Interaction of Insulin and Chlorpromazine in Teratogenesis

Abstract

IT has been shown that treatment of chicken embryos with insulin will produce malformations of quite different kinds according to the developmental stage at which the hormone is administered. During the earliest period of incubation rumplessness is the typical insulin-induced defect, that is, a partial or complete suppression of the tail skeleton and its related soft tissues^1–3. When, however, insulin is injected after 4 or 5 days of incubation the tail structures remain intact, but the embryos are likely (incidence and severity always depending on dosage) to have disproportionately short legs (micromelia) and abnormalities of the facial skeleton, most commonly expressed as a shortening of the upper beak⁴. During the second period of response embryos can be effectively protected against the teratogenic activity of insulin by supplying them with supplementary nicotinamide, whereas during early stages only a limited lowering of the teratogenic activity of insulin is achieved by nicotinamide supplementation^5,6.