Horm Metab Res 1977; 9(5): 389-394
DOI: 10.1055/s-0028-1093488
Originals

© Georg Thieme Verlag KG Stuttgart · New York

The Effect of Lipids on Prolactin and Growth Hormone Secretion

W. M. Fraser , W. G. Blackard
  • Department of Medicine and the Clinical Research Center, Medical College of Virginia, Richmond, Virginia, U.S.A.
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Publication History

Publication Date:
23 December 2008 (online)

Abstract

Paired TRH (thyrotropin releasing hormone) and CPZ (chlorpromazine) stimulation tests were performed on 3 and 5 normal male volunteers respectively. During one of the paired tests, Intralipid plus heparin was administered i.v. for 3 hours to assess the effect of FFA and TG elevations on prolactin (PRL) secretion. At the end of the first hour of Intralipid plus heparin (or saline for control stimulations), either CPZ (25 mg i.m.) or TRH (250 units i.v.) was given. In the Intralipid experiments, plasma TG and FFA values more than doubled. The PRL responses to CPZ and TRH were not significantly affected by the lipid infusion. In addition, intravenous lipid did not suppress the elevated prolactin levels observed in drug induced chronic hyperprolactinemia.

Since earlier investigations using "metabolic" stimuli (insulin, arginine) have shown inhibition of GH response by lipids, and since the stimuli used for the above experiments were "nonmetabolic", it was proposed that the response of GH and PRL to different types of stimuli might be controlled by different mechanisms, the "metabolic" mechanism being affected by FFA. To investigate this possibility, a non-metabolic stimulus for GH (L-dopa) and a metabolic stimulus for PRL (insulin) were employed using the above experimental design. The GH response to L-dopa was significantly inhibited by the lipid infusion. However, the PRL response to insulin was not suppressed by the lipid infusion. These data show that FFA and TG have no inhibitory effect on the response of prolactin to metabolic as well as non-metabolic stimuli, whereas the GH response to both types of stimuli is inhibited by lipids.

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