Related Experiment Video
Updated: Aug 4, 2026

The WinCF Model - An Inexpensive and Tractable Microcosm of a Mucus Plugged Bronchiole to Study the Microbiology of Lung Infections
Published on: May 8, 2017
Abnormalities in zinc homeostasis in young infants with cystic fibrosis
N F Krebs1, J E Westcott, T D Arnold
1Department of Pediatrics, University of Colorado School of Medicine, Denver 80262, USA.
Insights
Infants with cystic fibrosis show impaired zinc homeostasis, with higher fecal losses linked to fat excretion. This suggests a reason for low zinc status in these infants before treatment.
Area of Science:
- Pediatric Nutrition
- Mineral Metabolism
- Gastroenterology
Background:
- Low plasma zinc concentrations are observed in about 30% of infants with cystic fibrosis detected via newborn screening.
- Cystic fibrosis (CF) can impact nutrient absorption and metabolism.
- Understanding zinc status is crucial for managing CF in early life.
Purpose of the Study:
- To investigate zinc homeostasis in infants with cystic fibrosis using stable isotope techniques.
- To compare zinc absorption and metabolism between breast-fed and formula-fed infants with CF.
- To identify factors contributing to suboptimal zinc status in this population.
Main Methods:
- Stable isotope methodology (70Zn and 67Zn) was employed to track zinc absorption and excretion.
- Fifteen infants with CF (mean age 1.8 months) participated.
- Measurements included fractional zinc absorption, total absorbed zinc, endogenous fecal zinc, net absorbed zinc, and fecal fat excretion.
Main Results:
- Fractional zinc absorption was significantly higher in breast-fed infants (0.40) compared to formula-fed infants (0.13).
- Total absorbed zinc was higher in formula-fed infants due to greater dietary intake.
- Endogenous fecal zinc excretion was twofold higher in formula-fed infants, correlating with fecal fat excretion (r=0.89).
- Net zinc absorption was negative in both feeding groups.
Conclusions:
- Infants with cystic fibrosis exhibit impaired zinc homeostasis, regardless of feeding type.
- Increased endogenous fecal zinc losses, associated with high fecal fat, suggest impaired zinc conservation.
- These findings provide a potential explanation for the common suboptimal zinc status observed in infants with CF prior to intervention.
Abstract:
Low plasma zinc concentrations have been reported in approximately 30% of young infants with cystic fibrosis identified by newborn screening. The objective of this study was to examine zinc homeostasis in this population by application of stable isotope methodology. Fifteen infants with cystic fibrosis (9 male, 6 female; 7 breast-fed, 8 formula-fed) were studied at a mean (+/-SD) age of 1.8 +/- 0.7 mo. On d 1, 70Zn was administered intravenously, and 67Zn was quantitatively administered with all human milk/formula feeds during the day. Three days later, a 3-d metabolic period was initiated, during which time intake was measured and complete urine and fecal collections were obtained. Fractional zinc absorption, total absorbed zinc, endogenous fecal zinc, and net absorbed zinc were measured; fecal fat excretion was also determined. Fractional absorption was significantly higher for the breast-fed infants (0.40 +/- 0.21) compared with the formula-fed group (0.13 +/- 0.06) (p = 0.01), but with the significantly higher dietary zinc intake of the formula-fed group, total absorbed zinc was higher for those receiving formula (p = 0.01). In 1 infants with complete zinc metabolic data, excretion of endogenous zinc was twofold greater for the formula-fed infants (p < 0.05); net absorption (mg zinc/d) was negative for both feeding groups: -0.04 +/- 0.52 for breast-fed; -0.28 +/- 0.57 for formula-fed. Endogenous fecal zinc losses correlated with fecal fat excretion (r = 0.89, n = 9, p = 0.001), suggesting interference with normal conservation of endogenously secreted zinc. These findings indicate impaired zinc homeostasis in this population and suggest an explanation for the observations of suboptimal zinc status in many young infants with cystic fibrosis prior to diagnosis and treatment.
Related Concept Videos
Sex-linked Disorders
Cystic Fibrosis: Pathogenesis
CF is primarily caused by a genetic mutation in a chromosome 7 gene coding for the cystic fibrosis transmembrane conductance regulator (CFTR) protein. The most common gene mutation leading to CF is the ΔF508 mutation, but...
Vitamins

