Inhibitory effects of interleukin-1 on growth hormone secretion in conscious male rats.

Wada, Yoshinaru; Sato, Makoto; Niimi, Michio; Tamaki, Miho; Ishida, Toshihiko; Takahara, Jiro

doi:10.1210/endo.136.9.7649102

Cited by 29 publications

(11 citation statements)

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“…or i.c.v. administration of IL-1 and to a lesser extent IL-1 , inhibited GH secretion (Wada et al 1995). These discrepancies may be due to the dosage, since other authors have described a biphasic effect of central IL-1 administration on GH secretion, with a stimulatory effect at low doses and an inhibitory effect at higher doses of IL-1 (Payne et al 1992).…”

Section: Discussionmentioning

confidence: 96%

Effects of endotoxin lipopolysaccharide administration on the somatotropic axis

Soto¹,

Martin²,

Millán³

et al. 1998

Journal of Endocrinology

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The aim of this work was to study the effect of chronic activation of the immune system on the somatotropic axis. Accordingly, the changes in growth hormone (GH) secretion, circulating insulin-like growth factor-I (IGF-I) and IGF binding proteins (IGFBPs) in response to endotoxin lipopolysaccharide (LPS) administration were examined in adult male Wistar rats. Acute LPS injection (2·5, 25 or 250 µg/kg) increased serum corticosterone in a dosedependent manner and decreased serum levels of insulin and IGF-I, serum GH concentration declined linearly as the LPS dose increased. Western ligand blot showed an increase in the 33 kDa band (corresponding to IGFBP-1 and IGFBP-2) in the rats that received the highest dose of LPS (250 µg/kg). Chronic LPS administration (250 µg/kg daily for 8 days) significantly decreased body weight, serum levels of IGF-I and pituitary GH content, whereas it increased circulating IGFBP-3 (47 kDa band), IGFBP-1 and IGFBP-2 (33 kDa band) and the 24 kDa band (which possibly corresponds to IGFBP-4). Serum concentration of corticosterone and hypothalamic somatostatin content were also increased by chronic LPS treatment. These data suggest that the decrease in GH and IGF-I secretion and the increase in circulating IGFBPs are important mechanisms in body weight loss during chronic inflammation.

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Section: Discussionmentioning

confidence: 96%

Effects of endotoxin lipopolysaccharide administration on the somatotropic axis

Soto¹,

Martin²,

Millán³

et al. 1998

Journal of Endocrinology

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“…Studies in children with other chronic diseases characterized by elevated circulating levels of inflammatory mediators such as juvenile rheumatoid arthritis also show reduced fitness and IGF-I (28, 29); and inflammatory cytokines like IL-6 and TNF-␣ can directly inhibit bioactivity of the GH→IGF-I axis (9,30,31). Circulating IL-6 was substantially elevated in the subjects with CF.…”

Section: Discussionmentioning

confidence: 99%

Fitness, Acute Exercise, and Anabolic and Catabolic Mediators in Cystic Fibrosis

Tirakitsoontorn

Nussbaum

Moser

et al. 2001

Am J Respir Crit Care Med

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Exercise can stimulate catabolic inflammatory cytokines even in healthy children. For patients with cystic fibrosis (CF), this may be problematic because CF is characterized by increased inflammation and suppressed growth. We examined fitness and the response to brief exercise of interleukin-6 (IL-6), tumor necrosis factor-␣ (TNF-␣ ), insulinlike growth factor-I (IGF-I), and IGF binding protein-1 (IGFBP-1) in 14 subjects with CF (10.5 Ϯ 0.8 yr of age), 9 of whom were treated with ibuprofen, and 14 healthy control subjects (11.6 Ϯ 0.5 yr of age, NS). Subjects performed brief intermittent, constant work rate protocol (scaled to each individual's exercise capacity) with blood and urine sampling. Peak O 2 was correlated with IGF-I (r ϭ 0.68, p Ͻ 0.01) in control subjects but not in subjects with CF. In subjects with CF, baseline IL-6 was 79% greater (p Ͻ 0.05) and IGF-I was 47% lower than in control subjects (p Ͻ 0.05). Post hoc analysis revealed a progressive increase in the IL-6 response to exercise, with the lowest increase observed in control subjects (11.8 Ϯ 4.6 pg/L/kJ), higher increases in patients with CF treated with ibuprofen (23.4 Ϯ 7.7 pg/L/kJ), and highest in subjects with CF not receiving ibuprofen (29.2 Ϯ 7.5 pg/L/kJ). Qualitatively similar results were observed for TNF-␣ . Exercise also significantly increased IGFBP-1 in both control subjects and subjects with CF. Brief exercise can increase even chronically elevated inflammatory mediators in CF, and this response may be attenuated by ibuprofen.

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“…The data do however show clearly that the GH responses to exogenous corticosterone and annexin 1 Ac2 ± 26 are readily inhibited by central but not peripheral administration of IL-1b. There is already substantial published evidence that IL-1b acts within the hypothalamus to suppress GH release (Wada et al, 1995) via mechanisms which involve increased somatostatin release (Honegger et al, 1991) and possibly also decreased secretion of GHRH (McCann et al, 1998). Our ®nding that central but not peripheral injection of IL-1b inhibits the rise in serum GH provoked by corticosterone or annexin 1 Ac2 ± 26 accords with this concept although, in contrast to other studies (Peisen et al, 1995;Wada et al, 1995), we found no e ects of the cytokine on the basal release of GH.…”

Section: Discussionmentioning

confidence: 99%

“…There is already substantial published evidence that IL-1b acts within the hypothalamus to suppress GH release (Wada et al, 1995) via mechanisms which involve increased somatostatin release (Honegger et al, 1991) and possibly also decreased secretion of GHRH (McCann et al, 1998). Our ®nding that central but not peripheral injection of IL-1b inhibits the rise in serum GH provoked by corticosterone or annexin 1 Ac2 ± 26 accords with this concept although, in contrast to other studies (Peisen et al, 1995;Wada et al, 1995), we found no e ects of the cytokine on the basal release of GH. It has been suggested that the positive e ects of IL-1b on the somatostatin secretion are secondary to the increase in CRH secretion the cytokine provokes (Peisen et al, 1995).…”

Section: Discussionmentioning

confidence: 99%

Opposing influences of glucocorticoids and interleukin‐1β on the secretion of growth hormone and ACTH in the rat in vivo: role of hypothalamic annexin 1

Philip

John

Cover

et al. 2001

British J Pharmacology

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This study exploited established immunoneutralization protocols and an N‐terminal annexin 1 peptide (annexin 1Ac2 – 26) to advance our knowledge of the role of annexin 1 as a mediator of acute glucocorticoid action in the rat neuroendocrine system in vivo. Rats were treated with corticosterone (500 μg kg−1, i.p.) or annexin 1Ac2 – 26 (0.1 – 10 ng rat−1, i.c.v.) and 75 min later with interleukin 1β (IL‐1β, 10 ng rat−1, i.c.v. or 500 μg kg−1, i.p). Blood was collected 1 h later for hormone immunoassay. Where appropriate, anti‐annexin 1 polyclonal antiserum (pAb) was administered subcutaneously or centrally prior to the steroid challenge. Corticosterone did not affect the resting plasma corticotrophin (ACTH) concentration but suppressed the hypersecretion of ACTH induced by IL‐1β (i.p. or i.c.v.). Its actions were quenched by anti‐annexin 1 pAb (s.c. or i.c.v) and mimicked by annexin 1Ac2 – 26. By contrast, corticosterone provoked an increase in serum growth hormone (GH) which was ablated by central but not peripheral administration of anti‐annexin 1 pAb. IL‐1β (i.c.v. or i.p.) did not affect basal GH but, when given centrally but not peripherally, it abolished the corticosterone‐induced hypersecretion of GH. Annexin 1Ac2 – 26 (i.c.v.) also produced an increase in serum GH which was prevented by central injection of IL‐1β. The results support the hypothesis that the acute regulatory actions of glucocorticoids on hypothalamo‐pituitary‐adrenocortical function require annexin 1. They also provide novel evidence that the positive influence of the steroids on GH secretion evident within this timeframe is effected centrally via an annexin 1‐dependent mechanism which is antagonized by IL‐1β. British Journal of Pharmacology (2001) 134, 887–895; doi:10.1038/sj.bjp.0704324

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Inhibitory effects of interleukin-1 on growth hormone secretion in conscious male rats.

Cited by 29 publications

References 0 publications

Effects of endotoxin lipopolysaccharide administration on the somatotropic axis

Effects of endotoxin lipopolysaccharide administration on the somatotropic axis

Fitness, Acute Exercise, and Anabolic and Catabolic Mediators in Cystic Fibrosis

Opposing influences of glucocorticoids and interleukin‐1β on the secretion of growth hormone and ACTH in the rat in vivo: role of hypothalamic annexin 1

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