Abstract

Although intestinal trefoil factor (ITF) can alleviate the burn-induced intestinal mucosa injury, the underlying mechanisms remains elusive. In this study, we investigated if ITF alters glutamine transport on the brush border membrane vesicles (BBMVs) of the intestines in Sprague-Dawley rats inflicted with 30% TBSA and the underlying mechanisms. We found that ITF significantly stimulated intestinal glutamine transport in burned rats. Mechanistically, ITF enhanced autophagy, reduces endoplasmic reticulum stress (ERS), and alleviates the impaired PDI, ASCT2, and B0AT1 in IECs and BBMVs after burn injury likely through AMPK activation. Therefore, ITF may protect intestinal epithelial cells from burn-induced injury through improving glutamine transport by alleviating ERS.

Highlights

  • Intestinal trefoil factor (ITF) can alleviate the burn-induced intestinal mucosa injury, the underlying mechanisms remains elusive

  • The results showed that the total transport abilities of Gln in brush border membrane vesicles (BBMVs) and intestinal epithelial cells (IECs) were significantly reduced after burn injury (P < 0.05) (Fig. 1a,d), and that sodium-dependent Gln transport was especially attenuated (P < 0.05) (Fig. 1b,e)

  • Glutamine in the intestinal lumen is transported to IECs mainly through microvilli that are neatly arranged in the brush border[42]

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Summary

Introduction

Intestinal trefoil factor (ITF) can alleviate the burn-induced intestinal mucosa injury, the underlying mechanisms remains elusive. A series of studies have confirmed that Gln administration can significantly improve intestinal energy metabolism and promote ATP production in the postburn animals and patients, thereby alleviating intestinal mucosal injury and promoting mucosal repair[6,7,8,9]. Our previous study revealed that intestinal trefoil factor (ITF), an intestine-specific growth factor, can significantly improve the bioavailability of Gln when administered intragastrically to the burned animals[26]. It remains unclear whether ITF exerts this effect by modifying intestinal Gln transporters though ERS alleviation in IECs after burn injury

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