Anti-inflammatory Effects of Enriched Enteral Nutrition During Human Experimental Endotoxemia

The Effect of Enriched Enteral Nutrition on Inflammation and Sub-clinical Organ Dysfunction During Human Endotoxemia

Status

Completed

Phases

Study type

Interventional

Source

ClinicalTrials.gov

Registry ID

NCT01100996

Acronym

VIHE

Enrollment

Registered

2010-04-09

Start date

2010-02-28

Completion date

2011-04-30

Last updated

2011-06-07

For informational purposes only — not medical advice. Sourced from public registries and may not reflect the latest updates. Terms

Conditions

Endotoxemia

Keywords

enteral nutrition, endotoxemia, innate immunity, nutritional anti-inflammatory pathway, intestinal damage

Brief summary

During sepsis and septic shock the immune response can be overwhelming leading to excessive tissue damage, organ failure and death. Ideally, the inflammatory response is modulated leading to both adequate protection to invading pathogens as well as limitation of an exuberant immune response. In the last years, experimental evidence has been accumulating that enteral administration of lipid-enriched nutrition attenuates inflammation and preserves organ integrity in several inflammatory models. The current study investigates the immune-modulating potential of enriched enteral nutrition in a human setting of experimental endotoxemia.

Interventions

OTHERcontrol enteral nutrition

This feeding consists of 20en% fat, 16en% protein and 49en% carbohydrates

OTHERenriched enteral feeding

This feeding contains 46 energy percent (en%) fat, 24en% protein and 30en% carbohydrates and is enriched with phospholipids.

Study design

Allocation

RANDOMIZED

Intervention model

PARALLEL

Primary purpose

TREATMENT

Masking

TRIPLE (Subject, Investigator, Outcomes Assessor)

Eligibility

Sex/Gender

MALE

Age

18 Years to 35 Years

Healthy volunteers

Yes

Inclusion criteria

* Age ≥ 18 and ≤ 35 yrs * Male * Written informed consent * non-smoking

Exclusion criteria

* Use of any medication (e.g. NSAID's, antibiotics, gastrointestinal motility altering medicine, corticosteroids) * Smoking in the past year * History, signs or symptoms of cardiovascular disease * (Family; first degree) history of cerebrovascular disease * Previous vagal collapse * Hypertension (defined as RR systolic \> 160 or RR diastolic \> 90) * Hypotension (defined as RR systolic \< 100 or RR diastolic \< 50) * Renal impairment (defined as plasma creatinin \>120 μmol/l) * Liver enzyme abnormalities ( ASAT \> 60 U/L, ALAT \> 75 U/L, Gamma-GT \> 60 U/L) * Positive hepatitis serology * Positive HIV test * Allergy to milk and/or soy proteins

Design outcomes

Primary

Measure	Time frame
circulating cytokines	several time points from LPS administration until 24 hours

Secondary

Measure	Time frame
markers for sub-clinical organ damage (kidney, endothelium, intestine)	several time points from LPS administration until 24 h

Countries

Netherlands

Outcome results

None listed

Source: ClinicalTrials.gov · Data processed: Feb 4, 2026