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For: Kobayashi K, Amemiya S, Kobayashi K, Sawanobori E, Mochizuki M, Ishihara T, Higashida K, Miura M, Nakazawa S. The involvement of growth hormone-binding protein in altered GH-IGF axis in IDDM. Endocr J 1999;46 Suppl:S67-9. [PMID: 12054124 DOI: 10.1507/endocrj.46.suppl_s67] [Citation(s) in RCA: 3] [Impact Index Per Article: 0.1] [Reference Citation Analysis] [What about the content of this article? (0)] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 01/28/2023] Open

For:	Kobayashi K, Amemiya S, Kobayashi K, Sawanobori E, Mochizuki M, Ishihara T, Higashida K, Miura M, Nakazawa S. The involvement of growth hormone-binding protein in altered GH-IGF axis in IDDM. Endocr J 1999;46 Suppl:S67-9. [PMID: 12054124 DOI: 10.1507/endocrj.46.suppl_s67] [Citation(s) in RCA: 3] [Impact Index Per Article: 0.1] [Reference Citation Analysis] [What about the content of this article? (0)] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 01/28/2023] Open

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Cited by Other Article(s)

Gallego M, Alday A, Urrutia J, Casis O. Transient outward potassium channel regulation in healthy and diabetic heartsThis article is one of a selection of papers from the NATO Advanced Research Workshop on Translational Knowledge for Heart Health (published in part 1 of a 2-part Special Issue). Can J Physiol Pharmacol 2009;87:77-83. [DOI: 10.1139/y08-106] [Citation(s) in RCA: 18] [Impact Index Per Article: 1.1] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/14/2022]

Scarth JP. Modulation of the growth hormone-insulin-like growth factor (GH-IGF) axis by pharmaceutical, nutraceutical and environmental xenobiotics: an emerging role for xenobiotic-metabolizing enzymes and the transcription factors regulating their expression. A review. Xenobiotica 2006;36:119-218. [PMID: 16702112 DOI: 10.1080/00498250600621627] [Citation(s) in RCA: 29] [Impact Index Per Article: 1.5] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/21/2022]

Abstract

The growth hormone-insulin-like growth factor (GH-IGF) axis has gained considerable focus over recent years. One cause of this increased interest is due to a correlation of age-related decline in plasma GH/IGF levels with age-related degenerative processes, and it has led to the prescribing of GH replacement therapy by some practitioners. On the other hand, however, research has also focused on the pro-carcinogenic effects of high GH-IGF levels, providing strong impetus for finding regimes that reduce its activity. Whereas the effects of GH/IGF activity on the action of xenobiotic-metabolizing enzyme systems is reasonably well appreciated, the effects of xenobiotic exposure on the GH-IGF axis has not received substantial review. Relevant xenobiotics are derived from pharmaceutical, nutraceutical and environmental exposure, and many of the mechanisms involved are highly complex in nature, not easily predictable from existing in vitro tests and do not always predict well from in vivo animal models. After a review of the human and animal in vivo and in vitro literature, a framework for considering the different levels of direct and indirect modulation by xenobiotics is developed herein, and areas that still require further investigation are highlighted, i.e. the actions of common endocrine disruptors such as pesticides and phytoestrogens, as well as the role of xenobiotic-metabolizing enzymes and the transcription factors regulating their expression. It is anticipated that a fuller appreciation of the existing human paradigms for GH-IGF axis modulation gained through this review may help explain some of the variation in levels of plasma IGF-1 and its binding proteins in the population, aid in the prescription of particular dietary regimens to certain individuals such as those with particular medical conditions, guide the direction of long-term drug/nutraceutical safety trials, and stimulate ideas for future research. It also serves to warn athletes that using compounds touted as performance enhancing because they promote short-term GH release could in fact be detrimental to performance in the long-run.

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Li JB, Wang CY, Chen JW, Feng ZQ, Ma HT. Expression of liver insulin-like growth factor 1 gene and its serum level in rats with diabetes. World J Gastroenterol 2004;10:255-9. [PMID: 14716834 PMCID: PMC4717015 DOI: 10.3748/wjg.v10.i2.255] [Citation(s) in RCA: 24] [Impact Index Per Article: 1.1] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/15/2022] Open

Abstract

AIM: To explore the effect of diabetic duration and blood glucose level on insulin like growth factor 1 (IGF-1) gene expression and serum IGF-1 level.

METHODS: Diabetes was induced into Sprague Dawley rats by alloxan and then the rats were subdivided into different groups with varying blood glucose level and diabetic duration. The parameters were measured as follows: IGF-1 mRNA by reverse transcriptase- polymerase chain reaction (RT-PCR), IGF-1 peptide and serum IGF-1 concentration by enzyme-linked immunosorbent assay (ELISA).

RESULTS: During early diabetic stage (week 2), in comparison with normal control group (NC), IGF-1 mRNA (1.17 ± 0.069 vs 0.79 ± 0.048, P < 0.001; 1.17 ± 0.069 vs 0.53 ± 0.023, P < 0.0005, respectively), IGF-1 peptide contents [(196.66 ± 14.9) ng·mg^-1vs (128.2 ± 11.25) ng·mg^-1, P < 0.0005; (196.66 ± 14.9) ng·mg^-1vs (74.43 ± 5.33) ng·mg^-1, P < 0.0001, respectively] were reduced in liver tissues of diabetic rats. The IGF-1 gene downregulation varied with glucose control level of the diabetic state, and deteriorated gradually further with duration of diabetes. By month 6, hepatic tissue IGF-1mRNA was 0.71 ± 0.024 vs 1.12 ± 0.056, P < 0.001; 0.47 ± 0.021 vs 1.12 ± 0.056, P < 0.0005, respectively. IGF-1 peptide was (114.35 ± 8.09) ng·mg^-1vs (202.05 ± 15.73) ng·mg^-1, P < 0.0005; (64.58 ± 3.89) ng·mg^-1vs (202.05 ± 15.73) ng·mg^-1, P < 0.0001 respectively. Serum IGF-1 was also lowered in diabetic group with poor control of blood glucose. On week 2, serum IGF-1 concentrations were (371.0 ± 12.5) ng·mg^-1vs (511.2 ± 24.7) ng·mg^-1, P < 0.0005, (223.2 ± 9.39) ng·mg^-1vs (511.2 ± 24.7) ng·mg^-1, P < 0.0001 respectively. By month 6, (349.6 ± 18.62) ng·mg^-1vs (520.7 ± 26.32) ng·mg^-1, P < 0.0005, (188.5 ± 17.35 vs 520.7 ± 26.32) ng·mg^-1, P < 0.0001, respectively. Serum IGF-1 peptide change was significantly correlated with that in liver tissue (r = 0.99, P < 0.001). Furthermore, No difference was found in the above parameters between diabetic rats with euglycemia and non-diabetic control group.

CONCLUSION: The influence of diabetic status on IGF-1 gene expression in liver tissues is started from early diabetic stage, causing down regulation of IGF-1 expression, and progresses with the severity and duration of diabetic state. Accordingly serum IGF-1 level decreases. This might indicate that liver tissue IGF-1 gene expression is greatly affected in diabetes, thus contributing to reduction of serum IGF-1 level.

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