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Research Paper|Volume 15, Issue 16|pp 7909—7921

Reorganization of pancreas circadian transcriptome with aging

Deepak Sharma1, Caitlin R. Wessel1, Mahboobeh Mahdavinia2, Fabian Preuss3, Faraz Bishehsari1,4,5
  • 1Rush Center for Integrated Microbiome and Chronobiology Research, Rush University Medical Center, Chicago, IL 60612, USA
  • 2Division of Allergy and Immunology, Department of Internal Medicine, Rush University Medical Center, Chicago, IL 60612, USA
  • 3University of Wisconsin-Parkside, Department: Biological Sciences, Kenosha, WI 53144, USA
  • 4Department of Internal Medicine, Division of Gastroenterology, Rush University Medical Center, Chicago, IL 60612, USA
  • 5Department of Anatomy and Cell Biology, Rush University Medical Center, Chicago, IL 60612, USA
Received: May 31, 2023Accepted: July 11, 2023Published: August 29, 2023
https://doi.org/10.18632/aging.204929

Copyright: © 2023 Sharma et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

The evolutionarily conserved circadian system allows organisms to synchronize internal processes with 24-h cycling environmental timing cues, ensuring optimal adaptation. Like other organs, the pancreas function is under circadian control. Recent evidence suggests that aging by itself is associated with altered circadian homeostasis in different tissues which could affect the organ’s resiliency to aging-related pathologies. Pancreas pathologies of either endocrine or exocrine components are age-related. Whether pancreas circadian transcriptome output is affected by age is still unknown. To address this, here we profiled the impact of age on the pancreatic transcriptome over a full circadian cycle and elucidated a circadian transcriptome reorganization of pancreas by aging. Our study highlights gain of rhythms in the extrinsic cellular pathways in the aged pancreas and extends a potential role to fibroblast-associated mechanisms.