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Nicotinamide mononucleotide ameliorates hypertriglyceridemia pancreatitis via NAD⁺/SIRT1-mediated TXNIP suppression

Hongtao Duan¹, Rui Zhang², Aiminuer Asikaer¹

¹School of Pharmacy and Bioengineering, Chongqing University of Technology, Chongqing 405400, China.

International Immunopharmacology

|April 11, 2025

Summary

Nicotinamide mononucleotide (NMN) treats hypertriglyceridemia-induced acute pancreatitis (HTG-AP) by protecting pancreatic cells and resolving inflammation. NMN therapy shows promise for HTG-AP treatment and repair.

Keywords:

Hypertriglyceridemia pancreatitis NOTCH Nicotinamide mononucleotides SIRT1 TXNIP

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Published on: December 2, 2022

Area of Science:

Biochemistry
Cell Biology
Immunology

Background:

Hypertriglyceridemia-induced acute pancreatitis (HTG-AP) is a severe condition that hinders pancreatic healing.
Nicotinamide mononucleotide (NMN), a NAD+ precursor, is used to restore NAD+ levels, but its role in HTG-AP is unknown.

Purpose of the Study:

To investigate the effects of NMN on HTG-AP.
To elucidate the underlying mechanisms of NMN action in HTG-AP.

Main Methods:

Bioinformatics analysis and in vivo experiments in mice.
In vitro studies using pancreatic acinar cells and macrophage cell lines (BMDM, RAW 264.7, THP-1).
Assessment of mitochondrial function, cellular injury, inflammatory markers, lipid levels, ROS, and macrophage polarization.

Main Results:

NMN protected pancreatic acinar cells from lipid-induced injury by suppressing TXNIP via NAD+/SIRT1 signaling.
NMN treatment reduced pancreatic injury, inflammation, serum lipids, and ROS in mice.
NMN inhibited the NOTCH pathway, promoting M2 macrophage polarization and enhancing inflammation resolution.

Conclusions:

NMN ameliorates pancreatic injury in HTG-AP through NAD+/SIRT1-mediated TXNIP suppression.
NMN influences macrophage polarization via NOTCH inhibition, offering a potential therapeutic strategy for HTG-AP.