Membrane potential dependence of Fe(III) uptake by mouse duodenum.

Area of Science:

• Cell Biology
• Physiology
• Nutritional Science

Background:

• Intestinal iron absorption is crucial for maintaining iron homeostasis.
• The precise mechanism of energy coupling for iron uptake remains incompletely understood.
• Previous studies indicated metabolic dependence but lacked clarity on specific ion involvement.

Purpose of the Study:

• To elucidate the role of sodium and membrane potential in intestinal iron (Fe3+) uptake.
• To investigate the energy coupling mechanisms involved in duodenal iron absorption.
• To examine the effects of specific ion substitutions and ionophores on iron transport.

Main Methods:

• In vitro studies using mouse duodenal fragments.
• Substitution of sodium (Na+) with potassium (K+) or rubidium (Rb+) in incubation media.
• Assessment of iron uptake with and without phloridzin, valinomycin, and nigericin.
• In vivo studies using tied-off intestinal segments.

Main Results:

• Fe3+ uptake was inhibited by replacing Na+ with K+ or Rb+, and this inhibition was reversible.
• Glucose uptake was not affected by Na+ substitution, ruling out indirect effects.
• Ionophores like valinomycin modulated both glucose and Fe3+ uptake, with concentration-dependent effects.
• In vivo experiments confirmed the inhibitory effect of univalent cations and enhanced absorption with ionophores.

Conclusions:

• Intestinal Fe3+ uptake is not directly Na+-dependent.
• The findings strongly suggest a dependence of the iron uptake process on the brush-border membrane potential.
• Modulation of membrane potential offers a potential avenue for influencing intestinal iron absorption.