The mitotic rate of stem cells is a major determinant of cancer risk.
Insulin-like growth factors (IGFs) are virtually obligate stimulants of cell turnover in nearly every tissue.
IGF activity is subject to rapid modulation by hepatic release of IGF binding protein-1 (IGFBP-1), a factor whose synthesis is suppressed by insulin and increased by glucagon.
Up-regulation of IGFBP-1 production can be expected to decrease IGF activity and thereby diminish cancer risk.
Measures that sensitize peripheral tissues to insulin, and thereby down-regulate insulin secretion, can be expected to increase IGFBP-1 synthesis, provided that they do not unduly sensitize hepatocytes as well.
Prolonged aerobic exercise and caloric restriction also increase IGFBP-1 production.
Since IGF-I suppresses hepatic synthesis of sex hormone binding globulin (SHBG), down-regulation of IGF activity will increase SHBG levels and thus diminish the availability of free sex hormones - an effect that should further decrease cancer risk in sex hormone-responsive tissues.
These considerations rationalize many findings in animal and epidemiologic studies, and suggest that non-diabetic insulin resistance may be a significant cancer risk factor.
Increased IGF activity associated with insulin resistance may also promote benign hyperplasias - most notably atherosclerosis.
Hyperinsulinemia stimulates intimal hyperplasia indirectly, via IGF.
Mots-clés Pascal : Carcinogenèse, Prévention, Régulation, Facteur croissance IGF, Exercice physique, Bilan calorique, Restriction modification, Epidémiologie, Modèle animal, Article synthèse, Tumeur maligne, Activité biologique
Mots-clés Pascal anglais : Carcinogenesis, Prevention, Regulation(control), Insulin like growth factor, Physical exercise, Caloric balance, Restriction modification, Epidemiology, Animal model, Review, Malignant tumor, Biological activity
Notice produite par :
Inist-CNRS - Institut de l'Information Scientifique et Technique
Cote : 97-0320449
Code Inist : 002B04E05. Création : 12/09/1997.