Key result
Low-dose endotoxemia induced a rapid 25-fold increase in plasma TNF-alpha and a 100-fold increase in IL-6 (p < 0.001 for both), leading to adipose tissue inflammation and systemic insulin resistance without overt clinical symptoms.
Why the study?
Does low-dose intravenous LPS induce adipose tissue inflammation and systemic insulin resistance in healthy human volunteers?
Population
10 healthy human volunteers (50% male, 90% Caucasian, mean age 22.7 ± 3.8)
Comparison
Intravenous lipopolysaccharide 0.6 ng/kg during… vs Placebo during a separate 36-hour inpatient visit
Design
RCT, randomized, double-masked, placebo-controlled
Follow-up
36 hours per visit
Authors
Loading...
Provides a safe human model for inflammation-driven insulin resistance; extends translational tools for cardio-metabolic disease research.
RCT (n=10)
Double-blind
Random sequence
No
Does low-dose intravenous LPS induce adipose tissue inflammation and systemic insulin resistance in healthy human volunteers?
Effect estimate: 25-fold induction of TNF-alpha and 100-fold increase in IL-6
p-value: p=<0.001
Very low-dose experimental endotoxemia safely induces adipose tissue inflammation and systemic insulin resistance without overt clinical symptoms, providing a viable human model for studying cardio-metabolic disease.
Mehta et al. (2012) conducted an RCT in Healthy volunteers (n=10). Lipopolysaccharide (LPS) vs. Placebo (saline) was evaluated on Plasma TNF-alpha and IL-6 levels (25-fold induction of TNF-alpha and 100-fold increase in IL-6, p=<0.001). Low-dose endotoxemia induced a rapid 25-fold increase in plasma TNF-alpha and a 100-fold increase in IL-6 (p < 0.001 for both), leading to adipose tissue inflammation and systemic insulin resistance without overt clinical symptoms.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: