The GH-IGF-1 axis alters through the menstrual cycle. During the periovulatory period when oestrogen levels have risen serum growth hormone (GH) levels increase 2-fold. IGF-1 levels have been reported as unchanged or modestly increased in the periovulatory period. Similarly exogenous oestrogens also increase GH levels while IGF-1 levels have been reported as reduced, unchanged or increased. Peripheral responsiveness to GH as reflected by the IGF-1 response to an acute bolus of GH is reduced in women on exogenous oestrogens suggesting a state of relative GH resistance. It is unknown if endogenous oestrogen has a similar impact on the GH-IGF-1 axis. To investigate this possibility further normal women were challenged with the IGF-1 generation test at different stages of the menstrual cycle.
Nine healthy women (age 38(6)years (mean (sd)); BMI 25(4)kg/m2) with a regular menstrual cycle were recruited . An IGF-1 generation test, which involves a sc injection of 21IU (7mg) of GH,was performed in the early follicular(EF), periovulatory(PO) and midluteal(ML) phases . At baseline serum samples were assayed for oestradiol. Serum IGF-1 levels were measured at baseline and 24 hours after GH administration.
As expected oestradiol levels were lower in the EF compared with PO or ML phases (32.6(7.8)vs 69.6(16.2)vs 66.6(23.6)pg/ml respectively (p<0.001)). Baseline IGF-1 was lower whereas increment IGF-1 (peak minus baseline) was higher in the EF compared with PO or ML (Baseline:297.4(48.9)vs 335.0(55.2)vs 346.6(78.2)ng/ml (p=0.01); Increment IGF-1:234.4(69.7)vs 194.7(37.8)vs 185.2(37.3)ng/ml (p=0.008)). Peak IGF-1 was unchanged throughout (531.9(69.7)vs 529.7(60.0)vs 531.8(66.7)ng/ml (p=1)).
In conclusion baseline IGF-1 increases from mid-cycle onwards presumably due to an increase in GH secretion secondary to increased oestrogen. The reduction in increment IGF-1 from mid-cycle onwards may represent a reduction in peripheral sensitivity to GH, however the constant peak IGF-1 level throughout the menstrual cycle suggests that maximal capacity to generate IGF-1 is unchanged. Therefore the changes seen in the GH-IGF-1 axis with endogenous oestrogen differ from those seen in response to exogenous oestrogen.
22 - 24 Mar 2004
British Endocrine Societies