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\n[https://doi.org/10.1007/s00018-023-04855-z](https://doi.org/10.1007/s00018-023-04855-z) Cellular and Molecular Life Sciences  \nIntrapancreatic fat, pancreatitis, and pancreatic cancer  \nAnna C. Lilly1,2 · Igor Astsaturov1,3 · Erica A. Golemis1,4  \nReceived: 15 March 2023 / Revised: 29 June 2023 / Accepted: 3 July 2023 / Published online: 15 July 2023 © The Author(s) 2023  \nAbstract  \nPancreatic cancer is typically detected at an advanced stage, and is refractory to most forms of treatment, contributing to poor survival outcomes. The incidence of pancreatic cancer is gradually increasing, linked to an aging population and increasing rates of obesity and pancreatitis, which are risk factors for this cancer. Sources of risk include adipokine signaling from fat cells throughout the body, elevated levels of intrapancreatic intrapancreatic adipocytes (IPAs), inflammatory signals arising from pancreas-infiltrating immune cells and a fibrotic environment induced by recurring cycles of pancreatic obstruction and acinar cell lysis. Once cancers become established, reorganization of pancreatic tissue typically excludes IPAs from the tumor microenvironment, which instead consists of cancer cells embedded in a specialized microenvironment derived from cancer-associated fibroblasts (CAFs) . While cancer cell interactions with CAFs and immune cells have been the topic of much investigation, mechanistic studies of the source and function of IPAs in the pre-cancerous niche are much less developed. Intriguingly, an extensive review of studies addressing the accumulation and activity of IPAs in the pancreas reveals that unexpectedly diverse group of factors cause replacement of acinar tissue with IPAs, particularly in the mouse models that are essential tools for research into pancreatic cancer. Genes implicated in regulation of IPA accumulation include KRAS, MYC, TGF-β, periostin, HNF1, and regulators of ductal ciliation and ER stress, among others. These findings emphasize the importance of studying pancreas-damaging factors in the pre-cancerous environment, and have significant implications for the interpretation of data from mouse models for pancreatic cancer.  \nKeywords Ductal cells · Cilia · Pancreatic steatosis · PDAC · Lipids  \nIntroduction  \nRates and degree of obesity have been rising across the globe for several decades; as of 2016, 39% of adults were classified as overweight and 13% as obese [1, 2]. In the United States, a 2017–2018 survey estimated that 31.1% of adults are overweight, and over 42% of adults are obese [3]. Obesity causes  \n* Erica A. Golemis [Erica.Golemis@fccc.edu](Erica.Golemis@fccc.edu)  \n1 Program in Cancer Signaling and Microenvironment, Fox Chase Cancer Center, 333 Cottman Ave., Philadelphia, PA 19111, USA  \n2 Molecular & Cell Biology & Genetics (MCBG) Program, Drexel University College of Medicine, Philadelphia, PA 19102, USA  \n3 The Marvin & Concetta Greenberg Pancreatic Cancer Institute, Fox Chase Cancer Center, Philadelphia, PA 19111, USA  \n4 Department of Cancer and Cellular Biology, Lewis Katz School of Medicine, Philadelphia, PA 19140, USA  \ncomplex changes in multiple organ systems, but is typically characterized by adipocyte expansion, fat deposits, immune cell recruitment, and low-grade chronic inflammation [2, 4, 5] . These changes are associated with increased risk for and exacerbation of diseases affecting multiple organ systems.  \nIncidence of diseases of the pancreas, including acute and chronic pancreatitis [6 , 7] and pancreatic cancer [8], are rising globally, with the highest rates of these diseases observed in North America and Europe. These rising rates have been linked to a number of modifiable factors, including increased preference of individuals for high calorie and high fat diets that promote obesity; the role of obesity in inducing and exacerbating pancreatitis [9, 10] and pancreatic cancer [11–15] has been appreciated for over a d","cbCaihm94V83GO0z","https://ap.wps.com/l/cbCaihm94V83GO0z","pdf",2831386,25,"English","# Abstract\n# Keywords\n# Introduction","[{\"question\":\"Why is pancreatic cancer often difficult to treat?\",\"answer\":\"Pancreatic cancer is typically detected late and is refractory to most treatments, resulting in poor survival outcomes.\"},{\"question\":\"What factors link obesity and pancreatitis to pancreatic cancer risk?\",\"answer\":\"Obesity and pancreatitis contribute through mechanisms such as adipokine signaling, increased intrapancreatic adipocytes, inflammatory signals from immune cells, and a fibrotic environment.\"},{\"question\":\"How might intrapancreatic adipocytes (IPAs) influence early pancreatic disease development?\",\"answer\":\"IPAs can accumulate in pre-cancerous niches and promote replacement of acinar tissue, with activity shaped by multiple regulatory genes and pathways identified in review evidence.\"}]","Intrapancreatic fat, pancreatitis, and pancreatic cancer | PDF",1790215422,63]