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Activation of TLRs Triggers GLP-1 Secretion in Mice

التفاصيل البيبلوغرافية
العنوان: Activation of TLRs Triggers GLP-1 Secretion in Mice
المؤلفون: Lorène J. Lebrun, Alois Dusuel, Marion Xolin, Naig Le Guern, Jacques Grober
المصدر: International Journal of Molecular Sciences, Vol 24, Iss 6, p 5333 (2023)
بيانات النشر: MDPI AG, 2023.
سنة النشر: 2023
المجموعة: LCC:Biology (General)
LCC:Chemistry
مصطلحات موضوعية: glucagon-like peptide 1, toll-like receptors, polymicrobial infection, cecal ligation puncture, inflammation, Biology (General), QH301-705.5, Chemistry, QD1-999
الوصف: The gastrointestinal tract constitutes a large interface with the inner body and is a crucial barrier against gut microbiota and other pathogens. As soon as this barrier is damaged, pathogen-associated molecular patterns (PAMPs) are recognized by immune system receptors, including toll-like receptors (TLRs). Glucagon-like peptide 1 (GLP-1) is an incretin that was originally involved in glucose metabolism and recently shown to be rapidly and strongly induced by luminal lipopolysaccharides (LPS) through TLR4 activation. In order to investigate whether the activation of TLRs other than TLR4 also increases GLP-1 secretion, we used a polymicrobial infection model through cecal ligation puncture (CLP) in wild-type and TLR4-deficient mice. TLR pathways were assessed by intraperitoneal injection of specific TLR agonists in mice. Our results show that CLP induces GLP-1 secretion both in wild-type and TLR4-deficient mice. CLP and TLR agonists increase gut and systemic inflammation. Thus, the activation of different TLRs increases GLP-1 secretion. This study highlights for the first time that, in addition to an increased inflammatory status, CLP and TLR agonists also strongly induce total GLP-1 secretion. Microbial-induced GLP-1 secretion is therefore not only a TLR4/LPS-cascade.
نوع الوثيقة: article
وصف الملف: electronic resource
اللغة: English
تدمد: 1422-0067
1661-6596
Relation: https://www.mdpi.com/1422-0067/24/6/5333; https://doaj.org/toc/1661-6596; https://doaj.org/toc/1422-0067
DOI: 10.3390/ijms24065333
URL الوصول: https://doaj.org/article/4674c7e6bf2546d39261728a3d2d5cea
رقم الأكسشن: edsdoj.4674c7e6bf2546d39261728a3d2d5cea
قاعدة البيانات: Directory of Open Access Journals
الوصف
تدمد:14220067
16616596
DOI:10.3390/ijms24065333