1. Figure 1. Serum concentrations of IGF-I (A), IGF-II (B), IGFBP-3 (C), and ALS (D) throughout life in GHD (closed circles) and healthy control (open circles) subjects.
Effect of Severe Growth Hormone (GH) Deficiency due to a Mutation in the GH-Releasing Hormone Receptor on Insulin-Like Growth Factors (IGFs), IGF-Binding Proteins, and Ternary Complex Formation Throughout Life1
J Clin Endocrinol Metab. 1999;84(11): doi: /jcem
J Clin Endocrinol Metab | Copyright © 1999 by The Endocrine Society

2. Figure 2. Comparison of molar ratios of IGF-I and IGF-II to IGFBP-3 in GHD and control children (A) and in GHD and control adults (B). Boxes represent the interquartile range.
Effect of Severe Growth Hormone (GH) Deficiency due to a Mutation in the GH-Releasing Hormone Receptor on Insulin-Like Growth Factors (IGFs), IGF-Binding Proteins, and Ternary Complex Formation Throughout Life1
J Clin Endocrinol Metab. 1999;84(11): doi: /jcem
J Clin Endocrinol Metab | Copyright © 1999 by The Endocrine Society

3. Figure 3. Theoretical partitioning of IGF-I between IGFBP-1, IGFBP-2, and IGFBP-3 in control (A) and GHD (B) subjects. Theoretical concentrations of IGF-I bound to IGFBP-1 (IGF-I/IGFBP-1), IGFBP-2 (IGF-I/IGFBP-2), and IGFBP-3 (IGF-I/IGFBP-3) were calculated from measured concentrations and affinity constants as described in Materials and Methods. Residual IGF-I corresponds to IGF-I bound to other IGFBPs or free IGF-I. The total height of each column is equivalent to median concentration of IGF-I measured by immunoassay in each subject group, and the median concentration of each theoretical quantity is represented by the individual boxes. The proportion of each theoretical quantity expressed as a percentage of the total IGF-I concentration is indicated.
Effect of Severe Growth Hormone (GH) Deficiency due to a Mutation in the GH-Releasing Hormone Receptor on Insulin-Like Growth Factors (IGFs), IGF-Binding Proteins, and Ternary Complex Formation Throughout Life1
J Clin Endocrinol Metab. 1999;84(11): doi: /jcem
J Clin Endocrinol Metab | Copyright © 1999 by The Endocrine Society

4. Figure 4. Theoretical partitioning of IGF-II between IGFBP-1, IGFBP-2, and IGFBP-3 in control (A) and GHD (B) subjects. Theoretical concentrations of IGF-II bound to IGFBP-1 (IGF-I/IGFBP-1), IGFBP-2 (IGF-I/IGFBP-2), and IGFBP-3 (IGF-I/IGFBP-3) were calculated from measured concentrations and affinity constants as described in Materials and Methods. Residual IGF-II corresponds to IGF-II bound to other IGFBPs or free IGF-II. The total height of each column is equivalent to median concentration of IGF-II measured by immunoassay in each subject group, and the median concentration of each theoretical quantity is represented by the individual boxes. The proportion of each theoretical quantity expressed as a percentage of the total IGF-II concentration is indicated.
Effect of Severe Growth Hormone (GH) Deficiency due to a Mutation in the GH-Releasing Hormone Receptor on Insulin-Like Growth Factors (IGFs), IGF-Binding Proteins, and Ternary Complex Formation Throughout Life1
J Clin Endocrinol Metab. 1999;84(11): doi: /jcem
J Clin Endocrinol Metab | Copyright © 1999 by The Endocrine Society

5. Figure 5. Theoretical partitioning of ALS between free ALS and the ternary complex in control (A) and GHD (B) subjects. Theoretical concentrations of free ALS, ternary complex containing IGF-I (TC[IGF-I]), and ternary complex containing IGF-II (TC[IGF-II]) were calculated from the measured concentration of total ALS and the theoretical concentrations of IGF/IGFBP-3 binary complexes. The total height of each column corresponds to the median concentration of total ALS in each group, measured by immunoassay, and the median concentration of each theoretical quantity is represented by the individual boxes. The amount of each theoretical quantity expressed as a percentage of total ALS concentrations is indicated.
Effect of Severe Growth Hormone (GH) Deficiency due to a Mutation in the GH-Releasing Hormone Receptor on Insulin-Like Growth Factors (IGFs), IGF-Binding Proteins, and Ternary Complex Formation Throughout Life1
J Clin Endocrinol Metab. 1999;84(11): doi: /jcem
J Clin Endocrinol Metab | Copyright © 1999 by The Endocrine Society