Abstract 484 Poster Session I, Saturday, 5/1 (poster 297)

Despite evidence that insulin resistance evolves during puberty, the underlying hormonal mechanism(s) responsible for it remain unresolved. Puberty related increases in GH and/or sex steroids are likely candidates. However, in a previous study four months of low-dose testosterone supplementation in adolescents with delayed puberty was not associated with deterioration of insulin action ( JCEM 82:3213, 1997). Therefore, in the present investigation the effects of four months of hGH (0.3 mg/kg/week) on body composition, protein, fat, and glucose metabolism and insulin sensitivity were evaluated in adolescents (age:14.0±0.6 yrs) with NGHD-SS. Body composition was assessed with dual energy x-ray absorptiometry. Whole body glucose, protein and fat turnover were measured with [6,6-2H2]glucose, [1-13C]leucine, and [2H5]glycerol. Invivo insulin action was assessed during a 3-hour hyperinsulinemic (40 mu/m2/min)-euglycemic clamp. (Table) In summary, short-term GH treatment in adolescents with non-GH deficient short stature led to: 1) increased lean body mass and decreased fat mass and leptin levels, 2) improved cardiovascular lipid risk profile, 3) increased hepatic glucose production and increased fasting insulin, and 4) decreased insulin-stimulated glucose uptake. We conclude that during puberty insulin resistance/ hyperinsulinemia is secondary to increased GH secretion and both act in unison to promote pubertal anabolism and enhance the growth spurt.

Table 1 No caption available.
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