Since 1911 the problem of placental permeability to insulin has been studied sporadically. Carlson, Drennan, Orr and Jones (1, 2) observed that pregnant dogs failed to develop glycosuria after pancreatectomy and concluded that the fetus pro- tected the mother against diabetes, presumably by diaplacental movement of some substance. Other investigators (3, 4), however, were unable to con- firm these early studies. Results of work with goats (5), rabbits (6, 7) and mice (8) were vari- able and suggest that species differences exist in the placental permeability to insulin. By in vitro techniques, systems for the proteolytic inactivation of insulin have been demonstrated in the rat (9) and human placenta (10).
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Buse et al. (1962) studied this question.
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