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Obesity Induced Colorectal Cancer

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Obesity Induced Colorectal Cancer Obesity Induced Colorectal Cancer THESIS Presented in Partial Fulfillment of the Requirements for the Degree Master of Mathematical Science in the Graduate School of The Ohio State University By Mauntell Ford, B.S. Graduate Program in Mathematics The Ohio State University 2013 Thesis Committee: Avner Friedman, Advisor Susan Olivo-Marston c Copyright by Mauntell Ford 2013 ABSTRACT More than 1.4 billion people in the world are overweight or obese [32]. Colorectal cancer takes the lives of 608,000 people each year[32]. It is important to study the negative impact of obesity on the body and population and the etiology of colorectal cancer. My goal was to create a mathematical model that relates obesity and insulin and captures the impact of increasing levels of insulin on the insulin growth factor -1 (IGF-1) pathway. The model is able to predict a risk of colorectal cancer based on a given insulin level. ii ACKNOWLEDGMENTS I would like to thank my advisors, Avner Friedman and Susan Olivo-Marston, for their support and guidance through the completion of my thesis. iii VITA 2007 . Wilson High School 2011 . B.Sc. in Mathematics from the Univer- sity of Kansas 2011-Present . Graduate Teaching Associate, The Ohio State University FIELDS OF STUDY Major Field: Mathematics Specialization: Mathematical Biology iv TABLE OF CONTENTS Abstract . ii Acknowledgments . iii Vita . iv List of Figures . vi List of Tables . vii CHAPTER PAGE 1 The relationship between obesity, insulin and colorectal cancer . 1 1.1 Obesity . 1 1.2 Hyperinsulinemia and colorectal cancer . 2 1.3 Obesity and diabetes . 2 1.4 Colorectal Cancer . 3 1.5 Insulin growth factor . 3 2 A mathematical approach . 5 2.1 Model Background . 5 2.2 Model Schematic . 6 2.3 Mathematical Model . 8 2.4 Discussion . 9 2.5 Conclusions . 11 Bibliography . 16 v LIST OF FIGURES FIGURE PAGE 2.1 Regression analysis based on data in the meta-analysis conducted by Moghaddam et al. [14]. 6 2.2 Relationship between BMI and insulin (pmol/l) [16] . 7 2.3 A model of the IGF1-R pathway leading to the development of colorec- tal cancer. Red bars represent inhibition and green arrows represent activation. 8 2.4 The top plots represent the levels of all of the proteins in the model. The bottom plots represent the varying levels of insulin and the re- spective level of colorectal cancer. Measurements are in µM. kIR = 10. As the final time increases, an increase in colorectal cancer is observed. 12 2.5 The top plots represent the levels of all of the proteins in the model. The bottom plots represent the varying levels of insulin and the re- spective level of colorectal cancer. As kIR decreases, the relationship between insulin and colorectal cancer changes. With small values of kIR, colorectal cancer is not increasing as quickly since the insulin is not activating the RAS, RAF, MAPK, ERK pathway as quickly. 13 2.6 The top plots represent the levels of all of the proteins in the model. The bottom plots represent the varying levels of insulin and the re- spective level of colorectal cancer. Measurements are in µM. Time is varied in these two plots. 14 2.7 The top plots represent the levels of all of the proteins in the model. The bottom plots represent the varying levels of insulin and the re- spective level of colorectal cancer. Measurements are in µM. Time is varied in these two plots. 15 vi LIST OF TABLES TABLE PAGE 2.1 Parameter values for the model. 10 vii CHAPTER 1 THE RELATIONSHIP BETWEEN OBESITY, INSULIN AND COLORECTAL CANCER 1.1 Obesity In 2008, more than 1.4 billion adults aged 20 or older, were overweight. Of these, more than 200 million men and nearly 300 million women were obese [32]. Obesity affects not only a staggering amount of adults but children as well. More than 40 million children under the age of five worldwide were overweight in 2010 [32]. Obesity is a global problem that is associated with an increased risk of premature death due to the complications associated with increased adipose tissue [12]. A meta-analysis showed that a 5 kg/m2 increase in body mass index (BMI) raises the risk of colon cancer by 24% in men [29]. Obesity has a direct and independent relationship with colorectal cancer [14]. It is the strongest determinant of insulin resistance and hyperinsulinemia [18]. Obesity is strongly associated with physiological function changes in adipose tissue causing problems such as insulin resistance, chronic inflammation and cancer [17][9]. 1 1.2 Hyperinsulinemia and colorectal cancer Childhood obesity is linked to adult health complications and hyperinsulinemia. The National Health and Nutrition Examination Study (NHANES) data from 1999-2000 estimated that 15.5% of 12-19 year olds and 15.3% of 6-11 year olds were overweight [9]. Being overweight in childhood and adolescence is significantly associated with insulin resistance in young adulthood [26]. The Bogalusa Heart Study reported that overweight schoolchildren, in comparison with their lean counterparts, were 12.6 times more likely to be hyperinsulinemic [26]. Hyperinsulinemia is a symptom of type 2 diabetes and associated with colorectal cancer [17]. A person with hyperinsulinemia has decreased IGF-binding protein (IGFBP) levels and increased free IGF-1 levels [10][18]. The risk of colorectal cancer is increased twofold for people with hyperinsu- linemia [18] because it may indirectly advance colorectal carcinogenesis by inducing changes in circulating IGF-1 and IGF binding proteins [21]. Increases in IGF-1 due to hyperinsulinemia may inhibit apoptosis of transformed and abnormal cells [21]. 1.3 Obesity and diabetes Obesity is correlated with type 2 diabetes, which is characterized by problematic insulin levels. Type 2 diabetes is caused by a resistance to the insulin produced by the β-cells in the pancreas. The blood sugar does not get into the fat, liver, or muscle cells for storage; therefore, high sugar levels build up [15]. In contrast, type 1 diabetes is an autoimmune process that destroys the pancreatic β-cells that synthesize insulin [30]. Risk of type 2 diabetes is nine fold higher for obese than for lean men [12]. Adolescents with type 2 diabetes mellitus are almost always obese [26]. Children and adolescents are more likely to develop full blown type 2 diabetes on a shorter time 2 scale than adults [9]. β-cell function problems and insulin resistance can be reversed by drastic and sustained energy deficits [13]. 1.4 Colorectal Cancer Colorectal cancer is the third most common cause of cancer deaths [19]. Each year more than 1 million cases of colorectal cancer are diagnosed worldwide [27]. TNF-α appears to contribute to the development of the tissue architecture necessary for tu- mor growth and metastasis [17]. TNF-α is involved in carcinogenesis because of its ability to activate NF-κB [17]. People with type 2 diabetes have up to a threefold increased risk of colorectal cancer compared to those without diabetes [10]. Hyper- insulinemia might contribute to cancer development through the growth-promoting effect of elevated levels of insulin [18]. Insulin has been shown to increase the growth of colon epithelial and carcinoma cells in vitro [21]. Diet is linked to as many as 70% kg of colorectal cancer deaths [1]. For a 2 increase in BMI, the risk of colorectal m2 cancer increased by 7% [14]. For a 2-cm increase in waist circumference, the risk increases by 4% [14]. The relative risk of colorectal cancer in obese was 1.46 (95% CI, 1.36-1.56) [14]. 1.5 Insulin growth factor When food is consumed the pancreas releases insulin. Insulin signals cells to store or use the glucose from the blood. Chronic excess energy intake causes obesity [18]. Increased adiposity leads to increased insulin resistance [26]. Insulin is less effective in obese than in non-obese in stimulating glucose uptake [20] because of dysregulation of circulating adipokines and cytokines [12]. Increased adiposity increases synthesis of proinflammatory cytokines, such as interleukin 6 (IL-6) [18] and TNF-α [9]. IL-6 3 regulates immune cell growth, cell differentiation and regulates chronic inflammation [17]. TNF-α inhibits insulin signaling and causes insulin resistance [10]. In response to insulin resistance, β-cells in the pancreas secrete more insulin, but the body is un- able to process the insulin and the blood glucose levels rise [21]. As time passes, β-cell function declines linearly [13]. Insulin resistance modifies the insulin growth factor (IGF) system[10], by activating liver production of IGF-1, both of which promote cancer cell proliferation because they act as growth factors [17]. Insulin is posi- tively related to IGF-1 bioavailability [21]. The IGF system consists of two ligands (IGF-1 and IGF-II), two receptors (IGF-1R and IGF-IIR), six high-affinity-binding proteins and several binding-protein proteases [18]. IGF-1 is produced by most body tissues [31], but predominantly in the liver [21]. It is important in cell growth and development and necessary for cell cycle progression [24]. Once insulin binds with its receptor, the mitogen-activated protein kinase (MAPK) and phosphatidylinositol 3-kinase (PI3K) pathways are activated [29]. The activation leads to increased prolif- eration and decreased apoptosis [10][21]. IGF-1 levels are elevated during obesity [29]. The concentration of IGF-1 is positively correlated with the risk of pre-menopausal breast, colorectal and prostate cancers [18]. The expression level of IGF-1R is asso- ciated with the tumor stage [24]. Increases in IGF-1 bioavailability over long periods of time may increase risk of colorectal cancer [21][17]. Blocking IGF-1R inhibits the growth and survival of human colorectal cancer cells [21].
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