Results: 5

1.
Fig. 4.

Fig. 4. From: Liver-Derived IGF-I Contributes to GH-Dependent Increases in Lean Mass and Bone Mineral Density in Mice with Comparable Levels of Circulating GH.

Loss of liver-derived IGF-I affects GH-induced changes in BMD, but not skeletal length. All mice treated with GH (+GH) had increased tip-to-tail length (A) and femoral length (B), and no differences were found between GH-treated Lit-Con and Lit-JAK2L mice. GH increased skeletal (C) and femoral (D) bone density in both groups, but GH-treated Lit-Con mice had significantly greater density than Lit-JAK2L mice (n = 15–18; *, P < 0.05; ***, P < 0.01; one-way ANOVA with Bonferroni post test).

Sarah M. Nordstrom, et al. Mol Endocrinol. 2011 July;25(7):1223-1230.
2.
Fig. 2.

Fig. 2. From: Liver-Derived IGF-I Contributes to GH-Dependent Increases in Lean Mass and Bone Mineral Density in Mice with Comparable Levels of Circulating GH.

Liver-derived IGF-I is necessary for a maximal GH-stimulated weight gain. A, All mice treated with GH (+GH) gained significantly more weight than untreated mice, but GH-treated Lit-Con mice gained more weight over time than GH-treated Lit-JAK2L mice (n = 15–18, P < 0.0001; two-way ANOVA). B, A separate comparison of final weights showed increased weights in both groups after GH treatment, but a significantly reduced final weight in GH-treated Lit-JAK2L mice vs. Lit-Con mice (n = 15–18; *, P < 0.05; ***, P < 0.001; one-way ANOVA with Bonferroni post test).

Sarah M. Nordstrom, et al. Mol Endocrinol. 2011 July;25(7):1223-1230.
3.
Fig. 1.

Fig. 1. From: Liver-Derived IGF-I Contributes to GH-Dependent Increases in Lean Mass and Bone Mineral Density in Mice with Comparable Levels of Circulating GH.

Lit-JAK2L mice have a more than 90% reduction in GH-dependent IGF-I production. A, Gene expression was determined by real-time PCR and 2−ΔΔCT analysis. GH increased liver Igf1 expression in Lit-Con mice but not in Lit-JAK2L mice (n = 7–8). B, Serum IGF-I was measured by ELISA at d 26. GH increased serum IGF-I in Lit-Con mice but not in Lit-JAK2L mice, resulting in a 93% reduction in circulating IGF-I in GH-treated Lit-JAK2L mice vs. GH-treated Lit-Con mice (n = 15–18). ****, P < 0.0001, one-way ANOVA with Bonferroni post test.

Sarah M. Nordstrom, et al. Mol Endocrinol. 2011 July;25(7):1223-1230.
4.
Fig. 3.

Fig. 3. From: Liver-Derived IGF-I Contributes to GH-Dependent Increases in Lean Mass and Bone Mineral Density in Mice with Comparable Levels of Circulating GH.

Liver-derived IGF-I is necessary for a maximal GH-induced increases in lean mass. A, Lean mass and fat mass were determined by dual energy x-ray absorptiometry scanning at d 26. GH increased lean mass increased in both groups, but GH-treated Lit-Con mice had significantly 12% greater lean mass than Lit-JAK2L mice. B, Fat mass was similar between untreated Lit-Con and Lit-JAK2L mice, and GH treatment did not alter the amount of fat in either genotype (n = 15–18; **, P < 0.01; ***, P < 0.001; one-way ANOVA with Bonferroni post test).

Sarah M. Nordstrom, et al. Mol Endocrinol. 2011 July;25(7):1223-1230.
5.
Fig. 5.

Fig. 5. From: Liver-Derived IGF-I Contributes to GH-Dependent Increases in Lean Mass and Bone Mineral Density in Mice with Comparable Levels of Circulating GH.

Circulating IGF-I is essential for GH-induced increases in spleen and kidney weight. Organs were weighed at d 26 and normalized body weight. A, Heart weights were comparable between all four groups. B, Liver weight increased in response to GH-treatment in both groups, but there were no differences between GH-treated Lit-Con and Lit-JAK2L mice. C, GH increased kidney weight in Lit-Con mice but not in Lit-JAK2L. D, There was also an increase in spleen weight in response to GH in Lit-Con mice but not in Lit-JAK2L mice (n = 15–18; *, P < 0.05; **, P < 0.01; ***, P < 0.001; one-way ANOVA with Bonferroni post test).

Sarah M. Nordstrom, et al. Mol Endocrinol. 2011 July;25(7):1223-1230.

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