Progestin-induced hypersecretion of growth hormone: an introductory review.
In the 1970s acromegalic features were reported in some dogs used in long-term toxicity studies of progestins. In 1980 confirmation that progestagen administration can lead to increased circulating growth hormone (GH) concentrations was obtained. This phenomenon appeared not to be confined to exogenous progestins, for an excess of GH was also found in bitches during the luteal phase of the oestrous cycle. In bitches with a progestin-induced excess of GH, GH secretion could neither be inhibited nor stimulated by well-known regulatory neurohormones, indicating autonomous secretion. Because it could not be attributed to a neoplasm and was reversible, an extra-pituitary site of GH production was investigated. The progestin-induced GH was found to originate from the mammary gland. This phenomenon seems to play a role in the mammary development that occurs during the luteal phase of the oestrous cycle. The increase in cell proliferative activity may also be responsible for the susceptibility of the mammary gland to neoplastic transformation. The discovery of mammary GH in the dog has recently become of wider importance now that expression of the GH gene has also been demonstrated in other species, namely, humans and cats.
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D000172:Acromegaly / Q000139:chemically induced / Q000662:veterinary*; D000818:Animals; D002415:Cats; D004283:Dog Diseases / Q000139:chemically induced*; D004285:Dogs; D005260:Female; D015870:Gene Expression; D013006:Growth Hormone / Q000235:genetics / Q000378:metabolism*; D006801:Humans; D008183:Luteal Phase; D008321:Mammary Glands, Animal / Q000378:metabolism*; D015674:Mammary Neoplasms, Animal / Q000139:chemically induced*; D011372:Progestins / Q000235:genetics / Q000633:toxicity*
D011372:Progestins; D013006:Growth Hormone