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Extra resources for Biology of IGF-1: Its Interaction with Insulin in Health and Malignant States (Novartis Foundation Symposia)

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30 DISCUSSION Kaaks: So you are arguing that peak height velocity is a better marker for cumulative exposure to IGF in the pubertal period, or just at a given point in time at which the peak height velocity is expressed? Holly: Peak height velocity tells you what is going in at the most rapid period of change. It’s like a car accident: the faster you are going the bigger the crash. LÖnning: There were some epidemiological studies back in Norway on young girls who went through puberty during the wartime period during 1940^45 when there were food restrictions (Nilsen & Vatten 2001).

This is enabled by paternal imprinting of the IGF-2 gene. In contrast, the mother needs to constrain the fetal development and balance nutrient extraction to ensure her own survival and reproductive competence for future potential fetuses, with potentially di¡erent fathers. This is enabled by maternal imprinting of the IGF-2 receptor gene (Reik et al 2003). As the pituitary develops and takes control of the endocrine system, pituitary GH drives systemic IGF-1 production which then plays a more dominant role in growth and development.

Carpentier: Here we speak about IGF-1 or the IGF-1 receptor, but each time we focus on only one component. I think we should consider the two elements. We should see whether if you have a high level of IGF-1 you will decrease the level of receptor. But if there is not such an e¡ect then you will probably have things going wrong. We always need to take into account both elements and not just focus on one. Kaaks: I am puzzled by what Je¡ Holly said about pubertal IGF levels. The vast majority of cross-sectional studies have shown no association whatsoever between ¢nal adult height attained and IGF levels.

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