Continuation of growth hormone (GH) substitution during fasting in GH-deficient patients decreases urea excretion and conserves protein synthesis

The consequences of GH deficiency during conditions in which endogenous GH release is acutely stimulated are largely unknown. Short-term fasting const itutes a robust GH stimulus, but the metabolic significance of GH during fa sting is uncertain. To address both of these issues, we therefore evaluated the effect of GH on substrate metabolism during fasting in adults with GH deficiency. Seven hy popituitary GH-deficient patients were each studied twice during a 40-h fas t: once with GH replacement continued and once with GH discontinued during the fast. After 40 h of fasting, protein synthesis and turnover were higher with than without GH replacement[phenylalanine incorporation (mu mol/kg fa t free mass/h): 36.6 +/- 1.2(GR) us. 32.8 +/- 1.4, P < 0.05; phenylalanine flux (mu mol/kg fat free mass/h): 41.3 +/- 1.0 (GH) us. 38.0 +/- 1.8, P < 0 .05]. During continued GH replacement, urea excretion decreased during nigh ttime [urea excretion (mmol/24 h): 269 +/- 51 (GH) us. 390 +/- 69, P < 0.05 ], and a significant decline in urea-N synthesis rate was found [urea-N syn thesis rate (mmol/h): 14.7 <plus/minus> 1.6 (GH) vs. 21.1 +/- 2.2, P < 0.01 ]. GH replacement was associated with increased lipid oxidation [lipid oxid ation (mg/kg per min): 0.91 +/- 0.07 (GH) vs. 0.70 +/- 0.03, P < 0.05]. Fin ally, continuation of GH induced moderate elevations in plasma glucose leve ls without significant changes in total glucose turnover or oxidation. In summary, continued GH substitution during fasting conserves nitrogen, wh ich involves stimulation or maintenance of protein synthesis. Our data supp ort the importance of GH replacement in hy, popituitary adults.