The binding and metabolism of low-density lipoprotein by skin fibroblasts of fetuses and newborns with anencephal

Abstract

We have previously demonstrated that the fetus with anencephaly is hypercholesterolemic. The plasma levels of total cholesterol and low-density lipoprotein cholesterol are threefold greater than those of normal fetuses. We have provided evidence that elevated low-density lipoprotein cholesterol levels were caused by reduced uptake and metabolism of low-density lipoprotein by atrophic adrenal glands deficient in low-density lipoprotein receptors. The purpose of the present investigation was to determine if other tissues, namely, skin fibroblasts, of the fetus with anencephaly were also deficient in low-density lipoprotein receptors. We compared the binding and metabolism of low-density lipoprotein by skin fibroblasts of fetuses with anencephaly and normal subjects. Cultures of skin fibroblasts were grown to confluency. Thereafter, the medium was changed to lipoprotein-deficient serum for 24 hours. The rate of uptake and degradation of iodine 125-iodo-LDL was determined as a function of time and concentration of low-density lipoprotein. The maximal specific binding of low-density lipoprotein was also determined. The rate of uptake, degradation, and the maximal binding of low-density lipoprotein was similar in skin fibroblasts of infants with anencephaly and normal subjects. We conclude that the elevated level of low-density lipoprotein cholesterol in cord blood of fetuses with anencephaly is not caused by deficiency of low-density lipoprotein receptors and metabolism in skin fibroblasts but instead by deficiency of low-density lipoprotein receptors and metabolism by atrophic adrenal glands.