Insulin-like growth factor-I (IGF-I) and clinical nutrition

2013 ◽  
Vol 125 (6) ◽  
pp. 265-280 ◽  
Author(s):  
Callum Livingstone
Keyword(s):  
Growth Factor ◽  
Nutritional Status ◽  
Nutritional Assessment ◽  
Peptide Hormone ◽  
Insulin Like Growth Factor ◽  
Nutritional Regulation ◽  
Factor I ◽  
Igf I ◽  
Growth Factor I ◽  
Nutritional Marker

IGF-I (insulin-like growth factor-I) is a peptide hormone, produced predominantly by the liver in response to pituitary GH (growth hormone), which is involved in a wide variety of physiological processes. It acts in an endocrine, paracrine and autocrine manner to promote growth. The production of IGF-I signals the availability of nutrients needed for its anabolic actions. Recently, there has been growing interest in its role in health and disease. IGF-I has long been known to be regulated by nutrition and dysregulated in states of under- and over-nutrition, its serum concentrations falling in malnutrition and responding promptly to refeeding. This has led to interest in its utility as a nutritional biomarker. A considerable evidence base supports utility for measurement of IGF-I in nutritional contexts. Its concentration may be valuable in providing information on nutritional status, prognosis and in monitoring nutritional support. However, it is insufficiently specific for use as a screening test for under nutrition as its serum concentration is influenced by many factors other than nutritional status, notably the APR (acute-phase response) and endocrine conditions. Concentrations should be interpreted along with clinical findings and the results of other investigations such as CRP (C-reactive protein). More recently, there has been interest in free IGF-I which holds promise as a nutritional marker. The present review covers nutritional regulation of IGF-I and its dysregulation in disease, then goes on to review recent studies supporting its utility as a nutritional marker in clinical contexts. Although not currently recommended by clinical guidelines, it is likely that, in time, measurement of IGF-I will become a routine part of nutritional assessment in a number of these contexts.

Nutrition and somatomedin XXII: Molecular regulation of insulin-like growth factor-I during fasting and refeeding in rats

1991 ◽  
Vol 6 (1) ◽  
pp. 33-43 ◽  
Author(s):  
S. Goldstein ◽  
J. B. Harp ◽  
L. S. Phillips
Keyword(s):  
Growth Factor ◽  
Hormonal Regulation ◽  
Cytoskeletal Proteins ◽  
Insulin Like Growth Factor ◽  
Nutritional Regulation ◽  
Factor I ◽  
Igf I ◽  
Fasting And Refeeding ◽  
Growth Factor I ◽  
Putative Precursor

ABSTRACT The liver is thought to be the locus of nutritional/hormonal regulation of circulating insulin-like growth factor-I (IGF-I). To probe the basis of nutritional regulation, we examined changes in serum IGF-I, hepatic content of extractable IGF-I immunoreactivity (a high Mr putative precursor) and hepatic IGF-I mRNA during fasting and refeeding in rats. Preliminary studies revealed that the hepatic level of IGF-I mRNA was consistently reduced only after food was withheld for 3 days, so the effects of refeeding were subsequently examined in such animals. After 3 days of fasting, animals lost 30% of their initial weight; weight regain was apparent within 3 h of refeeding ad libitum and, after 48 h, weight was comparable to initial fed levels. Fasting reduced levels of serum and extractable hepatic IGF-I to 19 and 26% of control (fed) values respectively (both P<0·005 vs control). There was no change in levels of serum IGF-I over the first 3 h of refeeding, but IGF-I rose above fasted levels at both 9 and 48 h (both P<0·005). Extractable hepatic IGF-I rose more slowly and was still below fasted levels after 9 h of refeeding, and modestly, but not significantly, greater than fasted levels after 48 h. The ratio of serum to hepatic IGF-I was decreased compared with control after 3 days of fasting, but increased after 3 and 9 h of refeeding (P<0·02 at 9 h). Northern blot analysis of total hepatic RNA revealed four species of IGF-I mRNA 0·8–1·1, 2·0, 4·0 and 7·5 kb in size. Each mRNA species fell to 15–28% of control levels after 3 days of fasting (all P<0·001). There was a prompt increase in each transcript after 3 h of refeeding, and all values were significantly (P<0·05) greater than fasted levels at 9 h but, at 48 h, most species were still below control levels. Levels of mRNA for the cytoskeletal proteins β-actin and cyclophilin also fell with fasting, but were restored more rapidly than IGF-I mRNA, to or above control levels after 3 h of refeeding. The observation that IGF-I expression was decreased at 3 h when β-actin and cyclophilin were normalized suggests specificity of regulation. Despite the temporal incongruity between IGF-I mRNA and serum and hepatic IGF-I, there were highly significant correlations (all P<0·002) between each pair of parameters. Since refeeding of fasted animals led to a rise in IGF-I mRNA which preceded rises in serum and hepatic IGF-I, our findings are consistent with the hypothesis that nutritional regulation of circulating IGF-I involves modulation at the level of hepatic IGF-I mRNA. The changes in the ratio of hepatic to serum IGF-I during fasting and refeeding indicate that there may also be regulation at the level of hepatic release.

Insulin-like growth factor i and demyelination: cytochemical evidence for free radical derived oxidant mediation

1995 ◽  
Vol 53 ◽  
pp. 966-967
Author(s):  
E. Ann Ellis ◽  
Maria B. Grant ◽  
Robert N. Mames
Keyword(s):  
Free Radical ◽  
Growth Factor ◽  
Nadh Oxidase ◽  
Peptide Hormone ◽  
Diabetic Patients ◽  
Insulin Like Growth Factor ◽  
Factor I ◽  
Igf I ◽  
Growth Factor I ◽  
Oxidant Production

The peptide hormone, insulin-like growth factor I (IGF-I) is a growth factor which has been shown in elevated concentrations in the serum and vitreous of diabetic patients with proliferative diabetic retinopathy. Studies with an animal model of IGF-I induced proliferative retinopathy2 showed demyelination in the optic nerves and along the medullary rays of rabbit eyes which received intravitreal injections of IGF-I, basic fibroblast growth factor (bFGF), or a combination of the two growth factors. Biochemical studies have demonstrated a role for oxidative injury in complications of diabetes including lipid peroxidation and demyelination in peripheral neuropathy. The cerium NADH-oxidase technique has been used to demonstrate free radical derived oxidant production in several pathological conditions including demyelination in experimental allergic encephalomyelitis (EAE). We investigated the role of free radical derived oxidants in growth factor-induced demyelination.Pigmented rabbits were injected intravitreally with 500 μg of IGF-I or bFGF and sacrificed at 4, 8,12 and 18 days.

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