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Testosterone Treatment in Adolescents with Delayed Puberty: Changes in Body Composition, Protein, Fat, and Glucose Metabolism¹

Division of Pediatric Endocrinology, Metabolism and Diabetes Mellitus, Children’s Hospital, University of Pittsburgh, Pittsburgh, Pennsylvania 15213

Address all correspondence and requests for reprints to: Silva Arslanian, Division of Endocrinology, Children’s Hospital of Pittsburgh, 3705 Fifth Avenue at DeSoto Street, Pittsburgh, Pennsylvania 15213. E-mail: arslans{at}chplink.chp.edu

Previously, we demonstrated decreased protein breakdown and insulin resistance in pubertal adolescents compared with prepubertal children. Puberty-related increases in sex steroids and/or GH could be potentially responsible. In the present study, the effects of 4 months of testosterone enanthate (50 mg im every 2 weeks) on body composition, protein, fat, and glucose metabolism and insulin sensitivity were evaluated in adolescents with delayed puberty. Body composition was assessed by H₂¹⁸O-dilution principle. Protein breakdown, oxidation, and synthesis were measured during primed constant infusion of [1-¹³C]leucine. Whole-body lipolysis was measured during primed constant infusion of [²H₅]glycerol. Insulin action in suppressing proteolysis and lipolysis and stimulating glucose disposal was assessed during a stepwise hyperinsulinemic (10 and 40 mU•m²•min) euglycemic clamp. Fat and glucose oxidation rates were calculated from indirect calorimetry measurements.

After 4 months of testosterone treatment, height, weight, and fat free mass (FFM) increased and fat mass, percent body fat, plasma cholesterol, high- and low-density lipoproteins, and leptin levels decreased significantly. Whole-body proteolysis and protein oxidation were lower after testosterone treatment (proteolysis, 0.49 ± 0.03 vs. 0.54 ± 0.04 g•h•kg FFM, P = 0.032; oxidation, 0.05 ± 0.01 vs. 0.09 ± 0.01 g•h•kg FFM, P = 0.015). Protein synthesis was not different, and resting energy expenditure was not different. Total body lipolysis was not affected by testosterone treatment, however, fat oxidation was higher after testosterone (pre-: 2.4 ± 0.7 vs. post-: 3.5 ± 0.7 µmol•kg•min, P = 0.031). During the 40 mU•m²•min hyperinsulinemia, insulin sensitivity of glucose metabolism was not affected with testosterone therapy (59.1 ± 8.8 vs. 57.1 ± 8.2 µmol•kg•min per µU/mL). However, metabolic clearance rate of insulin was higher posttestosterone (13.6 ± 1.1 vs. 16.7 ± 0.8 mL•kg•min, P = 0.004).

In conclusion, after 4 months of low-dose testosterone treatment in adolescents with delayed puberty 1) FFM increases and fat mass and leptin levels decrease; 2) postabsorptive proteolysis and protein oxidation decrease; 3) fat oxidation increases; and 4) insulin sensitivity in glucose metabolism does not change, whereas insulin clearance increases. These longitudinal observations are in agreement with our previous cross-sectional studies of puberty and demonstrate sparing of protein breakdown of approximately 1.2 g•kg•day FFM, wasting of fat mass, but no change in insulin sensitivity after short periods of low-dose testosterone supplementation.

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