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Updated: Jun 24, 2026

Assessment of Glutamine as a Fuel Source for Alveolar Macrophages Exposed to Chronic Ethanol Using an Extracellular Flux Bioanalyzer

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Glutamine attenuates nitric oxide synthase expression and mitochondria membrane potential decrease in

Jun Lu¹, Xin-ying Wang, Wen-hao Tang

¹General Surgery Department, Zhongda Hospital, Jiangsu Key Lab of Molecular and Function Image, Southeast University, Nanjing, China.

European Journal of Nutrition

|April 7, 2009

Summary

This summary is machine-generated.

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Nitric Oxide Signaling Pathway

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Nitric oxide (NO), an inorganic gas, acts as a potent second messenger in most animal and plant tissues. NO diffuses out of the cells that produce it and enters the neighboring cells to generate a downstream response. NO synthase (NOS) catalyzes NO production by the deamination of the amino acid arginine. There are three isoforms of NOS. Endothelial cells have endothelial NOS (eNOS), nerve and muscle cells have neuronal NOS (nNOS), and macrophages produce inducible NOS (iNOS) upon exposure to...

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Glutamine (Gln) protects liver cells from inflammation by reducing nitric oxide (NO) overproduction and preserving mitochondrial function. This study suggests Gln may down-regulate inducible nitric oxide synthase (iNOS) gene expression via an NF-kappaB independent pathway.

Area of Science:

Hepatology
Mitochondrial Biology
Immunology

Background:

Mitochondrial dysfunction from nitric oxide (NO) overproduction contributes to organ failure in severe diseases.
Glutamine (Gln) is reported to modify inducible nitric oxide synthase (iNOS) gene expression, potentially mediating its beneficial effects in critical illnesses.

Purpose of the Study:

To evaluate the effects of Gln on NO production, iNOS expression, and mitochondrial membrane potential (ΔΨm) in interleukin (IL)-1β-activated rat hepatocytes.
To investigate the role of nuclear factor-kappaB (NF-κB) in these processes.

Main Methods:

Primary rat hepatocytes were cultured and treated with IL-1β alone or with varying concentrations of Gln.
Nitrite, alanine aminotransferase (ALT), iNOS protein and mRNA levels, mitochondrial membrane potential (ΔΨm), and NF-κB activity were assessed.

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Last Updated: Jun 24, 2026

Assessment of Glutamine as a Fuel Source for Alveolar Macrophages Exposed to Chronic Ethanol Using an Extracellular Flux Bioanalyzer

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Published on: November 15, 2024

Main Results:

IL-1β increased NO production, ALT release, and iNOS expression, while decreasing ΔΨm. Gln dose-dependently inhibited these IL-1β-induced effects.
Gln significantly attenuated the IL-1β-induced decrease in ΔΨm.
IL-1β increased NF-κB activity, which was further augmented by Gln.

Conclusions:

Glutamine protects mitochondrial function in hepatocytes under inflammatory stress.
The protective effect of Gln may involve down-regulation of iNOS gene expression.
The mechanism appears to be independent of NF-κB signaling.