Glucose Activates Vagal Control of Hyperglycemia and Inflammation in Fasted Mice.
Animals
Cytokines
/ metabolism
Diabetes Mellitus, Experimental
/ metabolism
Dopamine
/ metabolism
Dopamine Agonists
/ pharmacology
Fasting
/ metabolism
Glucose
/ physiology
Hyperglycemia
/ metabolism
Inflammation
/ metabolism
Insulin
/ metabolism
Male
Mice
Mice, Inbred C57BL
Sepsis
/ metabolism
Vagus Nerve
Journal
Scientific reports
ISSN: 2045-2322
Titre abrégé: Sci Rep
Pays: England
ID NLM: 101563288
Informations de publication
Date de publication:
30 01 2019
30 01 2019
Historique:
received:
22
08
2018
accepted:
14
11
2018
entrez:
1
2
2019
pubmed:
1
2
2019
medline:
12
5
2020
Statut:
epublish
Résumé
Sepsis is a leading cause of death in hospitalized patients. Many experimental treatments may have failed in clinical trials for sepsis, in part, because they focused on immune responses of healthy animals that did not mimic the metabolic settings of septic patients. Epidemiological studies show an association between metabolic and immune alterations and over 1/3 of septic patients are diabetic, but the mechanism linking these systems is unknown. Here, we report that metabolic fasting increased systemic inflammation and worsened survival in experimental sepsis. Feeding and administration of glucose in fasted mice activated the vagal tone without affecting blood pressure. Vagal stimulation attenuated hyperglycemia and serum TNF levels in sham but only hyperglycemia in splenectomized mice. Vagal stimulation induced the production of dopamine from the adrenal glands. Experimental diabetes increased hyperglycemia and systemic inflammation in experimental sepsis. Fenoldopam, a specific dopaminergic type-1 agonist, attenuated hyperglycemia and systemic inflammation in diabetic endotoxemic mice. These results indicate that glucose activates vagal control of hyperglycemia and inflammation in fasted septic mice via dopamine.
Identifiants
pubmed: 30700738
doi: 10.1038/s41598-018-36298-z
pii: 10.1038/s41598-018-36298-z
pmc: PMC6354016
doi:
Substances chimiques
Cytokines
0
Dopamine Agonists
0
Insulin
0
Glucose
IY9XDZ35W2
Dopamine
VTD58H1Z2X
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
1012Subventions
Organisme : NIGMS NIH HHS
ID : R01 GM114180
Pays : United States
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