doses of the unlabeled [Ser8]GLP-1 either iv or by in situ brain perfusion, indicating the absence of a saturable transport system at the BBB. 3. Lack of modulation by short-term fasting and some other ingestive peptides that may interact with GLP-1, including leptin, glucagon, insulin, neuropeptide Y, and melanin-concentrating hormone. 4. No inhibition of influx by the selective GLP-1 receptor antagonist exendin(9-39), suggesting that the GLP-1 receptor is not involved in the rapid entry into brain. Similarly, there was no efflux system for [Ser8]GLP-1 to exit the brain other than following the reabsorption of cerebrospinal fluid (CSF). The fast influx was not associated with high lipid solubility. Upon reaching the brain compartment, substantial amounts of [Ser8]GLP-1 entered the brain parenchyma, but a large proportion was loosely associated with the vasculature at the BBB. Finally, the influx rate of [Ser8]GLP-1 was compared with that of GLP-1 in a blood-free brain perfusion system; radiolabeled GLP-1 had a more rapid influx than its analog and neither peptide showed the self-inhibition indicative of a saturable transport system. Therefore, we conclude that [Ser8]GLP-1 and the endogenous peptide GLP-1 can gain access to the brain from the periphery by simple diffusion and thus contribute to the regulation of feeding.

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Authors: Kastin, A. J., Akerstrom, V., & Pan, W.
Affiliations: Tulane University (US)
ORCID: Pan, Weihong
Venue: Journal of Molecular Neuroscience
Publisher: Springer Science and Business Media LLC
Published: 2002
Volume: 18
Issue: 1-2
Pages: 07-13
ISSN: 0895-8696 (ISSN-L)
DOI: 10.1385/jmn:18:1-2:07
OpenAlex: W2076140273
Cited by: 480
References: 28
Citations by year: 2026: 8 · 2025: 22 · 2024: 21 · 2023: 18 · 2022: 24 · 2021: 28 · 2020: 24 · 2019: 29 · 2018: 24 · 2017: 23 · 2016: 25 · 2015: 27 · 2014: 31 · 2013: 27 · 2012: 23
FWCI: 6.00
Type: journal article
Language: en
Open access: closed
Locations: Journal of Molecular Neuroscience (publishedVersion)
PubMed (publishedVersion)
Funders: U.S. Department of Veterans Affairs
National Institutes of Health
National Institute of Diabetes and Digestive and Kidney Diseases (DK-54880)
Topics: Life Sciences › Neuroscience › Neurology › Barrier Structure and Function Studies
Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Treatment and Management
Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
Keywords: glucagon-like peptide-1, blood-brain barrier, brain uptake, passive diffusion, GLP-1 receptor, exendin-9-39, satiety, food intake regulation, cerebrospinal fluid reabsorption
MeSH terms: Animals, Appetite Regulation, Blood-Brain Barrier, Brain, Cerebrovascular Circulation, Dose-Response Relationship, Drug, Food Deprivation, Glucagon, Hypothalamic Hormones, Insulin, Male, Melanins, Mice, Inbred ICR, Neuropeptide Y, Peptide Fragments, Pituitary Hormones, Protein Precursors, Leptin, Mice, Glucagon-Like Peptide 1

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Interactions of Glucagon-Like Peptide-1 (GLP-1) with the Blood-Brain Barrier

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