title: Obesity and cancer, a case for insulin signaling.
abstract: Obesity is a worldwide epidemic, with the number of overweight and obese individuals climbing from just over 500 million in 2008 to 1.9 billion in 2014. Type 2 diabetes (T2D), cardiovascular disease and non-alcoholic fatty liver disease have long been associated with the obese state, whereas cancer is quickly emerging as another pathological consequence of this disease. Globally, at least 2.8 million people die each year from being overweight or obese. It is estimated that by 2020 being overweight or obese will surpass the health burden of tobacco consumption. Increase in the body mass index (BMI) in overweight (BMI>25 kg/m(2)) and obese (BMI>30 kg/m(2)) individuals is a result of adipose tissue (AT) expansion, which can lead to fat comprising >50% of the body weight in the morbidly obese. Extensive research over the last several years has painted a very complex picture of AT biology. One clear link between AT expansion and etiology of diseases like T2D and cancer is the development of insulin resistance (IR) and hyperinsulinemia. This review focuses on defining the link between obesity, IR and cancer.
authors.affiliation: Division of Signaling Biology, Princess Margaret Cancer Centre/University Health Network, Toronto, Ontario, Canada.
authors.forename: Y
authors.initials: Y
authors.lastname: Poloz
authors.affiliation: Division of Signaling Biology, Princess Margaret Cancer Centre/University Health Network, Toronto, Ontario, Canada.|Department of Medical Biophysics, University of Toronto, Toronto, Ontario, Canada.
authors.forename: V
authors.initials: V
authors.lastname: Stambolic
mesh_terms: D000818:Animals; D006801:Humans; D006946:Hyperinsulinism / Q000188:drug therapy; D007328:Insulin / Q000378:metabolism*; D007333:Insulin Resistance; D009369:Neoplasms / Q000188:drug therapy / Q000378:metabolism*; D009767:Obesity, Morbid / Q000378:metabolism*; D015398:Signal Transduction
chemical_list: D007328:Insulin