Effects of Obesity and Exercise on Pancreatic Oxidative Stress, Morphology, and Health

Abstract

Obesity is concomitant with hyperglycemic conditions and increased oxidative stress. Under hyperglycemia, thioredoxin interacting protein (TXNIP) causes increased oxidative stress and β‐cell apoptosis within the pancreas.Lean rats (LZR) and obese rats (OZR) were randomly assigned to control (n=12) and exercise (n=12) groups. Exercise LZR (n=6) and OZR (n=6) underwent 8 weeks of multi‐lane motor treadmill running for 60 minutes at 60–70% maximum determined intensity. Pancreas tissue was harvested at approximately 20 weeks and mounted on cork using OTC freezing medium.Pancreas sections of 8μm thickness were cut and collected on slides then stained using DAPI and Alexa‐Fluor 546 targeting primary insulin antibodies. Slides were then imaged using the Zeiss LSM 510 Confocal microscope and Zeiss computer software; islet area and β‐cell number were determined. Nitrate analysis was measured using the Sievers Nitric Oxide Analyzer (NOA 280) using pancreas lysates. The WES system was used for Western analysis of TXNIP protein quantification.Body mass, glucose and insulin were significantly greater in OZR vs LZR (p<0.05). OZR also had higher beta‐cell numbers and islet areas to LZR (Table 1), although not significant. There was an almost 3‐fold increase in TXNIP in OZR compared to LZR (p=0.03). OZR that exercised experienced an approximate 2‐fold decrease in TXNIP expression when compared to the OZR control (p=0.02). No difference was observed between OZR exercised and LZR control (p=0.18).This study showed an increase in the expression of TXNIP in the pancreas of obese compared to lean groups. Eight weeks of treadmill running was associated with decreasing the expression of TXNIP in OZR to almost the same level as the LZR controls, suggesting that exercise may be used as a means to reduce oxidative stress even in a hyperglycemic obese environment.Current studies are being conducted to further assess markers of oxidative stress and nitric oxide associated with these perturbations, as well as pro‐apoptotic markers within the pancreas.Support or Funding InformationNIHGMS 5U54GM104942‐03 (PDC)This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.