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  • Author: D. L. Russell-Jones x
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Insulin-like growth factor-I gene expression is increased in the right ventricular hypertrophy induced by chronic hypoxia in the rat

D L Russell-Jones, R M Leach, J P T Ward, and C R Thomas

ABSTRACT

Rats were maintained in chambers and breathed air (control, n=8) or an atmosphere containing 10% oxygen (hypoxic, n=10) for 35 days. On completion of the experiment the hypoxic animals weighed less than the controls (hypoxic, 290 ± 11.7g; control, 339 ± 19.2g; means ± S.E.M., p<0.05). No differences in the left ventricular weights were found between groups but the right ventricular weights were greater in the hypoxic rats (hypoxic, 0.39 ± 0.02g; control, 0.27 ± 0.08g; p<0.01). The amount of mRNA for IGF-I in the ventricles was quantified by Northern blot analysis. There was no difference between groups in IGF-I mRNA levels in the left ventricles (hypoxic, 1.07 ± 0.41 absorbance units (AU); control, 0.73 ± 0.33 AU). In the right ventricles, IGF-I mRNA was greater in hypoxic than in control rats (hypoxic, 2.37 ± 0.75 AU; control, 0.64 ± 0.11 AU; p<0.05). This study demonstrates that expression of IGF-I mRNA is increased in the hypertrophied right ventricle of hypoxic rats; IGF-I may play a central role in the initiation and maintenance of this process.

DOI:
https://doi.org/10.1677/jme.0.0100099
Volume 10: Issue 1,
Pages:
99–102 (4 total)
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Intraperitoneal insulin is more potent than subcutaneous insulin at restoring hepatic insulin-like growth factor-I mRNA levels in the diabetic rat: a functional role for the portal vascular link

D. L. Russell-Jones, M. Rattray, V. J. Wilson, R. H. Jones, P. H. Sönksen, and C. R. Thomas

ABSTRACT

There is evidence that the hormonal control of hepatic IGF-I production is mediated by GH and insulin. To elucidate the role of these hormones further we administered s.c. or i.p. insulin (at 2·5 and 5·0 IU/day) and/or GH (0·8 IU/day) to rats made diabetic with streptozotocin 16 days previously. Hepatic IGF-I production was then assessed by quantifying hepatic IGF-I mRNA levels by autoradiography of Northern blots. Diabetes resulted in a fivefold reduction in hepatic IGF-I mRNA levels (optical density (OD) of the 0·7–1·1 kb band: controls, 1·3±0·09; diabetics, 0·28±0·08; P<0·01), which was not significantly changed by treatment with s.c. insulin (OD: low dose, 0·55±0·05; high dose, 0·58±0·05) or low dose i.p. insulin (OD: 0·40±0·03). High dose i.p. insulin enhanced hepatic IGF-I mRNA levels (OD: 0·93±0·23) compared with diabetic rats (P<0·01) and those given high dose s.c. insulin (P<0·04), despite the blood glucose values being similar in the treated groups (i.p., 4·72±0·29 mmol/l; s.c., 3·32±0·03 mmol/l). Administration of GH alone partially restored the hepatic IGF-I mRNA level (OD: GH-treated, 1·00±0·05; diabetic, 0·28±0·08; P<0·01), whilst having no effect on blood glucose values (diabetic, 36·35±0·45 mmol/l; GH-treated, 38·65±2·39 mmol/l). Additional administration of s.c. insulin completely restored IGF-I mRNA levels to those of controls (OD: low dose, 1·35±0·14; high dose, 1·27 ± 0·18). These observations indicate that insulin and GH are required for full expression of hepatic IGF-I mRNA and that insulin given i.p. is more potent than that given s.c. at stimulating hepatic synthesis of IGF-I.

DOI:
https://doi.org/10.1677/jme.0.0090257
Volume 9: Issue 3,
Pages:
257–263 (7 total)