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Hormone and Receptor Studies: Relationship to Linear Growth in Childhood and Puberty^*

Department of Medicine, Division of Endocrinology and Metabolism, and Department of Pathology, University of Florida Gainesville, Florida 32610

Address requests for reprints to: Thomas J. Merimee, M.D., Department of Medicine, Division of Endocrinology and Metabolism, University of Florida, Box J-226, JHMHC, Gainesville, Florida 32610–0226.

Preliminary data suggested different patterns of hormonal control of linear growth in males and females. To better define these patterns, serum samples were collected from 75–125 boys and a similar number from girls for each year of age between 3–16 yr (n = 2416). Fewer samples were collected from 2-yr-olds, newborns, and adults (n = 151). Samples for each age were aliquoted, combined, and assayed for GH, GHbinding protein (GHBP), insulin-like growth factor-I, and testosterone.

GHBP, expressed as a percentage of the [¹²⁵I[GH bound, increased yearly in males and females, with no relationship to the secretion of sex hormones. The increase in binding of [¹²⁵I[ GH and, by inference, GH receptors occurred at a greater rate between the ages of 2–10 yr than between 10–16 yr (in terms of absolute binding, 1.2 ± 0.11% vs. 0.38 ± 0.04% yearly; P < 0.001). In each age group, however, the increase in GHBP exhibited a strong positive correlation with linear height (r = 0.96–0.98 in males; r = 0.92–0.99 in females).

Before puberty, GH and insulin-like growth factor-I concentrations were consistently greater in females. Between 10–16 yr of age, height velocity (centimeters of growth per yr) correlated strongly with GH in girls (r = 0.86), but did not correlate with GH in boys of a similar age (r = –0.13). The major pubertal growth spurt in males strongly correlated with a rise in serum testosterone concentration beginning at age 11 yr (r = 0.92). Small peaks of GH secretion before and after the major period of accelerated growth in males possibly prolonged the major growth phase, but did not initiate it.

^* This work was supported in part by a grant (AM-18130) from the NIAMDD, NIH; grants from the General Clinical Research Center Program of the Division of Research Resources; and NIH (RR-00082). Also supported by a contract with the Department of Health and Rehabilitative Services of the State of Florida for the University of Florida Diabetes Research Education and Treatment Center.

Received February 19, 1991.

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