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Int J Mol Sci. 2018 Dec 18;19(12). pii: E4110. doi: 10.3390/ijms19124110.

Using Mouse and Drosophila Models to Investigate the Mechanistic Links between Diet, Obesity, Type II Diabetes, and Cancer.

Author information

1
School of Biological Sciences, Monash University, Clayton, Victoria 3800, Australia. coral.warr@utas.edu.au.
2
School of Medicine, College of Health and Medicine, University of Tasmania, Hobart, Tasmania 7000, Australia. coral.warr@utas.edu.au.
3
School of Biological Sciences, Monash University, Clayton, Victoria 3800, Australia. katherine.shaw@monash.edu.
4
School of Biological Sciences, Monash University, Clayton, Victoria 3800, Australia. arani.azim@monash.edu.
5
School of Biological Sciences, Monash University, Clayton, Victoria 3800, Australia. matthew.piper@monash.edu.
6
School of Biological Sciences, Monash University, Clayton, Victoria 3800, Australia. linda.parsons@monash.edu.

Abstract

Many of the links between diet and cancer are controversial and over simplified. To date, human epidemiological studies consistently reveal that patients who suffer diet-related obesity and/or type II diabetes have an increased risk of cancer, suffer more aggressive cancers, and respond poorly to current therapies. However, the underlying molecular mechanisms that increase cancer risk and decrease the response to cancer therapies in these patients remain largely unknown. Here, we review studies in mouse cancer models in which either dietary or genetic manipulation has been used to model obesity and/or type II diabetes. These studies demonstrate an emerging role for the conserved insulin and insulin-like growth factor signaling pathways as links between diet and cancer progression. However, these models are time consuming to develop and expensive to maintain. As the world faces an epidemic of obesity and type II diabetes we argue that the development of novel animal models is urgently required. We make the case for Drosophila as providing an unparalleled opportunity to combine dietary manipulation with models of human metabolic disease and cancer. Thus, combining diet and cancer models in Drosophila can rapidly and significantly advance our understanding of the conserved molecular mechanisms that link diet and diet-related metabolic disorders to poor cancer patient prognosis.

KEYWORDS:

Drosophila; cancer; diet; obesity; type II diabetes mellitus

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