ArticleWorld journal of gastroenterology2002
The role of endotoxin, TNF-alpha, and IL-6 in inducing the state of growth hormone insensitivity.
Article in World journal of gastroenterology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 73 citations in OpenAlex.
- A Theoretical Link Between the GH/IGF-1 Axis and Cytokine Family in Children: Current Knowledge and Future Perspectives.Children (Basel, Switzerland) · 2025Review
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- Gut Microbes and Circulating Cytokines in Preterm Infants with Growth Failure.The Journal of nutrition · 2023Article
- Classical and novel GH receptor signaling pathways.Molecular and cellular endocrinology · 2020Review
- Acromegaly, inflammation and cardiovascular disease: a review.Reviews in endocrine & metabolic disorders · 2020Review
- Signal Transduction for TNFα-Induced Type II SOCS Expression and Its Functional Implication in Growth Hormone Resistance in Carp Hepatocytes.Frontiers in endocrinology · 2020Article
- Chronic inflammation and the growth hormone/insulin-like growth factor-1 axis.Central-European journal of immunology · 2020Review
- Growth Hormone Receptor Regulation in Cancer and Chronic Diseases.Frontiers in endocrinology · 2020Review
- Age-dependent increase in angiopoietin-like protein 2 accelerates skeletal muscle loss in mice.The Journal of biological chemistry · 2018Article
- The pre-treatment characteristics and evaluation of the effects of recombinant human growth hormone therapy in children with growth hormone deficiency and celiac disease or inflammatory bowel disease.Central-European journal of immunology · 2018Article
- Characterization of Growth Hormone Resistance in Experimental and Ulcerative Colitis.International journal of molecular sciences · 2017Article
- Growth Hormone Resistance-Special Focus on Inflammatory Bowel Disease.International journal of molecular sciences · 2017Review
- Insulin-like growth factor-I and insulin-like growth factor binding protein-1 are related to cardiovascular disease biomarkers in obese adolescents.Pediatric diabetes · 2016Article
- Leptin's role in lipodystrophic and nonlipodystrophic insulin-resistant and diabetic individuals.Endocrine reviews · 2013Review
- Lipopolysaccharide-induced failure of the gut barrier is site-specific and inhibitable by growth hormone.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2013Article
- βTrCP controls GH receptor degradation via two different motifs.Molecular endocrinology (Baltimore, Md.) · 2012Article
- Immune activation and target organ damage are consequences of hydrodynamic treatment but not delivery of naked siRNAs in mice.Nucleic acid therapeutics · 2011Article
- Dragon (repulsive guidance molecule b) inhibits IL-6 expression in macrophages.Journal of immunology (Baltimore, Md. : 1950) · 2011Article
- Associations between plasma insulin-like growth factor-I and the markers of inflammation interleukin 6, C-reactive protein and YKL-40 in an elderly background population.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2010Article
- The role of insulin-like growth factor-I and its binding proteins in glucose homeostasis and type 2 diabetes.Diabetes/metabolism research and reviews · 2009Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimCritical illnesses such as sepsis, trauma, and burns cause a growth hormone insensitivity, which leads to an increased negative nitrogen balance. Endotoxin is generously released into blood under these conditions and stimulates the production of proinflammatory cytokines such as TNF-alpha, IL-6, and IL-1, which may play a very important role in inducing the growth hormone insensitivity. The objective of this current study was to investigate the role of endotoxin, TNF-alpha and IL-6 in inducing the growth hormone insensitivity at the receptor and post-receptor levels.
methodsSpague-Dawley rats were injected with endotoxin, TNF-alpha, and IL-6, respectively and part of rats injected with endotoxin was treated with exogenous somatotropin simultaneously. All rats were killed at different time points. The expression of IGF-I, GHR, SOCS-3 and beta-actin mRNA in the liver was detected by RT-PCR and the GH levels were measured by radioimmunoassay, the levels of TNF-alpha and IL-6 were detected by ELISA.
resultsThere was no significant difference in serous GH levels between experimental group and control rats after endotoxin injection, however, liver IGF-I mRNA expression had been obviously down-regulated in endotoxemic rats. Liver GHR mRNA expression also had a predominant down-regulation after endotoxin injection. The lowest regulation of liver IGF-I mRNA expression occurred at 12h after LPS injection, being decreased by 53% compared with control rats. For GHR mRNA expression, the lowest expression occurred at 8h and had a 81% decrease. Although SOCS-3 mRNA was weakly expressed in control rats, it was strongly up-regulated after LPS injection and had a 7.84 times increase compared with control rats. Exogenous GH could enhance IGF-I mRNA expression in control rats, but it did fail to prevent the decline in IGF-I mRNA expression in endotoxemic rats. Endotoxin stimulated the production of TNF-alpha and IL-6, and the elevated IL-6 levels was shown a positive correlation with increased SOCS-3 mRNA expression. The liver GHR mRNA expression was obviously down-regulated after TNF-alpha iv injection and had a 40% decrease at 8h, but the liver SOCS-3 mRNA expression was the 4.94 times up-regulation occurred at 40 min after IL-6 injection.
conclusionThe growth hormone insensitivity could be induced by LPS injection, which was associated with down-regulated GHR mRNA expression at receptor level and with up-regulated SOCS-3 mRNA expression at post-receptor level. The in vivo biological activities of LPS were mediated by TNF-alpha and IL-6 indirectly, and TNF-alpha and IL-6 may exert their effects on the receptor and post-receptor levels respectively.
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