Insulin resistance and hyperinsulinaemia in the development and progression of cancer.
Experimental, epidemiological and clinical evidence implicates insulin resistance and its accompanying hyperinsulinaemia in the development of cancer, but the relative importance of these disturbances in cancer remains unclear. There are, however, theoretical mechanisms by which hyperinsulinaemia could amplify such growth-promoting effects as insulin may have, as well as the growth-promoting effects of other, more potent, growth factors. Hyperinsulinaemia may also induce other changes, particularly in the IGF (insulin-like growth factor) system, that could promote cell proliferation and survival. Several factors can independently modify both cancer risk and insulin resistance, including subclinical inflammation and obesity. The possibility that some of the effects of hyperinsulinaemia might then augment pro-carcinogenic changes associated with disturbances in these factors emphasizes how, rather than being a single causative factor, insulin resistance may be most usefully viewed as one strand in a network of interacting disturbances that promote the development and progression of cancer.
Godsland
Ian F
IF
Endocrinology and Metabolic Medicine, Imperial College London, Praed Street, London W2 1PG, U.K. i.godsland@imperial.ac.uk
D051017:Apoptosis Regulatory Proteins / Q000502:physiology; D002471:Cell Transformation, Neoplastic / Q000378:metabolism; D006133:Growth Substances / Q000502:physiology; D006801:Humans; D006946:Hyperinsulinism / Q000150:complications* / Q000453:epidemiology; D007333:Insulin Resistance / Q000502:physiology*; D009369:Neoplasms / Q000453:epidemiology / Q000209:etiology* / Q000503:physiopathology; D017526:Receptor, IGF Type 1 / Q000502:physiology
D051017:Apoptosis Regulatory Proteins; D006133:Growth Substances; D017526:Receptor, IGF Type 1