The control on growth hormone release by free XXXX is maintained in @entity2012 .

@entity1 @entity7704 @entity1670 @entity2733 @entity2012 @entity42718 @entity1718 @entity413
Free @entity1718 (FFA) physiologically regulate GH release via a negative feedback. The aim of this study was to examine whether such feedback is preserved in @entity2012 , a condition in which alterations in other regulatory mechanisms of GH release occur. Eight acromegalic @entity1 (group 1: five @entity1 and three @entity1 , 43.0 +/- 4.2 yr old, mean +/- SE) received per os on two different days, at a 3 day-interval, in a random order, placebo or 250 mg of @entity42718 , an inhibitor of lipolysis analogous to @entity1670 , at 0700 and 1100 h. In both tests @entity7704 (1-29 @entity2733 ), 50 microg, was administered i.v. at 1300 h. Blood samples for GH, FFA, immunoreactive insulin (IRI), and @entity413 were taken from 0900 to 1500 h, and the time period considered for statistical analysis was 1200-1500 h, representative of steady-state condition for FFA, IRI, and @entity413 . Mean plasma FFA levels (1200-1500 h) were significantly lower after acipimox than after placebo (0.05 +/- 0.01 vs. 0.17 +/- 0.01 g/L, P < 0.01). In contrast, both mean basal GH levels (1200-1300 h) and the mean GH response to @entity7704 (GH delta area, 1300-1500 h) were significantly higher after acipimox than after placebo (12.0 +/- 1.9 vs. 7.8 +/- 1.2 microg/L, P < 0.01; 2937 +/- 959 vs. 1154 +/- 432 microg/L x 120 min, P < 0.01). The increase in both basal GH levels and GH delta area occurred in all eight @entity1 . Acipimox also reduced mean serum IRI (83 +/- 12 vs. 112 +/- 14 pmol/L) and blood @entity413 (5.1 +/- 0.1 vs. 5.7 +/- 0.1 mmol/L) levels, as compared with placebo (P < 0.03 or less). Eight acromegalic @entity1 (group 2: six @entity1 and two @entity1 , 46.6 +/- 5.7 yr old) underwent a constant i.v. 10% lipid infusion (150 mL/h), started at 0900 h and continued until 1500 h. Mean plasma FFA levels (1200-1500 h) were significantly higher during lipid infusion than after placebo (0.27 +/- 0.01 vs. 0.16 +/- 0.01 g/L, P < 0.02); in contrast, mean basal GH levels (1200-1300 h) were reduced by lipid infusion, as compared with placebo (9.9 +/- 3.1 vs. 16.6 +/- 4.4 microg/L, P < 0.01), and the same occurred for the GH delta area after @entity7704 (2498 +/- 1643 vs. 4512 +/- 1988 microg/L x 120 min, P < 0.01). Serum IRI and blood @entity413 levels were similar after placebo and during lipid infusion. These data indicate that, in @entity2012 , the acute reduction of circulating FFA levels results in increased GH release, whereas the increase in circulating FFA levels is accompanied by a reduced GH release. Taken together, these findings suggest that, in @entity2012 , the control of FFA on GH release is preserved.
