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Review
. 2018 Apr;118(4):555-567.
doi: 10.1016/j.jand.2017.07.005. Epub 2017 Sep 12.

Diabetes Mellitus and Obesity as Risk Factors for Pancreatic Cancer

Guido Eibl, Zobeida Cruz-Monserrate, Murray Korc, Maxim S Petrov, Mark O Goodarzi, William E Fisher, Aida Habtezion, Aurelia Lugea, Stephen J Pandol, Phil A Hart, Dana K Andersen; Consortium for the Study of Chronic Pancreatitis, Diabetes, and Pancreatic Cancer
Review

Diabetes Mellitus and Obesity as Risk Factors for Pancreatic Cancer

Guido Eibl et al. J Acad Nutr Diet. 2018 Apr.

Abstract

Pancreatic ductal adenocarcinoma (PDAC) is among the deadliest types of cancer. The worldwide estimates of its incidence and mortality in the general population are eight cases per 100,000 person-years and seven deaths per 100,000 person-years, and they are significantly higher in the United States than in the rest of the world. The incidence of this disease in the United States is more than 50,000 new cases in 2017. Indeed, total deaths due to PDAC are projected to increase dramatically to become the second leading cause of cancer-related deaths before 2030. Considering the failure to date to efficiently treat existing PDAC, increased effort should be undertaken to prevent this disease. A better understanding of the risk factors leading to PDAC development is of utmost importance to identify and formulate preventive strategies. Large epidemiologic and cohort studies have identified risk factors for the development of PDAC, including obesity and type 2 diabetes mellitus. This review highlights the current knowledge of obesity and type 2 diabetes as risk factors for PDAC development and progression, their interplay and underlying mechanisms, and the relation to diet. Research gaps and opportunities to address this deadly disease are also outlined.

Keywords: Obesity; Pancreatic cancer; Prevention; Review; Type 2 diabetes mellitus.

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Conflict of interest statement

Conflict of Interest disclosures: All authors declared no conflict of interest

Figures

Figure 1
Figure 1. Prevalence of diabetes mellitus (DM), Prevalence of Obesity, and Incidence of Pancreatic Cancer
Figure 1A (Top): Prevalence of DM (in quartiles) 2014 (from http://www.cdc.gov/diabetes/data). Figure 1B (Middle): Prevalence of Obesity expressed as Body Mass Index (in quartiles) 2015 (from http://www.cdc.gov/obesity/data). Figure 1C (Bottom): Incidence of Pancreatic Cancer, age adjusted, all races (in quartiles) 2009–2013 (from http://statecancerprofiles.cancer.gov/data-topics/incidence.html).
Figure 1
Figure 1. Prevalence of diabetes mellitus (DM), Prevalence of Obesity, and Incidence of Pancreatic Cancer
Figure 1A (Top): Prevalence of DM (in quartiles) 2014 (from http://www.cdc.gov/diabetes/data). Figure 1B (Middle): Prevalence of Obesity expressed as Body Mass Index (in quartiles) 2015 (from http://www.cdc.gov/obesity/data). Figure 1C (Bottom): Incidence of Pancreatic Cancer, age adjusted, all races (in quartiles) 2009–2013 (from http://statecancerprofiles.cancer.gov/data-topics/incidence.html).
Figure 1
Figure 1. Prevalence of diabetes mellitus (DM), Prevalence of Obesity, and Incidence of Pancreatic Cancer
Figure 1A (Top): Prevalence of DM (in quartiles) 2014 (from http://www.cdc.gov/diabetes/data). Figure 1B (Middle): Prevalence of Obesity expressed as Body Mass Index (in quartiles) 2015 (from http://www.cdc.gov/obesity/data). Figure 1C (Bottom): Incidence of Pancreatic Cancer, age adjusted, all races (in quartiles) 2009–2013 (from http://statecancerprofiles.cancer.gov/data-topics/incidence.html).
Figure 2
Figure 2. Adipose tissue dysfunction during obesity
Schematic overview of obesity-associated changes in white adipose tissue leading to hyperplasia/hypertrophy of adipocytes, recruitment and proliferation of immune cells, increased secretion of pro-inflammatory cytokines (e.g. TNF-α, IL-6) and adipokines (leptin), reduction of adiponectin, increase of free fatty acids (FFA), ultimately leading to insulin resistance and systemic and local inflammation (from van Kruijsdijk et al. Cancer Epidemiol Biomarkers Prev 2009; 18(10): 2569–78 with permission).
Figure 3
Figure 3. Promotion of PDAC by T2DM: Potential Role of Islet Factors
Illustration of the interplay and crosstalk between pancreatic pre-cancer (PanIN) and cancer (PDAC) cells, pancreatic stellate cells (PaSCs), immune cells (e.g. tumor-associated macrophages: TAMs), and islets.
See this image and copyright information in PMC

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