Figure 5.

Both hypothalamic somatostatin and liver-derived IGF-I reduce basal pituitary GH secretion. Proposed model is shown for the regulation of basal GH release from the pituitary by both intermittent somatostatin release from the hypothalamus and continuous IGF-I release from the liver in male rodents. The GH secretion in male rodents is intermittent, with low basal levels between pulses. In the normal situation (left panels), the low basal GH levels are due to suppression of GH release from the pituitary by pulses of hypothalamic somatostatin (upper left) that coincide with the low basal GH levels (middle left). In addition, basal GH levels are suppressed by continuous release of liver-derived IGF-I (lower left). Loss of either hypothalamic somatostatin (somatostatin depletion; central panels) or liver-derived IGF-I (liver IGF-I depletion; right panels) causes enhanced basal GH levels. Therefore, the effects of both somatostatin and IGF-I seem necessary to maintain low GH trough levels and thereby the masculinizing effect of pulsatile GH secretion in rodents. Arrows depict the effect of a GH pulse to initiate the somatostatin pulse during the next coming GH trough. Therefore, GH can inhibit its own secretion via a short loop feedback effect at the hypothalamic level, suggesting that the pulsatility of GH secretion is due to a reciprocal interplay between the hypothalamus and the pituitary and is not only due to an intrinsic rhythm of the hypothalamus itself.