Lack of association between insulin-like growth factor-I (IGF-I) gene polymorphism (rs35767) and power performance in professional, amateur athletes and non-athlete individuals in Iranian population

ABSTRACT The effects of feed restriction and refeeding on ovarian and hepatic insulin-like growth factor-I (IGF-I) gene expression, systemic and ovarian IGF-I concentrations and on associated metabolic changes were measured in prepubertal gilts. Eleven pairs of littermate gilts (70·7 ± 4·7 kg) were placed on a maintenance level of feeding for 7 days (days 1–7). On day 8, littermates were either fed at a maintenance level of energy or fed to appetite for a further 6 days. Blood samples were taken on day 13 (07.00–16.00 h) to determine plasma insulin and IGF-I, and on day 14 (02.00–06.00 h) to determine plasma GH levels. Following slaughter on day 14, one ovary from each animal was retained to measure follicular fluid IGF-I and oestradiol concentrations. The remaining ovary and a sample of liver were retained for IGF-I mRNA analysis using a ribonuclease protection assay. Six days of refeeding significantly increased plasma IGF-I (P<0·005) and basal insulin (P<0·05) but there was no effect on plasma GH. Ovarian follicular volume and diameter were significantly larger after refeeding (P<0·05), with no effect on follicular fluid oestradiol concentrations. Mean follicular fluid IGF-I concentrations were unaffected by treatment. However, the relationships between individual follicular IGF-I concentrations, absolute follicular fluid IGF-I contents and follicle volume were affected by feeding level (P<0·05). Regression analysis of the same data also revealed that at this stage of maturity, small follicles had greater follicular fluid concentrations of IGF-I than larger follicles. Refeeding increased the amount of IGF-I mRNA in hepatic but not ovarian tissue. We conclude that there is differential regulation of the IGF-I gene in porcine hepatic and ovarian tissues, and that ovarian factors other than, or as well as, IGF-I are involved in the regulation of ovarian responses to refeeding. Journal of Endocrinology (1993) 139, 143–152

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Commentary: A polymorphic CA repeat in the promoter region of the insulin-like growth factor I (IGF-I) gene

European Journal of Epidemiology ◽

10.1023/a:1023309321705 ◽

2002 ◽

Vol 18 (3) ◽

pp. 191-194 ◽

Cited By ~ 7

Author(s):

Ingrid Rietveld ◽

Joop A.M.J.L. Janssen ◽

Cornelia M. Van Duijn ◽

Steven W.J. Lamberts

Keyword(s):

Growth Factor ◽

Promoter Region ◽

Insulin Like Growth Factor ◽

Ca Repeat ◽

Factor I ◽

Igf I ◽

Growth Factor I ◽

I Gene

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20kDa Human Growth Hormone (20K hGH) Stimulates Insulin-Like Growth Factor-I (IGF-I) Gene Expression at Lower Concentrations than 22K hGH in hGH Receptor-Expressing Ba/F3 Cells

Endocrine Journal ◽

10.1507/endocrj.47.supplmarch_s37 ◽

2000 ◽

Vol 47 (SupplMarch) ◽

pp. S37-S40 ◽

Cited By ~ 3

Author(s):

HIDEO YOSHIZATO ◽

MINORU TANAKA ◽

TAKAHIKO FUJIKAWA ◽

YOSHIFUMI HIGASHIMOTO ◽

AYAKO SHIMIZU ◽

...

Keyword(s):

Gene Expression ◽

Growth Hormone ◽

Growth Factor ◽

Human Growth Hormone ◽

Human Growth ◽

Insulin Like Growth Factor ◽

Factor I ◽

Igf I ◽

Growth Factor I ◽

I Gene

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Defining human insulin-like growth factor I gene regulation

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.00212.2016 ◽

2016 ◽

Vol 311 (2) ◽

pp. E519-E529 ◽

Cited By ~ 9

Author(s):

Aditi Mukherjee ◽

Damir Alzhanov ◽

Peter Rotwein

Keyword(s):

Gene Expression ◽

Growth Factor ◽

Biological Effects ◽

Model Systems ◽

Trophic Factors ◽

Insulin Like Growth Factor ◽

Factor I ◽

Igf I ◽

Growth Factor I ◽

I Gene

Growth hormone (GH) plays an essential role in controlling somatic growth and in regulating multiple physiological processes in humans and other species. Insulin-like growth factor I (IGF-I), a conserved, secreted 70-amino acid peptide, is a critical mediator of many of the biological effects of GH. Previous studies have demonstrated that GH rapidly and potently promotes IGF-I gene expression in rodents and in some other mammals through the transcription factor STAT5b, leading to accumulation of IGF-I mRNAs and production of IGF-I. Despite this progress, very little is known about how GH or other trophic factors control human IGF1 gene expression, in large part because of the absence of any cellular model systems that robustly express IGF-I. Here, we have addressed mechanisms of regulation of human IGF-I by GH after generating cells in which the IGF1 chromosomal locus has been incorporated into a mouse cell line. Using this model, we found that physiological levels of GH rapidly stimulate human IGF1 gene transcription and identify several potential transcriptional enhancers in chromatin that bind STAT5b in a GH-regulated way. Each of the putative enhancers also activates a human IGF1 gene promoter in reconstitution experiments in the presence of the GH receptor, STAT5b, and GH. Thus we have developed a novel experimental platform that now may be used to determine how human IGF1 gene expression is controlled under different physiological and pathological conditions.

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