Abstract
Sepsis is characterized by a dysregulated immune response to infection. Nutrition is important in the care of septic patients, but the effects of specific nutrients on inflammation in sepsis are not well defined. Our prior work has shown benefits from early enteral dextrose infusion in a preclinical endotoxemia model of sepsis. In the current study, we extend our initial work to examine the effects of dextrose infusions, varying by route of administration, on inflammation and glycemic control in a more clinically relevant and translational model of Klebsiella pneumoniae (KP) bacteremia. Ten-week old C57BL6/J male mice (n = 31) underwent the implantation of indwelling vascular catheters, followed by inoculation with oropharyngeal KP. The mice were randomized 24 h after inoculation to (1) intravenous (IV) dextrose, (2) enteral dextrose, or (3) enteral saline (control) to study the effects on systemic inflammation, hemodynamics, and glycemic control. At 72 h, 77% of the control mice died, whereas IV dextrose induced 100% mortality, associated with increased inflammation, hyperglycemia, and hypotension. Enteral dextrose reduced mortality to 27%, promoted euglycemia, and reduced inflammation compared to IV dextrose. We conclude, in a bacteremic model of sepsis, that enteral (but not IV) dextrose administration is protective, suggesting that the route of nutrient support influences inflammation in sepsis.
Highlights
Sepsis induces a catabolic state characterized by metabolic dysregulation and muscle atrophy, contributing to an increased length of intensive care unit (ICU) stay, decreased quality of life, and increased long-term mortality [1,2,3,4]
We developed a preclinical model of sepsis using oropharyngeal Klebsiella pneumoniae because (a) Klebsiella infection is common in septic patients, (b) the lung is a common route of entry for pathogens in clinical sepsis, (c) Klebsiella pneumoniae readily disseminates after initial pulmonary infection, and (d) systemic inflammation and decompensation develop approximately one day after the initial insult, thereby modeling the course of septic patients
In a translationally relevant Klebsiella pneumoniae model of sepsis, the physiologic effects of exogenous dextrose varied by route of administration
Summary
Sepsis induces a catabolic state characterized by metabolic dysregulation and muscle atrophy, contributing to an increased length of intensive care unit (ICU) stay, decreased quality of life, and increased long-term mortality [1,2,3,4]. Nutrition therapy can counteract the effects of catabolism in sepsis and improve recovery [5,6,7,8] but is potentially associated with adverse consequences. Nutrition may be delivered to septic patients by either enteral or parenteral (intravenous (IV)). Intravenous nutrition has been linked to an increased incidence of hyperglycemia (which is independently associated with increased mortality), increased risk of infection, and increased morbidity in septic patients [9,10,11]. Enteral nutrition carries risk and has been associated with an increased incidence of diarrhea, nausea, vomiting, bowel ischemia, Nutrients 2020, 12, 2901; doi:10.3390/nu12102901 www.mdpi.com/journal/nutrients
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