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The effect of in utero insulin exposure on tissue iron status in fetal rats
M K Georgieff1, R J Kassner, W J Radmer
1Department of Pediatrics, University of Minnesota School of Medicine, Minneapolis 55455.
Insights
Fetal exposure to insulin in rats leads to lower iron concentrations in the liver and skeletal muscle, suggesting a link between maternal diabetes and infant iron status. This research highlights potential mechanisms for iron deficiency in infants of diabetic mothers.
Area of Science:
- Perinatal Medicine
- Developmental Biology
- Nutritional Biochemistry
Background:
- Infants born to diabetic mothers exhibit biochemical signs of iron deficiency.
- Fetal hyperinsulinemia in sheep is associated with decreased iron concentrations, likely due to increased hemoglobin synthesis.
- The impact of fetal insulin exposure on tissue iron concentrations requires further investigation.
Purpose of the Study:
- To investigate the effect of fetal insulin exposure on tissue iron concentrations in newborn rat pups.
- To determine if insulin administration to fetuses reduces iron levels in organs such as the liver, skeletal muscle, small intestine, heart, and brain.
Main Methods:
- Pregnant rats were injected with insulin or a diluent on day 19 of gestation.
- Fetuses were delivered at term (days 21 or 22) after insulin or diluent administration.
- Iron concentrations in various tissues (liver, skeletal muscle, small intestine, heart, brain) were measured in newborn pups.
Main Results:
- Insulin-treated rat pups had higher birth weights compared to controls.
- Fetuses treated with 2 U of neutral protamine Hagedorn insulin showed significantly lower liver iron concentrations.
- Higher doses of protamine zinc insulin resulted in significantly lower iron concentrations in both liver and skeletal muscle.
Conclusions:
- Fetal insulin exposure in rats is associated with reduced iron concentrations in the liver and skeletal muscle.
- These findings suggest a potential mechanism linking maternal diabetes during pregnancy to altered iron metabolism in offspring.
- Further research is warranted to elucidate the precise mechanisms and clinical implications for infants of diabetic mothers.
Abstract:
Newborn infants of diabetic mothers have serum biochemical signs of iron deficiency in cord blood directly related to elevations of cord erythropoietin and Hb concentrations. In sheep, chronic fetal hyperinsulinemia results in fetal hypoxemia, expansion of the red cell mass, and decreased iron concentrations, most likely due to increased iron utilization for Hb synthesis. To determine whether fetal insulin exposure also results in reduced tissue iron concentrations, we measured liver, skeletal muscle, small intestine, heart, and brain iron concentrations in newborn rat pups after s.c. fetal injection of insulin or diluent alone on d 19 of gestation. The fetuses of 11 pregnant rats were exteriorized, injected with 2 U neutral protamine Hagedorn insulin or diluent, replaced in utero, and delivered on d 22. To determine dose dependency, the fetuses of six pregnant rats were injected with 3 U of longer-acting protamine zinc insulin and delivered on d 21. At delivery, the insulin-treated groups had higher birth weights than the placebo-treated group, although plasma insulin concentrations were not different. The 2 U neutral protamine Hagedorn insulin-treated fetuses had significantly lower mean +/- SEM liver iron concentrations than the control fetuses (910 +/- 34 versus 1014 +/- 43 micrograms/g dry tissue weight; p less than 0.05), but had similar skeletal muscle iron concentrations. The 3 U protamine zinc insulin-treated fetuses had significantly lower liver and skeletal muscle iron concentrations compared to control and to 2 U neutral protamine Hagedorn insulin-treated fetuses (p less than 0.05). No differences in small intestine, heart, or brain iron concentrations were seen among groups.(ABSTRACT TRUNCATED AT 250 WORDS)