A. Rijnberk et Ja. Mol, PROGESTIN-INDUCED HYPERSECRETION OF GROWTH-HORMONE - AN INTRODUCTORY REVIEW, Journal of Reproduction and Fertility, 1997, pp. 335-338
In the 1970s acromegalic features were reported in some dogs used in l
ong-term toxicity studies of progestins. In 1980 confirmation that pro
gestagen administration can lead to increased circulating growth hormo
ne (GH) concentrations was obtained. This phenomenon appeared not to b
e 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 i
nhibited nor stimulated by well-known regulatory neurohormones, indica
ting autonomous secretion. Because it could not be attributed to a neo
plasm and was reversible, an extra-pituitary site of GH production was
investigated. The progestin-induced GH was found to originate from th
e mammary gland. This phenomenon seems to play a role in the mammary d
evelopment that occurs during the luteal phase of the oestrous cycle.
The increase in cell proliferative activity may also be responsible fo
r 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 demonstrat
ed in other species, namely, humans and cats.