Abstract
1. 1. 125I-labelled insulin binds in vitro to isolated mammary cells prepared by treating freshly excised murine mammary gland with bacterial collagenase. The binding is specific for insulin, and it is saturable with respect to insulin in the range of physiologic concentrations of the hormone. Small amounts (50 pg/ml) of native insulin effectively compete with labeled insulin for binding. The specific binding of insulin to mammary cells is destroyed by digesting the cells with trypsin. 2. 2. Physiologic concentrations (about 10 −10 M of insulin stimulate the incorporation of [ 3H] uridine into trichloroacetic acid-precipitable material by isolated mammary cells from pregnant mice, but not from adult virgin mice. Although a metabolic response to insulin is observed only in cells from pregnant animals, the characteristics of 125I-labelled insulin binding to cells from pregnant and virgin animals are very similar. Lactating cells bind 3–4 times more insulin than do cells from virgin or pregnant animals. 3. 3. Although proliferation of mammary cells during pregnancy may be stimulated or regulated by insulin following prolactin priming of these cells, the normal quiescence of the virgin tissue probably cannot be explained by the absence of insulin receptors. The absence of metabolic responses to insulin in the virgin tissue is probably explained by the improper function or incomplete nature of the hormone-receptor complex in the membrane.
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