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Pancreatic steatosis

an update

Ramkissoon, Reshama; Gardner, Timothy B.b

Current Opinion in Gastroenterology: September 2019 - Volume 35 - Issue 5 - p 440–447
doi: 10.1097/MOG.0000000000000566
PANCREAS: Edited by Timothy B. Gardner

Purpose of review Pancreatic steatosis is a clinical entity with emerging significance and impacts patient health in a multitude of ways. It has a high prevalence in the global population with predilections for different demographics by age, sex and ethnicity. Understanding the pathophysiology, clinical features and complications of this entity may be important to understanding the consequences of the ongoing obesity global epidemic.

Recent findings Obesity and metabolic syndrome contribute to metabolic derangements that result in lipid mishandling by adipocytes. Adipocytokine imbalances in circulation and in the pancreatic microenvironment cause chronic, low-grade inflammation. The resulting beta cell and acinar cell apoptosis leads to pancreatic endocrine and exocrine dysfunction. Furthermore, these adipocytokines regulate cell growth, differentiation, as well as angiogenesis and lymphatic spread. These consequences of adipocyte infiltration are thought to initiate carcinogenesis, leading to pancreatic intraepithelial neoplasia and pancreatic ductal adenocarcinoma.

Summary Obesity will lead to millions of deaths each year and pancreatic steatosis may be the key intermediate entity that leads to obesity-related complications. Enhancing our understanding may reveal strategies for preventing mortality and morbidity related to the global epidemic of obesity. Further research is needed to determine the pathophysiology, long-term complications and effective treatment strategies for this condition.

aDepartment of Internal Medicine

bSection of Gastroenterology and Hepatology, Dartmouth-Hitchcock Medical Center, Lebanon, New Hampshire, USA

Correspondence to Resham Ramkissoon, MD, Department of Internal Medicine, Dartmouth-Hitchcock Medical Center, One Medical Center Drive, Lebanon, NH 03756, USA. Tel: +1 603 650 7515; fax: +1 603 650 6122; e-mail:

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