دورية أكاديمية
Lipopolysaccharide Potentiates Insulin-Driven Hypoglycemic Shock.
| العنوان: | Lipopolysaccharide Potentiates Insulin-Driven Hypoglycemic Shock. |
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| المؤلفون: | Hagar JA; Department of Microbiology and Immunology, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599.; Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599.; Center for Gastrointestinal Biology and Disease, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599., Edin ML; Division of Intramural Research, National Institute for Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC 27709., Lih FB; Division of Intramural Research, National Institute for Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC 27709., Thurlow LR; Department of Microbiology and Molecular Genetics, University of Pittsburgh, Pittsburgh, PA 15219., Koller BH; Department of Genetics, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599., Cairns BA; Department of Microbiology and Immunology, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599.; Department of Surgery, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599; and.; North Carolina Jaycee Burn Center, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599., Zeldin DC; Division of Intramural Research, National Institute for Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC 27709., Miao EA; Department of Microbiology and Immunology, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599; emiao@med.unc.edu.; Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599.; Center for Gastrointestinal Biology and Disease, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599. |
| المصدر: | Journal of immunology (Baltimore, Md. : 1950) [J Immunol] 2017 Nov 15; Vol. 199 (10), pp. 3634-3643. Date of Electronic Publication: 2017 Oct 16. |
| نوع المنشور: | Journal Article |
| اللغة: | English |
| بيانات الدورية: | Publisher: American Association of Immunologists Country of Publication: United States NLM ID: 2985117R Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1550-6606 (Electronic) Linking ISSN: 00221767 NLM ISO Abbreviation: J Immunol Subsets: MEDLINE |
| أسماء مطبوعة: | Publication: Bethesda, MD : American Association of Immunologists Original Publication: Baltimore : Williams & Wilkins, c1950- |
| مواضيع طبية MeSH: | Congenital Hyperinsulinism/*drug therapy , Insulin/*therapeutic use , Salmonella Infections/*drug therapy , Salmonella typhimurium/*immunology , Sepsis/*drug therapy, Animals ; Caspases/genetics ; Caspases/metabolism ; Caspases, Initiator ; Cells, Cultured ; Complement System Proteins/metabolism ; Congenital Hyperinsulinism/immunology ; Female ; Humans ; Lipopolysaccharides/immunology ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Salmonella Infections/immunology ; Sepsis/immunology ; Signal Transduction ; Toll-Like Receptor 4/genetics ; Toll-Like Receptor 4/metabolism |
| مستخلص: | Critically ill patients typically present with hyperglycemia. Treatment with conventional insulin therapy (targeting 144-180 mg/dl) improves patient survival; however, intensive insulin therapy (IIT) targeting normal blood glucose levels (81-108 mg/dl) increases the incidence of moderate and severe hypoglycemia, and increases mortality. Septic patients are especially prone to IIT-induced hypoglycemia, but the mechanism remains unknown. Here, we show that codelivery of insulin with otherwise sublethal doses of LPS induced hypoglycemic shock in mice within 1-2 h. LPS impaired clearance of insulin, which amplified insulin receptor signaling. These effects were mediated by caspase-11, TLR4, and complement, each of which trigger eicosanoid production that potentiates insulin signaling. Finally, in an animal model of sepsis, we observed that Salmonella typhimurium -infected mice exhibited simultaneous impaired insulin clearance coexisting with insulin resistance. Our results raise the possibility that septic patients have impaired insulin clearance, which could increase their susceptibility to hypoglycemia during IIT, contraindicating its use. (Copyright © 2017 by The American Association of Immunologists, Inc.) |
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| معلومات مُعتمدة: | U54 AI057141 United States AI NIAID NIH HHS; R01 AI119073 United States AI NIAID NIH HHS; Z01 ES025034 United States ImNIH Intramural NIH HHS; R01 AR061491 United States AR NIAMS NIH HHS; R01 AI097518 United States AI NIAID NIH HHS; T32 AI007273 United States AI NIAID NIH HHS; ZIA ES025034-22 United States ImNIH Intramural NIH HHS |
| المشرفين على المادة: | 0 (Insulin) 0 (Lipopolysaccharides) 0 (Tlr4 protein, mouse) 0 (Toll-Like Receptor 4) 9007-36-7 (Complement System Proteins) EC 3.4.22.- (Casp4 protein, mouse) EC 3.4.22.- (Caspases) EC 3.4.22.- (Caspases, Initiator) |
| تواريخ الأحداث: | Date Created: 20171018 Date Completed: 20171120 Latest Revision: 20220317 |
| رمز التحديث: | 20240829 |
| مُعرف محوري في PubMed: | PMC5685187 |
| DOI: | 10.4049/jimmunol.1700820 |
| PMID: | 29038248 |
| قاعدة البيانات: | MEDLINE |
| تدمد: | 1550-6606 |
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| DOI: | 10.4049/jimmunol.1700820 |