OBJECTIVES: Obesity and insulin resistance cause fatty infiltration of many organs, including the pancreas (pancreatic steatosis [PS]) and the liver (nonalcoholic fatty liver disease [NAFLD]). In contrast to NAFLD, pathophysiological mechanisms and clinical relevance of PS remain unknown. This study aimed to identify a possible relation between PS and NAFLD. METHODS: In this study including postmortem collected material of 80 patients, clinical and histological data were collected and revised. Patients with hepatic or pancreatic disease and alcohol abuse were excluded. Nonalcoholic fatty liver disease activity score was used for grading the histology of the liver, whereas pancreatic lipomatosis score assessed PS. Ordinal logistic regression was used to analyze correlations. RESULTS: Interlobular and total pancreatic fat were both related to NAFLD activity score in patients without steatogenic medication (P = 0.02 and P = 0.03, respectively). When corrected for body mass index, no relation could be found. Total pancreatic fat was a significant predictor for the presence of NAFLD (P = 0.02). Presence of intralobular pancreatic fat was related to nonalcoholic steatohepatitis; however, total fat was not. CONCLUSIONS: This study demonstrates that NAFLD and PS are related. This relationship seems to be mediated by general obesity. Intralobular pancreatic fat is associated with nonalcoholic steatohepatitis.
OBJECTIVES:Obesity and insulin resistance cause fatty infiltration of many organs, including the pancreas (pancreatic steatosis [PS]) and the liver (nonalcoholic fatty liver disease [NAFLD]). In contrast to NAFLD, pathophysiological mechanisms and clinical relevance of PS remain unknown. This study aimed to identify a possible relation between PS and NAFLD. METHODS: In this study including postmortem collected material of 80 patients, clinical and histological data were collected and revised. Patients with hepatic or pancreatic disease and alcohol abuse were excluded. Nonalcoholic fatty liver disease activity score was used for grading the histology of the liver, whereas pancreatic lipomatosis score assessed PS. Ordinal logistic regression was used to analyze correlations. RESULTS: Interlobular and total pancreatic fat were both related to NAFLD activity score in patients without steatogenic medication (P = 0.02 and P = 0.03, respectively). When corrected for body mass index, no relation could be found. Total pancreatic fat was a significant predictor for the presence of NAFLD (P = 0.02). Presence of intralobular pancreatic fat was related to nonalcoholic steatohepatitis; however, total fat was not. CONCLUSIONS: This study demonstrates that NAFLD and PS are related. This relationship seems to be mediated by general obesity. Intralobular pancreatic fat is associated with nonalcoholic steatohepatitis.
Authors: Emily L Kullman; Karen R Kelly; Jacob M Haus; Ciaran E Fealy; Amanda R Scelsi; Mangesh R Pagadala; Chris A Flask; Arthur J McCullough; John P Kirwan Journal: J Appl Physiol (1985) Date: 2016-03-31
Authors: Lucia Pacifico; Michele Di Martino; Caterina Anania; Gian Marco Andreoli; Mario Bezzi; Carlo Catalano; Claudio Chiesa Journal: World J Gastroenterol Date: 2015-04-21 Impact factor: 5.742