Insulin-like growth factor I (IGF-I) has a role in the whole-body anabolism and promotes both normal and abnormal cell growth in several tissues. Although IGF-I is also synthesized locally at numerous other sites, the liver does constitute the major site of its synthesis, and circulating IGF-I is mainly of hepatic derivation. The production of IGF-I is stimulated by growth hormone (GH), the secretion of which is influenced by circulating IGF-I level through a negative feed-back mechanism. Oral estrogen treatment causes a significant decrease of the IGF-I serum level, probably through a hepatocellular effect due to the first hepatic passage. Treatment with transdermal estradiol (tdE2) at the currently used doses does not cause, on average, substantial variations in the IGF-I serum level. The addition of an androgenic progestin--with strong hepatocellular actions, opposite to those of estrogen--completely reverses the IGF-I decrease induced by oral estrogens, and even causes a trend to IGF-I increase when tdE2 is used. Conversely, the addition of a non androgenic progestin, like dydrogesterone, does not cause interference with the estrogen effect.
Effect of progestins on IGF-I serum level in estrogen-treated postmenopausal women.
BIGLIA, Nicoletta;
1997-01-01
Abstract
Insulin-like growth factor I (IGF-I) has a role in the whole-body anabolism and promotes both normal and abnormal cell growth in several tissues. Although IGF-I is also synthesized locally at numerous other sites, the liver does constitute the major site of its synthesis, and circulating IGF-I is mainly of hepatic derivation. The production of IGF-I is stimulated by growth hormone (GH), the secretion of which is influenced by circulating IGF-I level through a negative feed-back mechanism. Oral estrogen treatment causes a significant decrease of the IGF-I serum level, probably through a hepatocellular effect due to the first hepatic passage. Treatment with transdermal estradiol (tdE2) at the currently used doses does not cause, on average, substantial variations in the IGF-I serum level. The addition of an androgenic progestin--with strong hepatocellular actions, opposite to those of estrogen--completely reverses the IGF-I decrease induced by oral estrogens, and even causes a trend to IGF-I increase when tdE2 is used. Conversely, the addition of a non androgenic progestin, like dydrogesterone, does not cause interference with the estrogen effect.
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