Overview

This trial is active, not recruiting.

Condition obesity
Treatment ibuprofen
Sponsor Swiss Federal Institute of Technology
Collaborator University of Monterrey, Mexico
Start date April 2016
End date December 2016
Trial size 40 participants
Trial identifier NCT02745925, Fe_Abs_Ibu

Summary

The main iron regulatory protein in the human metabolism is hepcidin. In normal weight, healthy subjects, hepcidin is regulated through the iron status of the body: low iron status results in low hepcidin concentrations, which facilitates dietary iron absorption. In obesity, which is an inflammatory state, hepcidin concentrations are increased and iron absorption is reduced despite low iron stores, leading to iron deficiency over time. Whether lowering the chronic low-grade inflammation during a limited treatment period and thereby lowering hepcidin concentration can improve iron absorption is uncertain.

United States No locations recruiting
Other Countries No locations recruiting

Study Design

Allocation non-randomized
Endpoint classification bio-availability study
Intervention model parallel assignment
Masking open label
Primary purpose basic science
Arm
(Experimental)
normal-weight women
ibuprofen
(Experimental)
obese women
ibuprofen

Primary Outcomes

Measure
Fractional iron absorption
time frame: Days 15 and 45

Secondary Outcomes

Measure
Plasma ferritin
time frame: Days 1, 15, 30, 45
Hemoglobin
time frame: Days 1, 15, 30, 45
Transferrin receptor
time frame: Days 1, 15, 30, 45
Hepcidin
time frame: Days 1, 15, 30, 45
c-reactive protein
time frame: Days 1, 15, 30, 45
interleukin-6
time frame: Days 1, 15, 30, 45
alpha-1-acid-glycoprotein
time frame: Days 1, 15, 30, 45

Eligibility Criteria

Female participants from 18 years up to 45 years old.

Inclusion Criteria: - normal-weight (BMI18.5-24.9kg/m2) or obesity (BMI 30-35kg/m2) - pre-menopausal - no chronic illness and no significant medical conditions that could influence iron or inflammatory status other than obesity - no-smoking Exclusion Criteria: - Diagnosed chronic disease or gastrointestinal disorders - Metabolic disorders (e.g. diabetes) - Regular use of medication (except oral contraceptives) - Subject on a weight loss diet or planning to start a weight loss diet during the duration of the study - Pregnancy or lactation

Additional Information

Official title Mechanism of Decreased Iron Absorption in Obesity: Controlling Adiposity-related Inflammation
Principal investigator Isabelle Herter-Aeberli, PhD
Description In states of high hepcidin concentration, intestinal iron absorption (through enterocytes) and recycling of iron (through macrophages) is reduced. The extent to which non-heme iron is absorbed from the diet is influenced by the composition of the diet. Ascorbic acid is a potent enhancer of non-heme iron absorption. It's mechanism of action is luminal reduction of dietary ferric iron (Fe3+) to more soluble ferrous iron (Fe2+). A study in the inestigator's laboratory showed that the enhancing effect of ascorbic acid on non-heme iron absorption is reduced in overweight and obese individuals. Possible explanations for this fact are the different sites of action of ascorbic acid and serum hepcidin on the enterocytes in dietary iron absorption. Increased hepcidin reduces iron efflux into the circulation at the basolateral membrane of the enterocyte. Therefore the improved iron transport into enterocytes through ascorbic acid at the luminal side (via the divalent metal transporter (DMT)-1), by reducing Fe3+ to Fe2+ seems to be less successful. To improve iron absorption in obese subjects, an intervention at the basolateral membrane of the enterocyte would be needed.
Trial information was received from ClinicalTrials.gov and was last updated in October 2016.
Information provided to ClinicalTrials.gov by Swiss Federal Institute of Technology.