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The Effect of Free Fatty Acids on Growth Hormone(GH)-Releasing Hormone-Mediated GH Secretion in Man^*

The Salk Institute for Biological Studies (N.L.), La Jolla, California 92037 La Jolla, California 92037
Department of Medicine, Institute of Clinical Endocrinology, Tokyo Women’s Medical College, 10 Ichigaya-Kawada-cho, Shinjuku-ku, Tokyo 162, Japan; and Laboratories for Neuroendocrinology, The Salk Institute for Biological Studies (N.L.), La Jolla, California 92037 La Jolla, California 92037

Address requests for reprints to: Dr. Toshihiro Imaki, Departmentof Medicine, Tokyo Women’s Medical College, 10 Ichigaya-Kawadacho,Shinjuku-ku, Tokyo 162, Japan.

The effect of FFA on GH-releasing hormone(GHRH)-mediated secretion of GH was examined in six normalyoung men. Three of the men were infused with 250 ml of alipid-heparin solution at 1.67 ml/min for 150 min, and the otherthree were given an equivalent volume of saline in the samemanner. Thirty minutes after the start of infusion, 100 µg GHRH (the 44-amino acid form) were injected iv, and plasmaGH and FFA were measured. One week later, the same menparticipated in an identical experiment, but the ones who hadreceived lipid-heparin previously were given saline and vice versa. In both experiments, plasma FFA increased to 2.25 ± 0.16meq/liter (mean ± SEM) 60 min after the start of lipid-heparininfusion, whereas FFA levels did not change significantly in thesaline-treated group. Mean plasma GH levels reached peakconcentrations in both groups 30 min after GHRH treatment.However, the peak GH response when lipid-heparin was givenwas significantly diminished (8.4 ± 1.7 ng/ml), compared withthe peak response when saline was given (28.9 ± 7.1 ng/ml).These data suggest that plasma FFA elevations induced by lipidheparininfusion inhibit GH secretion induced by GHRH.

^* This work was supported by a grant from the Intractable Diseases Division, Public Health Bureau, Ministry of Health and Welfare, Japan, and NIH Grants AD-09690 and AM-18811.

Received June 21, 1984.

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