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01 30, 2019;9 (1): 1012.

Glucose Activates Vagal Control of Hyperglycemia and Inflammation in Fasted Mice.

Biju Joseph, Guilherme Shimojo, Zhifeng Li, Maria Del Rocio Thompson-Bonilla, Roshan Shah, Alexandre Kanashiro, Helio C Salgado, Luis Ulloa
Author Information
  1. Biju Joseph: Department of Surgery, Rutgers-New Jersey Medical School, Newark, NJ, 07103, USA.
  2. Guilherme Shimojo: Department of Surgery, Rutgers-New Jersey Medical School, Newark, NJ, 07103, USA.
  3. Zhifeng Li: Department of Surgery, Rutgers-New Jersey Medical School, Newark, NJ, 07103, USA.
  4. Maria Del Rocio Thompson-Bonilla: Department of Surgery, Rutgers-New Jersey Medical School, Newark, NJ, 07103, USA.
  5. Roshan Shah: Department of Surgery, Rutgers-New Jersey Medical School, Newark, NJ, 07103, USA.
  6. Alexandre Kanashiro: Department of Surgery, Rutgers-New Jersey Medical School, Newark, NJ, 07103, USA.
  7. Helio C Salgado: Department of Physiology, Medical School - University of São Paulo, Ribeirão Preto, SP, 14049-900, Brazil.
  8. Luis Ulloa: Department of Surgery, Rutgers-New Jersey Medical School, Newark, NJ, 07103, USA. Luis.Ulloa@Rutgers.edu. ORCID
PMID: 30700738 DOI: 10.1038/s41598-018-36298-z

Abstract

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.

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Grants

  1. R01 GM114180/NIGMS NIH HHS

MeSH Term

Animals
Cytokines
Diabetes Mellitus, Experimental
Dopamine
Dopamine Agonists
Fasting
Glucose
Hyperglycemia
Inflammation
Insulin
Male
Mice
Mice, Inbred C57BL
Sepsis
Vagus Nerve

Chemicals

Cytokines
Dopamine Agonists
Insulin
Glucose
Dopamine
Journal Article Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't
Article has an altmetric score of 1

Word Cloud

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