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. 2008 Oct 28;6(10):e254. doi: 10.1371/journal.pbio.0060254

Figure 4. GH/IGF-I Deficiency in Adult bIGF1RKO+/− .

Figure 4

(A) Hypothalamic GHRH was higher (left) and SRIH lower (middle) in bIGF1RKO+/− than control mice at age 9 mo. Pituitary GH was markedly low (right). The wet weight of the hypothalamus and total proteins extracted from hypothalamus in mutants did not differ from control values (bIGF1RKO+/− 1.55 ± 0.12 mg versus controls 1.53 ± 0.10 mg, p = 0.86, NS).

(B) GH immunoreactivity (red) was much lower in bIGF1RKO+/− than control pituitaries, here in frontal sections through the lateral half gland with DAPI (blue) nuclear counter-stain. aP, anterior pituitary; iP, intermediate pituitary; pP, posterior pituitary.

(C) Liver GH receptor (upper) and Jak2 (lower panel) were overphosphorylated upon administration of GH into the portal vein, indicating hypersensitivity of GHR (n = 4 per group; paired t-test). Right: representative western blots.

(D) IGF-binding protein-3 (IGFBP-3, left), ALS (middle), and circulating IGF-I (right) were significantly less abundant in bIGF1RKO+/− mice than controls, indicative of deficient peripheral GH action. IGFBP-3 and ALS (and also Spi2.1, see text) were determined only in males.