Mukherjee S, Maheshwari D, Pal R, Sachdeva N. Pancreatic fat in type 2 diabetes: Causal or coincidental? World J Meta-Anal 2023; 11(3): 68-78 [DOI: 10.13105/wjma.v11.i3.68]
Corresponding Author of This Article
Naresh Sachdeva, MSc, PhD, Professor, Department of Endocrinology, Post Graduate Institute of Medical Education and Research, Endocrinology Lab, Research Block-B Post Graduate Institute of Medical Education and Research, Chandigarh 160012, India. naresh_pgi@hotmail.com
Research Domain of This Article
Endocrinology & Metabolism
Article-Type of This Article
Minireviews
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 Meta-Anal. Mar 2, 2023; 11(3): 68-78 Published online Mar 2, 2023. doi: 10.13105/wjma.v11.i3.68
Pancreatic fat in type 2 diabetes: Causal or coincidental?
Soham Mukherjee, Deep Maheshwari, Rimesh Pal, Naresh Sachdeva
Soham Mukherjee, Deep Maheshwari, Rimesh Pal, Naresh Sachdeva, Department of Endocrinology, Post Graduate Institute of Medical Education and Research, Chandigarh 160012, India
Author contributions: Mukherjee S and Maheshwari D performed the literature search and wrote the manuscript; Pal R wrote a portion of the manuscript; Sachdeva N drafted the structure of the manuscript and edited the whole manuscript.
Conflict-of-interest statement: All the authors declare that there are no conflicts of interest associated with this manuscript.
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: https://creativecommons.org/Licenses/by-nc/4.0/
Corresponding author: Naresh Sachdeva, MSc, PhD, Professor, Department of Endocrinology, Post Graduate Institute of Medical Education and Research, Endocrinology Lab, Research Block-B Post Graduate Institute of Medical Education and Research, Chandigarh 160012, India. naresh_pgi@hotmail.com
Received: September 17, 2022 Peer-review started: September 17, 2022 First decision: October 30, 2022 Revised: December 27, 2022 Accepted: February 15, 2023 Article in press: February 15, 2023 Published online: March 2, 2023 Processing time: 165 Days and 0.1 Hours
Abstract
Type 2 diabetes (T2D) is a multifactorial metabolic disorder affecting more than 450 million people across the globe. With the increasing prevalence of T2D and obesity, the role of fat accumulation at sites other than subcutaneous adipose tissue has received significant attention in the pathophysiology of T2D. Over the past decade and a half, a pressing concern has emerged on investigating the association of pancreatic fat accumulation or pancreatic steatosis with the development of disease. While a few reports have suggested a possible association between pancreatic fat and T2D and/or impaired glucose metabolism, a few reports suggest a lack of such association. Pancreatic fat has also been linked with genetic risk of developing T2D, prediabetes, reduced insulin secretion, and beta cell dysfunction albeit some confounding factors such as age and ethnicity may affect the outcome. With the technological advancements in clinical imaging and progress in assessment of pancreatic beta cell function, our understanding of the role of pancreatic fat in causing insulin resistance and development of various etiologies of T2D has significantly improved. This review summarizes various findings on the possible association of pancreatic fat accumulation with the pathophysiology of T2D.
Core Tip: The concomitant rise in the incidences of obesity and type-2 diabetes (T2D) has increased interest in understanding the role of pancreatic fat accumulation or pancreatic steatosis in causing T2D. In the past few years, various researchers have attempted to decipher whether pancreatic fat has any causative role in the pathogenesis of T2D. While a few cross-sectional and retrospective studies have shown a positive association between pancreatic fat and T2D, there is a lack of well-controlled, prospective, and long-term follow-up studies that could clearly establish the role of pancreatic fat in causing T2D. Therefore, in light of the presently available evidence, the role of pancreatic fat as an independent predictor of T2D must be interpreted with caution.
