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Effects of growth hormone administration on dehydroepiandrosterone sulphate, androstenedione, testosterone and Cortisol metabolism during nutritional repletion
Author(s) -
Ziegler Thomas R.,
Barbieri Robert L.,
Young Lorraine S.,
FerrariBaliviera Elizabetta,
Wilmore Douglas W.
Publication year - 1991
Publication title -
clinical endocrinology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.055
H-Index - 147
eISSN - 1365-2265
pISSN - 0300-0664
DOI - 10.1111/j.1365-2265.1991.tb03767.x
Subject(s) - endocrinology , medicine , androstenedione , dehydroepiandrosterone , androgen , testosterone (patch) , excretion , dehydroepiandrosterone sulfate , hormone
Summary This study evaluated whether pharmacological doses of recombinant human growth hormone (hGH) influences androgen or Cortisol metabolism during nutritional repletion following prolonged illness. Stable hospitalized adults (three male, seven female) receiving constant calorie and protein intake were studied. An initial control week was followed by a treatment period during which hGH (10 mg/day s.c.) was administered daily. Prior to hGH treatment, serum and 24‐h urinary concentrations of dehydroepiandrosterone sulphate (DS) were below the normal range; serum androstenedione and testosterone concentrations were within the lower limit of normal. In contrast, serum Cortisol (F) and 24‐h urinary F excretion were normal. During hGH treatment, nitrogen balance became positive and plasma insulin‐like growth factor I (IGF‐I) concentrations rose five to seven‐fold. However, serum DS, androstenedione, testosterone and F, and urinary F excretion did not change, while 24‐h urinary DS excretion fell significantly. Growth hormone administration markedly stimulated protein anabolism but did not increase the low concentrations of circulating androgens or alter the disassociation between adrenal androgen and F release in stable hospitalized males and females. Thus, hGH does not appear to function as a cortical adrenal androgen stimulating hormone (CASH) or regulate adrenal Cortisol or gonadal androgen release in this clinical setting.