Ko J, Skudder-Hill L, Cho J, Bharmal SH, Petrov MS. Pancreatic enzymes and abdominal adipose tissue distribution in new-onset prediabetes/diabetes after acute pancreatitis. World J Gastroenterol 2021; 27(23): 3357-3371 [PMID: 34163117 DOI: 10.3748/wjg.v27.i23.3357]
Corresponding Author of This Article
Maxim S Petrov, MD, MPH, PhD, Professor, School of Medicine, University of Auckland, 28 Park Avenue, Auckland 1142, New Zealand. m.petrov@auckland.ac.nz
Research Domain of This Article
Gastroenterology & Hepatology
Article-Type of This Article
Case Control Study
Open-Access Policy of This Article
This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
World J Gastroenterol. Jun 21, 2021; 27(23): 3357-3371 Published online Jun 21, 2021. doi: 10.3748/wjg.v27.i23.3357
Pancreatic enzymes and abdominal adipose tissue distribution in new-onset prediabetes/diabetes after acute pancreatitis
Juyeon Ko, Loren Skudder-Hill, Jaelim Cho, Sakina H Bharmal, Maxim S Petrov
Juyeon Ko, Loren Skudder-Hill, Jaelim Cho, Sakina H Bharmal, Maxim S Petrov, School of Medicine, University of Auckland, Auckland 1142, New Zealand
Author contributions: Ko J, Skudder-Hill L, Cho J, and Bharmal SH collected data; Ko J wrote the manuscript; Ko J, Skudder-Hill L, Cho J, Bharmal SH, and Petrov MS reviewed the manuscript; Petrov MS conceived and supervised the study.
Institutional review board statement: The study was approved by the Health and Disability Ethics Committee (New Zealand).
Informed consent statement: All study participants or their legal guardians provided informed written consent about personal and medical data collection prior to study enrolment.
Conflict-of-interest statement: The authors have no conflict of interest.
Data sharing statement: No additional data are available.
STROBE statement: The authors have read the STROBE Statement—checklist of items, and the manuscript was prepared and revised according to the STROBE Statement—checklist of items.
Open-Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/Licenses/by-nc/4.0/
Corresponding author: Maxim S Petrov, MD, MPH, PhD, Professor, School of Medicine, University of Auckland, 28 Park Avenue, Auckland 1142, New Zealand. m.petrov@auckland.ac.nz
Received: January 29, 2021 Peer-review started: January 29, 2021 First decision: April 5, 2021 Revised: April 14, 2021 Accepted: June 7, 2021 Article in press: June 7, 2021 Published online: June 21, 2021 Processing time: 140 Days and 3.6 Hours
ARTICLE HIGHLIGHTS
Research background
Abdominal adipose tissue distribution is an important factor in the pathogenesis of diabetes in general and new-onset diabetes after acute pancreatitis in particular.
Research motivation
The role of pancreatic enzymes in the pathogenesis of new-onset diabetes after acute pancreatitis is unknown.
Research objectives
The objective was to compare head-to-head abdominal adipose tissue distribution in new-onset prediabetes or diabetes after acute pancreatitis (NODAP), type 2 prediabetes or diabetes, and healthy controls.
Research methods
The design was a case-control study. Intra-pancreatic fat, liver fat, skeletal muscle fat, visceral fat, and subcutaneous fat were quantified in a blinded fashion with the use of magnetic resonance imaging. Circulating levels of pancreatic amylase, pancreatic lipase, and chymotrypsin were determined.
Research results
The intra-pancreatic fat percentage was 9.4 ± 1.8%, 9.8 ± 1.1%, and 7.8 ± 1.9% in NODAP, type 2 prediabetes or diabetes, and healthy controls, respectively (P < 0.001). The visceral fat volume was 2205 ± 1098 cm3, 2622 ± 1172 cm3, and 1209 ± 808 cm3 in NODAP, type 2 prediabetes or diabetes, and healthy controls, respectively (P < 0.001). The other fat phenotypes did not differ between the groups. The amount of intra-pancreatic fat and visceral fat was significantly associated with circulating levels of pancreatic amylase in NODAP (but not type 2 prediabetes or diabetes or healthy controls).
Research conclusions
Excess intra-pancreatic fat deposition is a key factor in the pathogenesis of new-onset diabetes after acute pancreatitis. There is a significant inverse relationship between circulating levels of pancreatic amylase and intra-pancreatic fat.
Research perspectives
Human studies on the role of pancreatic amylase in new-onset diabetes after acute pancreatitis are warranted.
