The DOI matches its Crossref record; 65 of the 65 references it cites were found in a registry or an index.
Lipopolysaccharides-Mediated Increase in Glucose-Stimulated Insulin Secretion: Involvement of the GLP-1 Pathway
Open accessAbstract
Lipopolysaccharides (LPS) of the cell wall of gram-negative bacteria trigger inflammation, which is associated with marked changes in glucose metabolism. Hyperglycemia is frequently observed during bacterial infection and it is a marker of a poor clinical outcome in critically ill patients. The aim of the current study was to investigate the effect of an acute injection or continuous infusion of LPS on experimentally induced hyperglycemia in wild-type and genetically engineered mice. The acute injection of a single dose of LPS produced an increase in glucose disposal and glucose-stimulated insulin secretion (GSIS). Continuous infusion of LPS through mini-osmotic pumps was also associated with increased GSIS. Finally, manipulation of LPS detoxification by knocking out the plasma phospholipid transfer protein (PLTP) led to increased glucose disposal and GSIS. Overall, glucose tolerance and GSIS tests supported the hypothesis that mice treated with LPS develop glucose-induced hyperinsulinemia. The effects of LPS on glucose metabolism were significantly altered as a result of either the accumulation or antagonism of glucagon-like peptide 1 (GLP-1). Complementary studies in wild-type and GLP-1 receptor knockout mice further implicated the GLP-1 receptor-dependent pathway in mediating the LPS-mediated changes in glucose metabolism. Hence, enhanced GLP-1 secretion and action underlies the development of glucose-mediated hyperinsulinemia associated with endotoxemia.
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“bacterial LPS were recently shown to enhance GLP-1 secretion, suggesting the involvement of TLR's in L cell activity (Larraufie et al., 2017;Nguyen et al., 2014).”
From The Microbiota-Gut-Brain Axis (2019) · cites this paper as Nguyen et al., 2014
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Cites
Metabolic Endotoxemia Initiates Obesity and Insulin Resistance
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Decoding the Patterns of Self and Nonself by the Innate Immune System
Medzhitov, R., & Janeway, C. A. (2002) · Science · doi:10.1126/science.1068883 · Cited by 2,154
Glucagon-like peptide-1 7–36: a physiological incretin in man
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The NICE-SUGAR Study Investigators (2012) · New England Journal of Medicine · doi:10.1056/nejmoa1204942 · Cited by 1,009
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Self-citationGlucagon-like peptide-1 receptor is involved in learning and neuroprotection
During, M. J., Cao, L., Zuzga, D. S., Francis, J. S., Fitzsimons, H. L., Jiao, X., Bland, R. J., Klugmann, M., Banks, W. A., Drucker, D. J., et al. (2003) · Nature Medicine · doi:10.1038/nm919 · Cited by 851
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Self-citationBacterial Endotoxin Is an Active Component of Cigarette Smoke
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Cryan, J. F., O'Riordan, K. J., Cowan, C. S. M., Sandhu, K. V., Bastiaanssen, T. F. S., Boehme, M., Codagnone, M. G., Cussotto, S., Fulling, C., Golubeva, A. V., et al. (2019) · Physiological Reviews · doi:10.1152/physrev.00018.2018 · Cited by 5,286
Mechanisms of Action and Therapeutic Application of Glucagon-like Peptide-1
Drucker, D. J. (2018) · Cell Metabolism · doi:10.1016/j.cmet.2018.03.001 · Cited by 2,170
Self-citationEnteroendocrine Cells: Chemosensors in the Intestinal Epithelium
Gribble, F. M., & Reimann, F. (2016) · Annual Review of Physiology · doi:10.1146/annurev-physiol-021115-105439 · Cited by 683
The Cardiovascular Biology of Glucagon-like Peptide-1
Drucker, D. J. (2016) · Cell Metabolism · doi:10.1016/j.cmet.2016.06.009 · Cited by 665
Self-citationThe Influence of the Gut Microbiome on Host Metabolism Through the Regulation of Gut Hormone Release
Martin, A. M., Sun, E. W. L., Rogers, G. B., & Keating, D. J. (2019) · Frontiers in Physiology · doi:10.3389/fphys.2019.00428 · Cited by 402
Metadata
- Authors
- Nguyen, A. T., Mandard, S., Dray, C., Deckert, V., Valet, P., Besnard, P., Drucker, D. J., Lagrost, L., & Grober, J.
- Affiliations
- Inserm (FR)
- Université Toulouse III - Paul Sabatier (FR)
- Mount Sinai Hospital (CA)
- ORCID
- Venue
- Diabetes
- Publisher
- American Diabetes Association
- Published
- 2014-01-16
- Volume
- 63
- Issue
- 2
- Pages
- 471-482
- ISSN
- 0012-1797 (ISSN-L)
- 1939-327X
- OpenAlex
- W2129911161
- Cited by
- 161
- References
- 65
- Citations by year
- 2026: 11 · 2025: 16 · 2024: 12 · 2023: 13 · 2022: 19 · 2021: 12 · 2020: 13 · 2019: 19 · 2018: 9 · 2017: 11 · 2016: 12 · 2015: 8 · 2014: 6
- FWCI
- 8.53
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Diabetes (publishedVersion, cc-by-nc-nd)
- PubMed (publishedVersion)
- HAL (submittedVersion, other-oa)
- Funders
- Agence Nationale de la Recherche (ANR-11-LABX-0021)
- Topics
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Pancreatic function and diabetes
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Treatment and Management
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Hyperglycemia and glycemic control in critically ill and hospitalized patients
- Keywords
- lipopolysaccharide, endotoxemia, glucose-stimulated insulin secretion, glucagon-like peptide-1, GLP-1 receptor, hyperinsulinemia, glucose metabolism, hyperglycemia, phospholipid transfer protein, glucose tolerance, bacterial infection
- MeSH terms
- Glucagon-Like Peptide-1 Receptor, Animals, Blood Glucose, Glucose, Insulin, Lipopolysaccharides, Receptors, Glucagon, Mice, Knockout, Phospholipid Transfer Proteins, Mice, Glucagon-Like Peptide 1
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