Insulin-Like Growth Factors and Their Binding Proteins: Biological Actions*

Jones, John I.; Clemmons, David R.

doi:10.1210/edrv-16-1-3

Cited by 2,497 publications

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“…The lack of a transmembrane anchor may affect its effectiveness as a dominant-negative inhibitor because there are a family of secreted IGF-binding proteins (insulin-like growth factor binding proteins), which bind IGFs with equal or even greater affinity than the IGF1R. 3,[28][29][30] IGFBPs are present at high levels in specific embryonic tissues and could potentially outcompete a dominant-negative IGF1R that does not contain an appropriate membrane anchor, thereby reducing the knockdown efficacy in those tissues.…”

Section: Discussionmentioning

confidence: 99%

Insulin-like growth factor signaling regulates zebrafish embryonic growth and development by promoting cell survival and cell cycle progression

et al. 2007

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Although much is known about the global effects of insulin-like growth factor 1 receptor (IGF1R)-mediated signaling on fetal growth and the clinical manifestations resulting from IGF/IGF1R deficiencies, we have an incomplete understanding of the cellular actions of this essential pathway during vertebrate embryogenesis. In this study, we inhibited IGF1R signaling during zebrafish embryogenesis using antisense morpholino oligonucleotides or a dominant-negative IGF1R fusion protein. IGF1R inhibition resulted in reduced embryonic growth, arrested development and increased lethality. IGF1R-deficient embryos had significant defects in the retina, inner ear, motoneurons and heart. No patterning abnormalities, however, were found in the brain or other embryonic tissues. At the cellular level, IGF1R inhibition increased caspase 3 activity and induced neuronal apoptosis. Coinjection of antiapoptotic bcl2-like mRNA attenuated the elevated apoptosis and rescued the retinal and motoneuron defects, but not the developmental arrest. Subsequent cell cycle analysis indicated an increased percentage of cells in G1 and a decreased percentage in S phase in IGF1R-deficient embryos independent of apoptosis. These results provide novel insight into the cellular basis of IGF1R function and show that IGF1R signaling does not function as an anteriorizing signal but regulates embryonic growth and development by promoting cell survival and cell cycle progression.

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Section: Discussionmentioning

confidence: 99%

Insulin-like growth factor signaling regulates zebrafish embryonic growth and development by promoting cell survival and cell cycle progression

et al. 2007

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“…These hypotheses suggests that obesity precipitates insulin resistance and the resulting prolonged hyperinsulinaemia in Obesity, overweight and cancer GD Batty et al itself acts as a tumour growth promoter. 44 Additionally, higher levels of insulin-like growth factor (IGF-I)Fa multifunctional, circulating peptide that encourages tumour growth through its mitosis and antiapoptosis properties 45 Fare positively associated with prostate and colorectal cancer risk, 46 both energy-related malignancies. While IGF-I is also positively related to BMI, the gradient is in fact nonlinear (at obese levels it decreases).…”

Section: Plausible Mechanismsmentioning

confidence: 99%

Obesity and overweight in relation to organ-specific cancer mortality in London (UK): findings from the original Whitehall study

Batty

Shipley

Jarrett³

et al. 2005

Int J Obes

125

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OBJECTIVE:To examine the relation of obesity and overweight with organ-specific cancer mortality. METHODS: In the Whitehall prospective cohort study of London-based government employees, 18 403 middle-age men participated in a medical examination between 1967 and 1970. Subjects were followed up for cause-specific mortality for up to 35 y (median: interquartile range (25th-75th centile); 28.1 y: 18.6-33.8). RESULTS: There were over 3000 cancer deaths in this cohort. There was a raised risk of mortality from carcinoma of the rectum, bladder, colon, and liver, and for lymphoma in obese or overweight men following adjustment for range of covariates, which included socioeconomic position and physical activity. These relationships held after exclusion of deaths occurring in the first 20 y of follow-up. CONCLUSION: Avoidance of obesity and overweight in adult life may reduce the risk of developing some cancers.

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“…Insulin has the ability to stimulate IGFs which are important mitogens, necessary for the cell to progress from G1 to the S phase of the cell cycle (Aaronson, 1991). Ninety-five percent of IGF-1 circulates bound to IGF binding protein-3 (IGFBP-3), which controls the availability of free IGF-1 by modulating its access to the IGF-1 receptor (Jones & Clemmons, 1995;Collett-Solberg & Cohen 1996). IGF-1 promotes cell growth by stimulating tyrosine-specific protein kinase activity both in its own receptors as well as in the insulin receptors.…”

Section: Glycemic Index In Chronic Disease Ls Augustin Et Almentioning

confidence: 99%

Glycemic index in chronic disease: a review

et al. 2002

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Aim: The intent of this review is to critically analyze the scientific evidence on the role of the glycemic index in chronic Western disease and to discuss the utility of the glycemic index in the prevention and management of these disease states. Background: The glycemic index ranks foods based on their postprandial blood glucose response. Hyperinsulinemia and insulin resistance, as well as their determinants (eg high energy intake, obesity, lack of physical activity) have been implicated in the etiology of diabetes, coronary heart disease and cancer. Recently, among dietary factors, carbohydrates have attracted much attention as a significant culprit, however, different types of carbohydrate produce varying glycemic and insulinemic responses. Low glycemic index foods, characterized by slowly absorbed carbohydrates, have been shown in some studies to produce beneficial effects on glucose control, hyperinsulinemia, insulin resistance, blood lipids and satiety. Method: Studies on the short and long-term metabolic effects of diets with different glycemic indices will be presented and discussed. The review will focus primarily on clinical and epidemiological data, and will briefly discuss in vitro and animal studies related to possible mechanisms by which the glycemic index may influence chronic disease.

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Insulin-Like Growth Factors and Their Binding Proteins: Biological Actions*

Cited by 2,497 publications

References 0 publications

Insulin-like growth factor signaling regulates zebrafish embryonic growth and development by promoting cell survival and cell cycle progression

Insulin-like growth factor signaling regulates zebrafish embryonic growth and development by promoting cell survival and cell cycle progression

Obesity and overweight in relation to organ-specific cancer mortality in London (UK): findings from the original Whitehall study

Glycemic index in chronic disease: a review

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