Nutrition, insulin, IGF-1 metabolism and cancer risk

A summary of epidemiological evidence

Rudolf Kaaks, Lonning, Laron

Research output: Contribution to journalArticle

88 Citations (Scopus)

Abstract

A Western lifestyle - characterized by low physical activity, and high dietary intake, animal protein, saturated fats and rapidly digestible carbohydrates - is associated with increased risks of many cancers. It has been postulated that, at least in part, these increases may be mediated by alterations in the metabolism of insulin and insulin-like growth factors (IGFs), related to nutritional lifestyle. Insulin regulates energy metabolism and increases the bio-activity of IGF-1 by enhancing its synthesis and by decreasing several of its binding proteins (IGFBP-1 and 2). Insulin and IGF-1 both stimulate anabolic processes as a function of available energy and elementary substrates (e.g. amino acids). The anabolic signals by insulin or IGF-1 can promote tumour development by inhibiting apoptosis, and by stimulating cell proliferation. Epidemiological evidence is accumulating and suggests that the risk of cancers of the colon, pancreas, endometrium, breast and prostate are related to circulating levels of insulin, IGF-1, or both. Nutritional energy balance, macronutrient composition of the diet and physical activity levels appear to be major determinants of IGF-1 bioactivity.

Original languageEnglish (US)
Pages (from-to)247-264
Number of pages18
JournalNovartis Foundation symposium
Volume262
StatePublished - Dec 1 2004

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Somatomedins
Insulin
Neoplasms
Life Style
Insulin-Like Growth Factor Binding Protein 2
Insulin-Like Growth Factor Binding Protein 1
Endometrium
Pancreatic Neoplasms
Colonic Neoplasms
Energy Metabolism
Prostate
Carrier Proteins
Breast
Fats
Carbohydrates
Cell Proliferation
Apoptosis
Diet
Amino Acids
Proteins

ASJC Scopus subject areas

  • Medicine(all)

Cite this

Nutrition, insulin, IGF-1 metabolism and cancer risk : A summary of epidemiological evidence. / Kaaks, Rudolf; Lonning; Laron.

In: Novartis Foundation symposium, Vol. 262, 01.12.2004, p. 247-264.

Research output: Contribution to journalArticle

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