Acipimox potentiates growth hormone response to growth hormone-releasing hormone by decreasing serum free fatty acid levels in hyperthyroidism

Eunjig Lee, Kyung Rae Kim, Hyun Chul Lee, Jae Hwa Cho, Moon Suk Nam, Su Youn Nam, Young Duk Song, Sungkil Lim, Kap Bum Huh

Research output: Contribution to journalArticle

7 Citations (Scopus)

Abstract

Hyperthyroidism is associated with an impairment of growth hormone (GH) responses to secretagogues. The aim of this study was to evaluate the effect of acipimox, an antilipolytic agent able to decrease free fatty acids (FFA), on GH response to GH-releasing hormone (GHRH) in hyperthyroid and normal control subjects. We studied six men with hyperthyroidism; seven normal men served as control subjects. Each subject underwent treatment with (1) 2 tablets of placebo orally or (2) 500 mg acipimox orally, 120 minutes before intravenous (IV) injection of 1 μg/kg GHRH-(1-29)NH2. GH response to GHRH in hyperthyroid patients was markedly reduced; the mean peak GH response (9.6 ± 1.0 μg/L) and the area under the GH response curve (12.9 ± 1.3 μg/L × 2 h) were lower than those of control subjects (25.7 ± 1.8 μg/L, P < .05; 28.7 ± 2.1 μg/L × 2 h, P < .05). Hyperthyroid patients had higher baseline levels of plasma FFA than control subjects (998.0 ± 38.9 v 498.0 ± 36.0 μEq/L, P < .01). Acipimox decreased FFA levels in both hyperthyroid and control subjects; the lowest FFA levels of hyperthyroid subjects induced by acipimox were similar to those of control subjects. After acipimox pretreatment, GH responses to GHRH increased significantly (P < .05); the mean peak plasma GH level (25.9 ± 4.6 μg/L) was similar to the peak GH levels of control subjects during the GHRH test, and the area under the GH response curve (41.1 ± 6.7 μg/L × 2 h) was even higher than that of control subjects with the GHRH test. However, the enhanced GH responses of hyperthyroid patients were still lower that those of control subjects during the acipimox plus GHRH test. We demonstrated that the decreased FFA levels induced by acipimox potentiate somatotrope responsiveness, likely acting at the pituitary level. Our results indicate that high FFA levels are responsible for impaired GH responses to GHRH in hyperthyroidism.

Original languageEnglish
Pages (from-to)1509-1512
Number of pages4
JournalMetabolism
Volume44
Issue number11
DOIs
Publication statusPublished - 1995 Jan 1

Fingerprint

Growth Hormone-Releasing Hormone
Hyperthyroidism
Nonesterified Fatty Acids
Growth Hormone
Serum
Hormones
acipimox
Intravenous Injections
Tablets
Placebos

All Science Journal Classification (ASJC) codes

  • Endocrinology, Diabetes and Metabolism
  • Endocrinology

Cite this

Lee, Eunjig ; Kim, Kyung Rae ; Lee, Hyun Chul ; Cho, Jae Hwa ; Nam, Moon Suk ; Nam, Su Youn ; Song, Young Duk ; Lim, Sungkil ; Huh, Kap Bum. / Acipimox potentiates growth hormone response to growth hormone-releasing hormone by decreasing serum free fatty acid levels in hyperthyroidism. In: Metabolism. 1995 ; Vol. 44, No. 11. pp. 1509-1512.
@article{02a607878d38492ebd26bfbb629aa2d1,
title = "Acipimox potentiates growth hormone response to growth hormone-releasing hormone by decreasing serum free fatty acid levels in hyperthyroidism",
abstract = "Hyperthyroidism is associated with an impairment of growth hormone (GH) responses to secretagogues. The aim of this study was to evaluate the effect of acipimox, an antilipolytic agent able to decrease free fatty acids (FFA), on GH response to GH-releasing hormone (GHRH) in hyperthyroid and normal control subjects. We studied six men with hyperthyroidism; seven normal men served as control subjects. Each subject underwent treatment with (1) 2 tablets of placebo orally or (2) 500 mg acipimox orally, 120 minutes before intravenous (IV) injection of 1 μg/kg GHRH-(1-29)NH2. GH response to GHRH in hyperthyroid patients was markedly reduced; the mean peak GH response (9.6 ± 1.0 μg/L) and the area under the GH response curve (12.9 ± 1.3 μg/L × 2 h) were lower than those of control subjects (25.7 ± 1.8 μg/L, P < .05; 28.7 ± 2.1 μg/L × 2 h, P < .05). Hyperthyroid patients had higher baseline levels of plasma FFA than control subjects (998.0 ± 38.9 v 498.0 ± 36.0 μEq/L, P < .01). Acipimox decreased FFA levels in both hyperthyroid and control subjects; the lowest FFA levels of hyperthyroid subjects induced by acipimox were similar to those of control subjects. After acipimox pretreatment, GH responses to GHRH increased significantly (P < .05); the mean peak plasma GH level (25.9 ± 4.6 μg/L) was similar to the peak GH levels of control subjects during the GHRH test, and the area under the GH response curve (41.1 ± 6.7 μg/L × 2 h) was even higher than that of control subjects with the GHRH test. However, the enhanced GH responses of hyperthyroid patients were still lower that those of control subjects during the acipimox plus GHRH test. We demonstrated that the decreased FFA levels induced by acipimox potentiate somatotrope responsiveness, likely acting at the pituitary level. Our results indicate that high FFA levels are responsible for impaired GH responses to GHRH in hyperthyroidism.",
author = "Eunjig Lee and Kim, {Kyung Rae} and Lee, {Hyun Chul} and Cho, {Jae Hwa} and Nam, {Moon Suk} and Nam, {Su Youn} and Song, {Young Duk} and Sungkil Lim and Huh, {Kap Bum}",
year = "1995",
month = "1",
day = "1",
doi = "10.1016/0026-0495(95)90154-X",
language = "English",
volume = "44",
pages = "1509--1512",
journal = "Metabolism: Clinical and Experimental",
issn = "0026-0495",
publisher = "W.B. Saunders Ltd",
number = "11",

}

Acipimox potentiates growth hormone response to growth hormone-releasing hormone by decreasing serum free fatty acid levels in hyperthyroidism. / Lee, Eunjig; Kim, Kyung Rae; Lee, Hyun Chul; Cho, Jae Hwa; Nam, Moon Suk; Nam, Su Youn; Song, Young Duk; Lim, Sungkil; Huh, Kap Bum.

In: Metabolism, Vol. 44, No. 11, 01.01.1995, p. 1509-1512.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Acipimox potentiates growth hormone response to growth hormone-releasing hormone by decreasing serum free fatty acid levels in hyperthyroidism

AU - Lee, Eunjig

AU - Kim, Kyung Rae

AU - Lee, Hyun Chul

AU - Cho, Jae Hwa

AU - Nam, Moon Suk

AU - Nam, Su Youn

AU - Song, Young Duk

AU - Lim, Sungkil

AU - Huh, Kap Bum

PY - 1995/1/1

Y1 - 1995/1/1

N2 - Hyperthyroidism is associated with an impairment of growth hormone (GH) responses to secretagogues. The aim of this study was to evaluate the effect of acipimox, an antilipolytic agent able to decrease free fatty acids (FFA), on GH response to GH-releasing hormone (GHRH) in hyperthyroid and normal control subjects. We studied six men with hyperthyroidism; seven normal men served as control subjects. Each subject underwent treatment with (1) 2 tablets of placebo orally or (2) 500 mg acipimox orally, 120 minutes before intravenous (IV) injection of 1 μg/kg GHRH-(1-29)NH2. GH response to GHRH in hyperthyroid patients was markedly reduced; the mean peak GH response (9.6 ± 1.0 μg/L) and the area under the GH response curve (12.9 ± 1.3 μg/L × 2 h) were lower than those of control subjects (25.7 ± 1.8 μg/L, P < .05; 28.7 ± 2.1 μg/L × 2 h, P < .05). Hyperthyroid patients had higher baseline levels of plasma FFA than control subjects (998.0 ± 38.9 v 498.0 ± 36.0 μEq/L, P < .01). Acipimox decreased FFA levels in both hyperthyroid and control subjects; the lowest FFA levels of hyperthyroid subjects induced by acipimox were similar to those of control subjects. After acipimox pretreatment, GH responses to GHRH increased significantly (P < .05); the mean peak plasma GH level (25.9 ± 4.6 μg/L) was similar to the peak GH levels of control subjects during the GHRH test, and the area under the GH response curve (41.1 ± 6.7 μg/L × 2 h) was even higher than that of control subjects with the GHRH test. However, the enhanced GH responses of hyperthyroid patients were still lower that those of control subjects during the acipimox plus GHRH test. We demonstrated that the decreased FFA levels induced by acipimox potentiate somatotrope responsiveness, likely acting at the pituitary level. Our results indicate that high FFA levels are responsible for impaired GH responses to GHRH in hyperthyroidism.

AB - Hyperthyroidism is associated with an impairment of growth hormone (GH) responses to secretagogues. The aim of this study was to evaluate the effect of acipimox, an antilipolytic agent able to decrease free fatty acids (FFA), on GH response to GH-releasing hormone (GHRH) in hyperthyroid and normal control subjects. We studied six men with hyperthyroidism; seven normal men served as control subjects. Each subject underwent treatment with (1) 2 tablets of placebo orally or (2) 500 mg acipimox orally, 120 minutes before intravenous (IV) injection of 1 μg/kg GHRH-(1-29)NH2. GH response to GHRH in hyperthyroid patients was markedly reduced; the mean peak GH response (9.6 ± 1.0 μg/L) and the area under the GH response curve (12.9 ± 1.3 μg/L × 2 h) were lower than those of control subjects (25.7 ± 1.8 μg/L, P < .05; 28.7 ± 2.1 μg/L × 2 h, P < .05). Hyperthyroid patients had higher baseline levels of plasma FFA than control subjects (998.0 ± 38.9 v 498.0 ± 36.0 μEq/L, P < .01). Acipimox decreased FFA levels in both hyperthyroid and control subjects; the lowest FFA levels of hyperthyroid subjects induced by acipimox were similar to those of control subjects. After acipimox pretreatment, GH responses to GHRH increased significantly (P < .05); the mean peak plasma GH level (25.9 ± 4.6 μg/L) was similar to the peak GH levels of control subjects during the GHRH test, and the area under the GH response curve (41.1 ± 6.7 μg/L × 2 h) was even higher than that of control subjects with the GHRH test. However, the enhanced GH responses of hyperthyroid patients were still lower that those of control subjects during the acipimox plus GHRH test. We demonstrated that the decreased FFA levels induced by acipimox potentiate somatotrope responsiveness, likely acting at the pituitary level. Our results indicate that high FFA levels are responsible for impaired GH responses to GHRH in hyperthyroidism.

UR - http://www.scopus.com/inward/record.url?scp=0029550385&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0029550385&partnerID=8YFLogxK

U2 - 10.1016/0026-0495(95)90154-X

DO - 10.1016/0026-0495(95)90154-X

M3 - Article

C2 - 7476342

AN - SCOPUS:0029550385

VL - 44

SP - 1509

EP - 1512

JO - Metabolism: Clinical and Experimental

JF - Metabolism: Clinical and Experimental

SN - 0026-0495

IS - 11

ER -